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Commercially available BDNF is human recombinant protein. Can you use it for stimulating primary neuronal cultures of mice and rats? If yes, what is the basis of this cross species activity?
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The BDNF protein has more than 95% sequence similarity among human, rat and mouse. In theory, it can be used to stimulate rat and mouse cells.
By the way, CUSABIO has the recombinant human BDNF work for you. Activity validated. Maybe it works for you.
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I will really appreciate it if somebody could share the software. My lab owns the stimulator but when we acquired it we didn't get the software nor the drivers. Grass doesn't exist anymore and "Natus" which is the company that bought it told me that "S88X" is a discontinued product and they do not longer provide support for it.
Its crucial for us to control the device from a PC.
Thanks in advance
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Hi David Martínez-Vargas Janelle M Fine Eric Kenji Lee ! Do any of you still have the Grass S88X Stimulator driver and software? If yes, can you please send it to me at apoorvar@umich.edu? Many thanks!!
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How do you research and bring work together?
You may use the technique of consilience without knowing it.
Read this definition and then let me know how you use consilience in your work.
Highlights:
In science and history, consilience (also convergence of evidence or concordance of evidence) is the principle that evidence from independent, unrelated sources can "converge" on strong conclusions. That is, when multiple sources of evidence are in agreement, the conclusion can be very strong even when none of the individual sources of evidence is significantly so on its own. Most established scientific knowledge is supported by a convergence of evidence: if not, the evidence is comparatively weak, and there will not likely be a strong scientific consensus.
The principle is based on the unity of knowledge; measuring the same result by several different methods should lead to the same answer. For example, it should not matter whether one measures distances within the Giza pyramid complex by laser rangefinding, by satellite imaging, or with a meter stick – in all three cases, the answer should be approximately the same. For the same reason, different dating methods in geochronology should concur, a result in chemistry should not contradict a result in geology, etc.
The word consilience was originally coined as the phrase "consilience of inductions" by William Whewell (consilience refers to a "jumping together" of knowledge).[1][2] The word comes from Latin com- "together" and -siliens "jumping" (as in resilience).[3]
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Dear Colleague Michael Marek,
Yes, this is so often the case. My husband who is an active observational planetary scientist says how often the "devil" is in the details of data analysis.
Our short story collection, Children of Steel, is being considered by Wayne State UP, BTW. It is a collection of short fiction by people who grew up in steel mill towns. I just noticed where you retired from teaching.
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I tried several approaches from different publications that describe in the methods section that PCPA (http://www.sigmaaldrich.com/catalog/product/sigma/c6506?lang=en&region=GB) was dissolved in 10N NaOH and the pH was then neutralised with HCl. But it did not work out for me.
I would be so grateful if anyone could explain me how exactly he/she managed to dissolve it.
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I am using saline with 2% Tween 80 for ip injections. It is still not perfect, you must homogenize the solution before each injection, but it is far more soluble than saline alone.
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The role of astroglia in brain function has been well studied since the use of fluorescence microscopy (in vitro and in vivo two-photon imaging) began in the 1990's.
Verkhratsky and Needergaard (2018) have shown, beyond reasonable scientific doubt, that astrocytes control chemical homeostasis in the whole brain. However, the role of calcium waves in this control of homeostasis is still not consensual among the experts.
The existence of large-scale calcium waves has been proven and imaged 'in vivo' with two-photon fluorescence microscopy. Thrane et al (2012) showed that general anesthetics selectively eliminate these waves. Recently the structure of these waves has been imaged and analysed, but their function(s) is (are) still not well identified.
References:
Thrane AS, Rangroo Thrane V, Zeppenfeld D, Lou N, Xu Q, Nagelhus EA, Nedergaard M. (2012) General anesthesia selectively disrupts astrocyte calcium signaling in the awake mouse cortex. Proc Natl Acad Sci U S A.109(46):18974-9.
Verkhratsky A, Nedergaard (2018) M. Physiology of Astroglia. Physiol Rev. 98(1):239-­‐389.
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The "paradox" above appears because astrocytes control brain homeostasis according to the valence of the stimulus. Therefore, excitation can be turned into inhibition, or vice-versa, according to the adaptive process in which the brain responds to stimulation, moves away from homeostatic equilibrium, and then reaches a stable region far from equilibrium, or recovers equilibrium after crossing a unstable phase. I mentioned this type of process in my 2010 paper with Furlan:
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I need to assay dopamine, noradrenaline and serotonin of rat brain during my research project, but I couldn't find ELISA kits which are suitable for rat brain samples.
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ELISA kits for dopamine and noradrenaline is still elusive. Right now HPLC is the best option.
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I have some EDA data from a colleague's project that I want to analyze. Looking into the data, I discovered that the sampling rate is relatively low - it is only 2 Hz. However, the literature I read suggested that the sampling rate should be at least 200 Hz. So, it seems the sampling rate is not high enough for analyzing the phasic components of EDA. Still, as I am completely new in the field of EDA, I would like to ask for your opinion:
Can I still conduct meaningful analysis of phasic SCRs?
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Indeed it is a low sampling ratio but even VarioPort, which is used for multi-channel physiology recordings in laboratory and ambulatory setups, has 25Hz frequency for EDA. Empatica E4 which is medically certified has sampling rate 4Hz. So, I am wondering which device could provide such a high ratio for EDA. What is more, the quality of physiological measurements may be affected by many factors (filtering process, inappropriate placement of sensors, movements during recording, alcohol or caffeine consumption, etc) except from sampling ratio.
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Please feel free to point me at papers, lecture notes, and books that would cover the basics as to allow a non specialist to start engaging with people whose occupation is to understand links between nervous system and behaviour in small animals / organisms (worms, insects, reptiles would be a good start).
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Hi again Herve,
Here are two short articles by Paul Katz- a former President of the ISN- one about the field itself, and the other a kind of "review" of the International Congress of Neuroethology that took place in Sapporo in 2014.
Enjoy!
Peter
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In specific could stimulation of the right DLPFC have a different effect to stimulation of the left hemisphere?
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Nice Contribution Michael A. Hunter
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Corpus callosum is the main bond between the brain’s left and right hemispheres. It is sometimes damaged or cut out because of a disease, this is called split brain, in this case the two halves of brain do not exchange information efficiently. In one experiment a word was flashed briefly to the right field of view of a split brain patient and the patient was asked what he saw and because the input from the right field of view is processed by the left hemisphere which is also responsible for verbal processing the patient’s answer matched the word, next the word was flashed to his left field of view and the experiment was repeated and the patient said that he did not see anything but when he was asked to draw a picture with his left hand he drew a picture of the word. The question is are there some stimuli in our environment that we can’t sense but affect our decisions? In other words do we decide or our behavior may be a reaction to the things that we are not aware of?
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It seems similar to what is told to happen in hypnosis: telling a person to do something after hypnosis, that person ( sometime) can do it after hypnosis without remembering the order.
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I am trying to design carbonate apatite nanoparticles that might cross the endothelial layer of brain capillary (blood brain barrier-BBB). Thus, an in vitro system would be a better option (easy to understand and faster) to check the permeability of particles before moving to an in vivo model. I am looking for an in vitro BBB system that can be used for this purpose. I have seen the co-culturing systems discussed by many researchers. Are the co-culturing system with the filter available commercially?
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You can look up Mimetas and easily make a BBB model with their OrganoPlate https://mimetas.com/overview-mimetas-applications/human-blood-brain-barrier
There was a paper published in February this year in Scientific Reports with this platform: https://www.nature.com/articles/s41598-018-20876-2
Hope it helps!
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the recent researches have shown that blind people react(smile) to the smile of a person in front of them. how this connection occures?
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Professor Zeashan Khan,
Thank you very much.
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I want to create separate masks for right and left hemispheres of the following regions:
ventro medial prefrontal ctx (vmPFC), dorso medial prefrontal ctx dmPFC), anterior middle cingulate ctx (mACC), posterior cingulate (PCC), precuneus (PC), inferior parietal lobule (IPL) and hippocampus (in parts if possble).
Any advice on which FSL atlas I could use greatly appreciated
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Hi Sean,
Sure, see attached. The readme file has the necessary info to create the ROIs. All the best!
-Ranga
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Hello,
I'm trying to image neurons every 15 min for 24 hours. My neurons don't even get past the 6h mark before dying. 
I plate my neurons on precoated ibidi chambers and use Dil at 5ul/1ml from 1mM stock with an incubation time of 5 minutes. After labeling, I replenish with fresh media plus some of the old media (growth factors) with added FBS. I've been adding 10% FBS because a neighboring lab found that longterm imaging without FBS of labeled neurons can cause the neurons to die.
The causes of death I'd like to rule out are (1) FBS or (2) Dil concentration/incubation time. Previously I had been imaging via phase contrast with phenol red in my media and that didn't seem to harm the neurons (although this was a 12 hr time lapse). 
If anyone can help me out I'd greatly appreciate it!! Thanks!
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 Hi Angelica,
Depending on the specifics of your experiment, you might also try doing transient transfection of a membrane bound fluorophore (e.g. mGFP https://www.addgene.org/14757/). I've done such transfections in on primary neural culture using CaPO4 method and Lipofectamine. In each case, the key was to optimize concentrations and incubation.
Best of luck, 
Joey 
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Two papers are using the method.
One attached and the other cited here: "Single rodent mesohabenular axons release glutamate and GABA" Root et al  2014
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Supplemental figure 3 and supplemental text from "Cho JH, Deisseroth K, Bolshakov VY. Synaptic encoding of fear extinction in mPFC-amygdala circuits. Neuron. 2013 Dec 18;80(6):1491-507." have a very nice explanation of the logic behind using TTX and 4-AP isolating monosynaptic inputs. They also show a positive control in which disynaptic inputs are not rescued by 4-AP. Here is a link to their supplemental materials: 
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Can we infer levels of one from the measures of the others?
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Dear Andrea, epigenetics certainly plays a role in regulating BDNF promoters activity. If you are interested in this topic, you may see these papers (among others). Kind regards, Enrico
Mallei A, Baj G, Ieraci A, Corna S, Musazzi L, Lee FS, Tongiorgi E, Popoli M. Expression and Dendritic Trafficking of BDNF-6 Splice Variant are Impaired in Knock-In Mice Carrying Human BDNF Val66Met Polymorphism. Int J Neuropsychopharmacol. 2015 Jun 24;18(12)
Chen KW, Chen L. Epigenetic Regulation of BDNF Gene during Development and Diseases. Int J Mol Sci. 2017 Mar 6;18(3).
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Reading papers I've found out that most interneurons express Calbindin, Calretinin and Parvalbumin, however I've also read that some pyramidal neurons do so as well, so I'm not too sure about using those genes for a interneuron molecular marker.
My intentions are not to study interneurons directly, but rather to localise them to rule them out of my actual research questions, that are related to pyramidal neurons.
Do you know of an interneuron molecular marker that:
1. Is expressed in most interneurons at developmental times AND
2. Is not expressed in pyramidal (excitatory) neurons
Thanks in advance!
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Hi Sebastian
The markers you mention (parvalbumin, calbindin and calretinin) may be useful in marking cortical interneurons but, as you correctly mention, they stain some excitatory neurons, particularly in the thalamus. We typically use GAD65/67 to label GABA-ergic interneurons, and ChAT to identify cholinergic interneurons of the striatum. I don't recall ever looking at glycinergic interneurons.
We previously attempted to use several different CAMKIIa antibodies to label cortical pyramidal neurons without success due to its presence in some neurons without a pyramidal morphology (perhaps it marks projection neurons generally rather than pyramidal neurons specifically?).
I hope you find this helpful.
Best wishes,
Daniel
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Does anyone know the best method to quantify cell viability/cell death in DRG neuronal primary culture from mice? One can it be detected with a change in morphology? I am looking for some colorimetric or flourescence based assays. I looked up some literature, and many have tried the MTT assay, but I am looking for something specific for neuronal cells. Any help will be appreciated in this regard.
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Dear Jagadeesh, I agree with Swati, you can use PI. I suggest another method, the double labelling of cleaved caspase-3(apoptosis) and MAP-2 (neurons). Thus, you can quantify by fow cytometry or by IF.  
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I am designing a stimulator for both muscle and cortical neurons stimulation to be used in physiology laboratory and after reading some papers I am still a bit puzzled about the best range of some of the parameters related to the outputs such as:
1.range and resolution of the amplitude of the output current ( I am using a 16-bit DAC)
2. maximum compliant voltage required to be adequate for the stimulation with most of the electrodes (in most cases it is mentioned that 12 volts is enough , although 80 or 100 volts has been mentioned in some other cases due to high impedance electrodes).
PS. 
I know that the amplitude of the output current depends on the distance of the electrode tip from the nerve and also the fact that the pulse duration also influences the proper amplitude.But I still need to know the best range for different applications.
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FYI, the stimulator I normally use for human muscle stimulation is the Digitimer DS7AH. We require the electrode-tissue impedance to be 10 kOhm or less when measured at 30 Hz. It typically is in the 5-10 kOhm range. Though in my previous post I said that some persons require up to 600 mA to optimally stimulate their quadriceps, most persons rarely require more than 400 mA. I also forgot to mention that we use a pulse duration of 0.2 ms.
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Hi,
We are working with an in vitro model of blood brain barrier (BBB) using bEND3 cells and oxygen/glucose deprivation procedure to study the BBB damage during a cerebral ischemia. We have realised that there is an important variability between plates and even between wells in the same plate. Is there someone with the same problem? Any idea?
Thanks for your answers,
Pau
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What are your end point measurements?
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Many of the epilepsy syndromes have their seizures linked to circadian rhythm like Infantile spasms, Benign rolandic epilepsy, Juvenile myoclonic epilepsy?
What happens in the body physiology particularly in the first 30 to 180 minutes upon awakening that lead to increase cortical excitability and hence the seizure occurrence? 
Is it hormonal like the cortisol awakening response ?
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Thanks Chaitra_Ramachandraiah
The paper was more descriptive of the Chronodependency in JME but yet it did not discuss why IEDs and seizurez do occur upon awakening !!
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In axons, action potentials can move both in ortho-dromic (normal) direction as well as in anti-dromic direction, if stimulated in the right way. But what happens if two action potentials are generated simultaneously, one in the distal axon end and one at the soma, that are moving towards each other to collide? Will they penetrate (move past each other) or annihilate?
According to classical Hodgkin-Huxley model and theory of neurophysiology they will annihilate due to the in-activation of the sodium conductance. This effect has also given rise to the experimental method called "the collision test", which is used to confirm axon projection from one brain region to another by means of antidromic stimulation. 
Nevertheless, a recent paper claims that two colliding action potentials will penetrate just as two colliding waves on a sea of water:
My question: Does anyone know the original literature about collision of action potentials? This must be back in the 1950'ties or 1940'ties. Who did the investigation and what are the publication references?  I have been trying to find the original papers, because I am sure that scientist investigated this back in those days. The only one I could find was this:
I. Tasaki, Collision of Two Nerve Impulses in the Nerve Fiber, Biochim. Biophys. Acta 3, 494 (1949).
thanks,
Rune
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Hello everyone.
Finally our rebuttal comment has been accepted for publication in Physical Review X, almost 2 years after our first submission. We could not reproduce the observation of penetration of action potentials by the Heimburg group. Instead we consistently observed annihilation of colliding action potentials.
Further we show that their measurements of action potential velocity was flawed and indicate that their measurement electrodes were so close to the stimulation electrodes, that 1) they could not contain two action potentials 2) passive propagation may explain part of their observations. 
Also, they did not demonstrate the All-or-none property of action potentials, which again suggest that they observe either activation of multiple nerves, or they generate passive electric signals. Attached is preprints and supplementary information.
Cheers!
Rune
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I have a trouble to carry out cerebellar slices in the cryostat. I have samples embedded in tissuetek and I'm cutting slices of 5 to 20 micrometers. However, the majority of slices has many holes. This is a trouble because I need to detect an a injury (with a tincion process, in the myelin), but if all whole sample its full of this holes I cant detect anything, in fact is like if all cerebellum has injury. The blades are new, I use 25-30° for cut and I use an antiroller (I haven't paraffin, then I use tissuetek). At beggining (one month ago aprox) the slices were fine, I mean, the cutting process was the same and the results are fine, but now I have this situation. Somebody can help me and giveme tips?
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Hi Abraham, there are several reasons why you are getting slices of poor quality. Firstly, check and make sure that your solutions are fresh and peoperly prepared (concentration and pH). Both, old PFA and wrong molarity of PBS may screw-up the quality of your slices. Secondly, make sure that the perfusion rate is not too fast. Check the literature and make adjustments according to the animals you use. Third, post-fixation i.e. keeping too long in PFA and poor dehydration prior to slicing can deteriorate the quality of your sections. The presence of water in frozen brain tissue can tear the tissue on parts. It is important therefore that the material is kept in sucrose until it floats to the surface. Finally, adjust the temperature of the cryo slicer as over-freezing the tissue may cause its breakage. If you follow these steps, the holes should vanish as they came. Best luck with your slices and let me know how you progress, SV
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Dear all,
I was wondering if anyone of you know of a comparative study between hardwired (cable) sleep measure and telemetry. Specifically, my interest is to know whether sleep stages are affected by being attached to a cable and if then the results are reliable.
Thanks,
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I would say telemetry is for sure better
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We have mice expressing a Flag-tagged protein (only one flag epitope) at endogenous levels. We have major problems (non specific labeling; particularly strong in the olfactory bulb) with most antibodies in our perfusion-fixed brain sections. Anyone has ever used anti-FLAG antibodies to label mouse brain proteins? Any advice? Best fixative to be used? Aware of a specfiic antibody?
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Dear Ivan,
no, we have never been able to solve this problem. Sorry I cannot help at the moment.
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Would like to know the feasibility and actual depth (areas of the brain) which could be reached with rTMD
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Dear Peter, as far as I know TMS acts by inducing an electrical field in the brain (i.e. spatial distribution of voltage) which in turn will produce electrical current depedning on the resitence that it finds. It is thought therefore that large collections of CSF may facilitate the presence of induced current. It has been long thought that in the interhemispheric fissure an efficient current could be developed in deeper structures than in the brain parenchima, probably due to the width of the inter-hemispheric sulcus. In older literature the induction of phosphenes was taken as a good measure of how deep stimulation can go in the inter-hemispheric fissure. Indeed, given the peculiar distribution of the retinotopic representation in V1, the wider the angle of the phosphene, the deeper you go with TMS. According to this view, depth of stimulatn was considered as much as 4 cm. This has been however challnged in recent work on the possible origin from extra-V1 (V2 and V3) cortices of TMS-induced phosphenes. In other words, there is little empirical data that can answer your question. You may find several works claiming that supplementary and pre-supplementary motor areas, with compatible behavioral effects. Putting together these data it seems that with conventional figure-of-8 coils you may reach as far as around 2 cm from the brain surface (my opinion! Not demonstrated!) You probably may find a better answer looking at the literature on modeling the electrical current (not electric field) in realistic brain models, whcih unfortunately  don't know much about. Good luck.
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Hello, all. My areas of research are memory and neurodegeneration, and I am not very well versed in the HIV-related dementia/HAND literature. So, if there is someone here reading this that is, I would be grateful for some feedback.
Basically, we have some data showing a strong correlation between a (relatively) novel memory measure we have been developing (recency ratio) and CD4 count, thus suggesting this memory measure is sensitive to infection levels. Of note, this is independent on general cognitive ability (MMSE) and was measured in a relatively young population. Also, CD4 does not appear to be correlated significantly with other measures of memory in this sample, including immediate recency (which has been reported in several papers before as a typical sign of cogntive impairment in HIV).
My question is: Is this finding of interest beyond simply reporting another cognitive correlate of decline in HIV? Is there any utility in this cognitive marker for screening and/or clinical assessment?
Thanks,
Davide
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HIV is associated with difficulties in many cognitive domains, including short term memory which eventually gets consolidated into long term memory and learning.
A full screen for cognitive functions is essential for all HIV patients, especially those that can expose themselves or others to harm from cognitive impairment.
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Currently, I'm using mT/mG reporter mice to check the cre activity of this Ert2 cre mice.
mT/mG mouse is supposed to autofluoresce without any additional staining or immunohistochemistry necessary. Nestin.CreERT2 is the transgenic mice that express CreERT2 under the control of the nestin promoter and enhancer. the cre will become activated by administration of tamoxifen.
After the cross breeding, my study is about neonatal brain,so the fist IP inject at P6 of pups, 0.25mg per body weight. 48h later, the second IP injection at P8, then 24h later, the P9 pups were perfused with cold 0.9% saline. After brain dissociation, brains were fixed 24h in PFA at 4, cryoprotected in 30% sucrose overnight at 4, and embedded in OCT for cryosection. 20 micrometer sections were mounted on slices directly.
the problem is I cannot see any fluorescence signal by using a traditional fluorescent microscope, even without any red fluorescence (mT, tdTomato), I'm thinking do I expose the slice in light a long time? Does this effect a lot? Is there some problems of the microscope? is it better change to confocal? Do I have some problems about the administration, such as the duration, the amount?
ANY SUGGESTIONS WILL BE APPRECIATED ?
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Hello Tao,
I don't know exactly which reporter line you are using, but are you sure that killing the animals 3 days after the first injection is enough time to have detectable expression of your reporter? For my experiments using inducible Cre lines I normally wait a week after injecting tamoxifen to have strong labelling.
Also, keep in mind that Nestin is only expressed in neural progenitor cells, and that depending on the timing of induction you will label different cells. Since you are injecting tamoxifen postnatally, when most of the neurogenesis is done, you will probably only label a small number of cells.
Look at Fig 1D of the following publication to have an idea of where you would expect to see labelled cells. Your samples should look be similar to what is shown in panel d4 (tamoxifen injected at P7).
I hope this helps!
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the neuron differentiate from neurosphere in Neurobasal+B27+LG is less than in neurobasal. I wonder the effect of B27 in the medium.
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Dear Zhi,
I've used the B27 for my neurospheres as well as for Astrocytes and Neurons differentiation. I used 3% B27 (50X) from Gibco along with   0.5% N2 (100X), 1% ABAM, 1% glutamax, 1% BSA and EGF for the first stages of proliferation then I switch the media by just replacing the EGF with FCS (still with B27) for the differentiation stages.The media improved my cells viability and proliferation. Basically, the astrocytes differentiation was very normal and their viability was perfect in the media containing the B27.
Hope you're gap is solved soon.
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Can I use Tail suspension test to evaluate the antidepressant using Rat? As I saw that TST is mostly utilized in mice, but I am looking for an authenticated reference of the use of Rats (however very few papers I found) please help me regarding this? 
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No, you shouldn't use the tail suspension test in rats as they are too heavy to be supported by the tips of their tails, unlike mice. You are always recommended to lift rats by the base of the tail (i.e. near the body) and only for short periods of time (i.e. moving from one cage to another). I typically lift rats by the base of the tail and place onto my forearm, holding the base of the tail firmly to prevent the rat from jumping off but not bearing any weight on the tail. The tail suspension test involves leaving a mouse suspended by the tip of the tail for 5-6 minutes; doing this in a rat would cause much higher levels of stress and pain to the rat. This would most likely mask any antidepressant effect you may be looking for.
As Leonardo suggests, the forced swim test would be the standard test to use with rats in such studies. To complement the forced swim test you could also time the amount of time spent grooming in an open field test (spontaneous grooming) and in the splash test (induced grooming). Taken together, you should have a good idea of whether your treatment is having an antidepressant effect. Obviously do the open field and splash tests in advance of the forced swim test as you do not want the stress of the forced swim test to have an effect on other tasks.
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If one uses antibodies against VGLUT1 and synaptophysin to stain in WT cultured hippocampal neurons, one expects the immunosignals to co-localize, since both are synaptic vesicle specific proteins. how to explain the finding of solely vglut1 signals? I understand if I have only synaptophysin signals, maybe I thereby detected vgat expressing neurons, but synaptic vesicles that are positive for vglut1 and not stained with anti synaptophysin antibody?
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I am not surprized by negative syn terminals
for example VGLUT2 and VGLUT3 (on which we work) very poorly colocalize with syn
and only half a gaba terminals are syn-positive
with VGLUT1 I would estmate that around 20% of VGLUT1-positive terminals are syn-negative
How to explain it ?? I don't know for sure
1) if you look at these synaptic proteins they are heterogeneous not only between synapses but also inside synapses
2) as far as I know the role of synaptophysin is not clear
3) and we do not have a generic marker of all synpases
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We aim to prepare and stimulate acute brain Slices from different fish species. Does anyone know if this has been done before?
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Dear Ida,
In addition to wonderful comments above, if you decide to go ahead with vibratom slices, have a look at my methods paper below for detailed description of how to cut brain slices in mice. You may need the modify the extracellular solution and some of the procedures as suggested by Kjetil, but the general principles should be pretty much the same.
Best wishes, Refik
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Neoangiogenesis makes some contribution to brain-blood barrier deteriorations, and to the progressive escalation of chronic epileptic manifestations. That is why it is of interest to clarify question on the role played by neoangiogenesis in kindled seizures development.
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Dear Nirmala, thanks a lot for your letter and recommended addresses (!)
Sincerely, Leon
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Sensory information from our limbs (touch and proprioception) reaches somatosensory I cortex (SI) by making two synapses (one at cuneate nucleus (medula) and one at VPN of thalamus). I wonder how this information is used to build a body integrity identity. What are the other pathways between SI, SII and other cortical regions that have role in body integrity identity?
I want to note that I found lots of cognitive studies, but I mostly wonder about the basic physiology of body integrity identiy.
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I think it is not motor shaping or self-experiencing input. Rather a delicate EPSP/IPSP dance goes on between ascending and descending inputs to insure reproduction of successful movement and not failed ones. We found that partial deafferentation by dorsal column or dorsal column nuclei lesion causes causes a permanent lose of fine finger actions. However dorsal rhizotomy from C2 to T5 results in full recovery of hand movement. This may show that unblocked sensory input becomes motor disduptive noise. Eliminate the noise and forelimb manipulative control of the hand returns to the monkey
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Dear all,
I want to build neural network based of data provided by Allen institute of brain. Before this, i need to reduce multi compartment neuron to single compartment neuron. Can anyone have tips, articles or other things that can help me?
Best,
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I do believe it is quite complicated if ever possible at all. The problem with such reduction is that: in real neuron, non-linear dendrites do spacial-temporal integration. Multicompartment models tend to describe this process in details (see for example Jarsky et al, 2005). The reduction of a multicompartment model to a point model totally removes spacial component, and remains only the temporal integration. If you have a mathematical background, you should understand the limits of possible reduction a partial differential equation to a single ODE.
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My antibody: rabbit-anti 5-HT from ImmunoStar (#20080). I am working w/ rat spinal cord tissue (cryo, 20um, longitudinal sections). I can't get my protocol to work, so any advice would be greatly appreciated!
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Hi Emma,
Immunofluorescence / immunohistochemistry can be tricky and quantitative analysis of the results even more difficult.  Positive and negative controls are essential, especially if antigen retrieval protocols are used.  The first manuscript details IF on cryo sections of rat brain (not SC). 
I have attached some of our publications from which you can get a some idea of the different protocols for 5-HT IF, although none used the ImmunoStar Rabbit anti-5HT. We have used their Goat anti-5HT.  
R.S. Rahim, A.C.B. Meedeniya & D.I. Crane (2014) Central serotonergic neuron deficiency in a mouse model of Zellweger syndrome. Neuroscience, 274, 229–241.
R., Raghupathi, M., D., Duffield, L., Zelkas, A., Meedeniya, S., JH Brookes, T., Chen Sia, D., A Wattchow, N., J Spencer, D., J Keating (2013) Identification of unique release kinetics of serotonin from guinea-pig and human enterochromaffin cells. J. Physiol. 591(23):5959-5975.
Meedeniya, A.C.B., Brookes, S.J.H., Hennig, G.W. & Costa M. (1998) The projections of 5-hydroxytryptamine-accumulating neurones in the myenteric plexus of the small intestine of the guinea-pig. Cell Tissue Res, 291, 375-384.
Maria N. Nguyen, Brenton Cavanagh, Tavia Davenport, Anwar Norazit, Adrian Meedeniya (2010) Tissue sectioning for epifluorescence microscopy. In: Méndez-Vilas,A., Díaz, J. (Eds.) Microscopy: Science, Technology, Applications and Education, Vol. 2: 907-913, Formatex, Badajoz, Spain.ISBN (13): 978-84-614-6190-5.
All the best,
Adrian
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I wonder if there is any test of visual working memory good to test  children aged 6-12? Is there any good test for selective attention of children aged 6-12? I will be very appreciated if I can know the advantages of the recommended test over other tests and if I get a link to some references. Thank you so much!
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There are a few tests out there. The most notable ones that I know of are the Corsi Block Test, which tests memorization of visuo-sptial information and sequencing. The Visual Pattern Test (or Task) does the same but without the sequencing aspect. Some research has found that the Corsi test engages different cognitive functioning than the VPT due to the absence or presence of sequencing. Another task I just read about asks the participant to compare patterns to one provided, bringing in decision-making and more executive functioning, as opposed to raw VS working memory. Personally, I'll be using the VPT, because sequencing adds another layer of cognitive processing.
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I am trying to understand the relationship between the healthy aging process and the development of the blood brain barrier disruption which might lead to several neurodegenerative diseases such as Alzheimer's disease.
Finding a cure for such complicated diseases requires a good understanding of the underlying mechanisms that lead to the development of the disease and a healthy blood brain barrier plays a major role in preventing such diseases.
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Aging and BBB dysfunction is an interesting topic because its a high risk factor for developing neurodegenerative diseases. To my knowledge most of recent studies point at loss of tight junction proteins of the BBB with aging which is likely due to neuroinflammation. Infiltration of circulatory leukocytes and blood borne immunoglobines into the brain is a marker of BBB leakage that happens in aged humans. In aged mice however, only loss of TJ proteins of BBB was observed. I think its not clear which come first, neuroinflammation or BBB leakage. It could be systemic inflammation disrupts the BBB first and lead to infiltration of toxins to the brain that trigger neuroinflammation. Not sure if the brain itself with aging would autonomously initiate inflammation due to certain malfunctioning in metabolic processes and clearance pathways to remove waste byproducts !?.. I would love to here comments from experts in the field..
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I am currently working with the technical team at ACD Biosystems to resolve some background staining that I observe when using their fluorescent multiplex kit (http://www.acdbio.com/rnascope%C2%AE-multiplex-fluorescent-assay). I am hoping this method will allow me to measure knockdown of an shRNA-targeted mRNA. Unfortunately, the positive and negative controls are showing some background staining that is nonspecific. I would like to know if anyone else has worked with the RNA Scope protocol and could provide input on how things worked out for you. Thanks! 
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I would NOT recommend RNAscope for neuronal cell cultures. I was unable to get this to work and the company was very frustrating. I will try again since we bought it and can let you know if I have more luck. The company wanted me to essentially invest my time and money to troubleshoot/develop their assay..
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I am a beginner of electrophysiology. To block NMDAR, people always use D-AP5 or D-AP7, though it seems that D-AP5 is more commonly used than D-AP7. But as for AMPAR, it seems that CNQX, DNQX and NBQX are equally used. What's the difference between these three antagonists? How to decide which one is suitable in what kind of recording?
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Hi Aifang,
as you indicate all of them are AMPA receptor antagonists however they differ in their selectivity and potency.
CNQX. Blocks AMPA/kainate but it is also an antagonist at the glycine site in NMDAR
DNQX. It is a selective NON-NMDAR antagonist (kainate & quisqualate)
NBQX. Potent and selective AMPA antagonist, although it also works on kainate.
If you just want to block AMPA I would use NBQX.
Hope this helps,
Ezequiel
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We need to inject drugs into rat brain regularly, but that would do too much damage given to the needed frequency. We tried nano particle strategy and  those commercial SR pumps, but they didn't work well in our experiments. So I wonder if there's any other validated ways to inject the drug once and let it perform sustained release itself. Many thanks.
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have you heard of the Alzet brain infusion system? We have used them in mice and it is basically an Alzet mini osmotic pump which you insert subcutaneously on the flank which is attached to a guide canulae inserted into which ever brain region is desired. The ones we have used give constant infusion but I think you can get ones where you can programme drug delivery at set time points. http://www.alzet.com/products/brain_infusion_kit/index.html
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Dear all, we are now trying to set our Electrophysiology machine. The referred unit in litterature which provides the settings with the unit of log cd s/m2, but for our machine we can only set it in the unit of cd s/m2. Hence I would like to ask how to convert this log cd s/m2 to cd s/m2.
So here is the question:  -5.45 log cd s/m2
A. 10-5.45 cd s/m2;
B. 2-5.45 cd s/m2;
C. e-5.45 cd s/m2.
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The answer is "A".  Visual physiology/photometric units use a base 10 log scale. 
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DG , CA1, CA2 and CA3 absent in fish. 
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Distinct type of  " Purkinje cells " not seen in mammals 
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Hello everyone. 
We are intending to study the effect of TBI on BF neurons. I did some literature search and found both FPI and CCI model have been used for this purpose. Between these two models, which one will be more appropriate to study the BF? 
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Dear Nanthini Jayabalan,
Both models are adequate to study TBI as are both well described in rats and other animals. I think I would choose the CCI model for this purpose (BF) because it can produce a more localized injury. Please take a time to read this paper, it may be of value to you:
Best regards,
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I am trying to do a ROS assay in Drosophila larval brain using 30uM DHE. But I have no reference image to compare to. Also, since the sample is too thick, most of the staining is superficial. How can I troubleshoot this?
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Dear Sourajit Das!
You can try to do embedding process in fresh tissues and reduce the concentration of staining, inhibition time and do one more time for destining process. i will be good observation... all the best
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It is known that women have higher brain perfusion than men, but I'm strugling on finding reportes about mice in physiological conditions. I'm using 8-10 month mice and DCE-MRI, but evidence from any other technique or rodent would be of great value. Thanks in advance!
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Thank you for the reference, however it refers to vessel diameter and not cerebral blood flow. Since females have larger vessel, does the perfusion is also smaller?
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Immediately after brain isolation hippocampus was isolated and with the help of tissue chopper 300 micron thick slices were prepared. The slices were incubated at 32 c in ACSF for about 60 minutes.When we tried to record the data with MEA2100 system I did not find any spontaneous activity with the slice.
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We use MEA2100 and compared chopped and vibratome cut slices. Vibratome cut is healthier. We put weight on the slice (silver coil, platinum would be better for sure) when we do the MEA recording on non-perforatted MEA.
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There are dozens of various EEG-patterns, separated during investigations on brain's electrophysiology. But are there any clues or identified association between these patterns and the processes in neuronetworks (at logical or even biochemical levels)? The interest lies especially in the set of pathological EEG-patterns, such as spike-waves etc.
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I recomend reading this one and some other works by R.I. Machinskaya who is a great expert in visual analysis of EEG patterns and their comparison with behavioral and cognitive deficits in children of defferent ages
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I have arguments this structure is of nodal-setting kind. How much animal brain is accessible for such examination?
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Hello Renzo
The exact form, as smth common for all engrams, evidently may not be presented as a scientifical result. These are much different evidently. But it is my hypothesis there is for all that the common structural form for long-memory engramms -- the nodal-setting form. The question is whether it may be proved or disproved.
More about it is here:
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Wondering how many synapses are formed by individual axons from medial entorhinal cortex onto individual dentate gyrus granule cells.
Has anyone ever estimated this by any chance ?
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This is what I could find from Lopez-Rojas & Kreutz, 2016 (http://www.sciencedirect.com/science/article/pii/S0149763415303171):
Granule cells have some features that predestine them for a function in pattern separation. They exhibit an unusual low firing rate (Jung and McNaughton, 1993 and Pernia-Andrade and Jonas, 2014), theoretically increasing the probability that different granule cells will encode similar inputs, and they outnumber both their presynaptic entorhinal partners and their postsynaptic CA3 pyramidal targets by an order of magnitude (in rats there are around 112,000 principal cells in layer II of the entorhinal cortex, 250,000 CA3 pyramidal cells and 1,200,000 granule cells). A single granule cell also has synaptic contacts with a reduced number (like a dozen) of CA3 pyramids. This results in a divergence in the projection from the entorhinal cortex to the dentate gyrus and a convergence from the dentate to the CA3 (Amaral et al., 1990, Amaral et al., 2007 and Schmidt et al., 2012) and it allows for an orthogonalization of the information that the dentate receives from the entorhinal cortex while it is relayed to the CA3 region (Aimone et al., 2011, Kesner and Rolls, 2015, Sahay et al., 2011b and Schmidt et al., 2012). Substantial experimental evidence supports this computational function of the dentate gyrus (Bakker et al., 2008, Gilbert et al., 2001 and Goodrich-Hunsaker et al., 2008). Interestingly pattern completion, the ability to recall information from a reduced number of inputs and classically attributed to CA3 region, has recently also been related to the dentate gyrus (Kropff et al., 2015, Nakashiba et al., 2012 and Temprana et al., 2015).
And from Amaral, Scharfman & Lavenex, 2008 (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2492885/):
The dentate granule cell
The principal cell type of the dentate gyrus is the granule cell (Figs. 4 and and5).5). The dentate granule cell has an elliptical cell body with a width of approximately 10 μm and a height of 18 μm (Claiborne et al., 1990). The granule cell bodies are tightly packed together and, in most cases, there is no glial sheath interposed between cells. The granule cell has a characteristic cone-shaped tree of spiny apical dendrites. The branches extend throughout the molecular layer and the distal tips of the dendritic tree end just at the hippocampal fissure or at the ventricular surface. The total length of the dendritic trees of granule cells located in the suprapyramidal blade are, on average, larger than those of cells in the infrapyramidal blade (3500 μm vs. 2800 μm, respectively). Dendrites of cells in the suprapyramidal blade have 1.6 spines/μm, whereas dendrites in the infrapyramidal blade have 1.3 spines/μm (Desmond and Levy, 1985). Thus, an estimate for the number of spines on the average suprapyramidal granule cell would be around 5600 and for an infrapyramidal cell 3640. Since virtually all of the excitatory inputs to granule cells are on these dendritic spines, these numbers indicate the approximate number of excitatory synapses that dentate granule cells receive from all sources. As noted earlier, the total number of granule cells in one dentate gyrus of the rat is ∼1.2 × 106 (West et al., 1991; Rapp and Gallagher, 1996). Although neurogenesis in the dentate gyrus persists into adulthood, and appears to be under environmental control, modern stereological studies have shown that the total number of granule cells does not vary in adult animals (Rapp and Gallagher, 1996). This implies that there is a steady state turnover of granule cells rather than a continuous
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Some people claim that this is correct bcause physical variables (such as brain measures or so) don't change across the country
It doesn't seem right, but I'm not sure how to argue against this from a medical perspective (I can using social and cultural definitions, but I need something "harder" more related to medicine).
Can anyone give me a hand? :-)
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In the drug abuse research field, an important distinction is whether subjects are treatment-seeking or non-treatment-seeking.
Here's an example from non-drug-abuse psychiatry:
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Does anybody of you know where to find nice pictures giving more information about how the brain is structured in detail ? (Like this one in the link.)
Same question for Neurotransmitter systems. Is there a nice collection and summary of what is known so far ?
Thanks !
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If it helps, the picture you posted is one of Thomas Deerinck's pictures of the cerebellum - see link: 
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Compared to other kind of fonts in the early stages of the acquisition of the processes of reading and writing
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Hello 
I do really appreciate  your wide contribution to our search!
I will start reading the material.
thanx again!
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can anyone help me about whether excitatory neuron and inhibitory neuron are colocalized or their locations are nearby? especially on drosophila, thanks a lot
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Hi,
your first approach should probably be antibody staining. You may be able to co-stain for glutamate and GABA in Drosophila, although the antibodies we've recently used are both in rabbit (see Perisse et al., 2016 and Owald et al., 2015).
If you have identified the neurons and have driver lines for it, ideally you can use a GAL4 and LexA combination with GFP/RFP to unambiguously see their overlap/proximity. Using tools such as GRASP you can also see if they potentially synapse onto one another. In our recent paper (Perisse et al., 2016), we have successfully shown GABAergic inhibition onto a glutamatergic neuron by ways of odour-stimulating the glutamatergic neuron while at the same time optogenetically exciting the GABAergic neuron, which led to a marked decrease in activity of the glutamatergic neuron.
One last note: glutamatergic doesn't have to mean excitatory in Drosophila. Most excitatory synapses are probably cholinergic, and glutamate was shown to be potentially inhibitory (Liu et al., 2013).
Let me know if you have further questions.
Oliver
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In psychiatric genetics, are we looking at genetic influences to explicate the intermediary neurobiological mechanisms of a condition or are we looking at intermediary neurobiological mechanisms to explain genetic risk and heritability? Or are we taking both approaches and if so, which one is more sound in you opinion?
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I think we're way past nature vs. nurture in terms of scientific studying of pathophysiological process. Even monozygotic twin studies never show 100% concordance between the siblings. Therefore, I agree with Sara, proceeding with both approaches will bring far more significant results in terms of acquiring knowledge with real imapct that might bring better treatments or understanding of the nature of certain pathology.
Best wishes,
Karlo
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I'm interested in investigating the nuclear role of ChAT, however all the published information I've been able to find is for human ChAT in the nucleus.  Anyone know if mouse ChAT also traffics into the nucleus?  It does have a predicted NLS, but I haven't found any studies specifically identifying ChAT in mouse nuclei.
I'm new to neuroscience work, so this may be a well-known thing that I'm just oblivious to
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Dear Maureen,
How did the previous studies identified/localised ChAT in the nucleus? What methods did they use specifically. If it is just immunolabelling, I would be very sceptical about it. In unhealthy cells, the nuclear membranes are disrupted and permeabilised to let antibodies and probes in the the nucleus. See my previous discussions on that subject below.
best wishes, Refik
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Does anyone know of a brain bank or researcher that will have brain tissue from patients that were born preterm? Is it something that is recorded??
thanks!
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Thank you Validimir. However the question is about ADULT brain samples from people who were born preterm. The practical issues of banking and ethics I understand, but it's the precise samples that I am after.
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When the neuron fires, there is a slow accumulation of potassium in the extracellular medium. However, I couldn't find the exact time scale of accumulation of potassium accumulation with respect to the firing activity of the neuron. Please help me in this regard as to after how long of persistent activity does the extracellular levels of potassium starts prominently increasing (inspite of the glial buffering activity).
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extracellular potassium accumulation is modelled as part of the paper:
The Sodium-Potassium Pump Controls the Intrinsic Firing of the Cerebellar Purkinje Neuron
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when we perform brain slice culture of cerebellum parts, should I also include the brain stem together to culture? or just cerebellum? Thanks,
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I thick  your slides should be restricted to cerebellum, because the two differ with respect to cellular compositions and functions.
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Sphingosine-1-phosphate1 (S1P1) regulates various molecular and cellular events in different body parts. Its expression pattern and functions are also varied dependent upon the cells types where it is expressed. Does anyone have any information regarding the effect of S1P1 in brain vasculature? Specially in ischemic condition (many paper suggests activation of S1P1 is neuroprotective in ischemic condition, however they lack the discussion on effect of S1P1 in brain vasculature). So if you have any information regarding the S1P1 signaling in brain vasculature, please do share !!!
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S1PR1 is one of the targets of the multiple sclerosis drug FTY720 (Fingolimod). Here is a review article about S1P and S1PRs: http://www.hindawi.com/journals/mi/2016/8606878/
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Hello.
I need know the mechanism of action BD1063. Is antagonist of sigma 1 receptor but I can't find a paper whit mechanism.
Thanks for your time.
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Rebeca, busca la siguiente referencia ( see the next reference):
Behav Brain Res. 2016 Jan 15;297:196-203. doi: 10.1016/j.bbr.2015.10.013. Epub 2015 Oct 14.
Ethanol-related behaviors in mice lacking the sigma-1 receptor.
Valenza M, DiLeo A, Steardo L, Cottone P, Sabino V.
Saludos!
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I interviewed over 100 formerly unconscious patients.  regardless of cause, they reported and increase in consciousness when moved.  During some of the time, they appeared to be unconscious externally but could hear, understand and emotionally respond to what was being said but couldn't move.  Trying to find a physiological explanation.
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I guess, neural correlates for these happenings could be understood from a few combined aspects of 'Narcolepsy' (where patients even though appear to be physically unconscious or asleep, they are aware of their surroundings), and 'Sleep Paralysis' (where one is unable to move or speak while remaining aware and conscious of one's surroundings). If one look for neural regions in the brain responsible for these two disorders, one may get some clue as to what may possibly create the phenomena you observed.
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How can i cut slices of cerebellum in a good way? I think someone who studies neuroscience. 
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If you are sectioning mouse samples, use paraffin. For larger animals, e.g. Rhesus macaques, use cryo: dry ice and obviously a larger microtome.
AFIP has a very good explanation of the methodology. ISBN 1-881041-00X
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What is the mechanism for enhancement of plasma triglycerides (TG) after feeding unsaturated fatty acid rich vegetable oils such as olive oil and Nigella sativa oil. I have found increased levels of plasma triglycerides (TG) in rat models. What are the molecular mechanisms/systems that increase TG in blood.
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You can get your answer from the Chapter about "Aspects of fat digestion and metabolism" which is descritive in details in http://www.fao.org/docrep/v4700e/v4700e08.htm
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Thank you all for your nice and enthralling response. The articles will definitely help me.
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Dear RG members, there is a belief that we use a very small percentage of our brain -  is it true? or how else can we measure the level of usage of a brain of different people of different level of thinking capacity. is there a perfect standard methodology to really measure the usage percentage of a human brain?
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here's an answer I once posted to another forum:
As far as we can tell we always use our brain's full capacity.
The issue starts with that there does not exist a single measure of brain "usage" or "activity". Neural functioning can be measured on the scale of genes, proteins, single neurons, groups of cells, or entire brains. Neuroscientists look at blood flow, glucose use, oxygen use, neurotransmitter levels, number of action potentials, intensity of various brain rhythms, connectivity patterns between areas, and hundreds, if not thousands, of things more. Clearly, there is no single all-encompassing way of quantifying brain usage.
That said, distinct brain regions and cell types certainly vary in their levels of activity on many of these measures. Activity levels vary across time, and they vary with the particular task the organism is performing. Indeed, this variation reflects how the brain processes information: in a way, it's how the brain works.
For other brain regions we have less of an idea "what they're for". But it has long been recognized that some brain functions aren't localized to any specific region. Rather, these functions are distributed over many areas. So you may be able to cut away a certain piece of brain tissue without grave consequences, but you will have reduced the brain's overall capacity for information processing.
Also, more is not always better. Bigger brains aren't smarter. Moreover, much higher blood flow through the brain would result in blood vessel ruptures, greatly increased neurotransmitter levels are toxic to the brain (cells die), and when neurons all over the brain fire action potentials as quickly as they possibly can we call that an epileptic seizure.
All of this doesn't mean we can't try out new psychological/cognitive strategies that optimize or enhance our functioning somehow (presumably by rearranging the information flow in our brains). And yes, "zapping" the brain with electric or magnetic pulses as well as some drugs can impressively alter behavior. But "impressive" for neuroscientists usually means a 50 percent change (of whatever it is we're looking at) that lasts for as long as the stimulation is on, or however long the drug remains active. And naturally, scientists then only look at what's improved, not at all the brain functions that may simultaneously be taking a beating...
Finally, there's an evolutionary argument. The human brain uses a massive amount of energy compared to our other organs. And foraging for food is no joke. So it's very unlikely nature would have put in 90 percent of idle brain tissue unless we really desperately needed it in order to survive.
Great TED clip attached as link
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I used Open field plus sucrose preferential. However, I receive this question when I'm presenting my stress-depression animal model. One of the questioner, a professor ask me this as he is using a substance that greatly affected the mouse prefrontal cortex and the mouse barely move. 
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Dear Hafiz,
Indeed, open-field test is carried out to show the locomotor activity of rodents before Forced Swimming Test (FST) to show that despite the normal locomotion of animals they are immobile in the FST test. I added some reviews that are useful to better understanding the immobility behavior in the FST. Under acute unpredictable and unavoidable stressful conditions, depressed people get despair and hopeless and, in fact, FST mimics similar conditions for rodents in which immobility time is considered as a depressive-like behavior. The Tail Suspension Test is similar to FST as well. Also, Climbing behavior in FST reflects the activity of adrenergic system and swimming is associated with serotonergic system activity.
Cryan, John F., and Andrew Holmes. "The ascent of mouse: advances in modelling human depression and anxiety." Nature reviews Drug discovery 4.9 (2005): 775-790.
Cryan, John F., Rita J. Valentino, and Irwin Lucki. "Assessing substrates underlying the behavioral effects of antidepressants using the modified rat forced swimming test." Neuroscience & Biobehavioral Reviews 29.4 (2005): 547-569.
Slattery, David A., and John F. Cryan. "Using the rat forced swim test to assess antidepressant-like activity in rodents." Nature protocols 7.6 (2012): 1009-1014.
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I am working now in research,trying to understand, is there are difference between swimmer ,karate player and non athletes in brain activity p300. so i need some related study in this topic.
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I guess that literature has evidenced certain effects in P300 amplitude during simple oddball tasks across different exercised-populations. Moreover, those studies have examined other features such as latency and area under the curve (AUC). 
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Philosopher Merleau-Ponty claimed that the feeling Self is the living body or its flesh. In this case, a conjecture can be made that siamese brothers or sisters would not have opposite feelings simultaneously (as one being happy and the other sad). Do you know any data that could help to support or disconfirm this conjecture?
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Dear Alfredo,
There are no many EEG studies on Siamese twins.
We find the following:
H.G. LENARD AND F.J. SCHULTE. Polygraphic sleep study in craniopagus twins. Journal of Neurology, Neurosurgery, and Psychiatry, 1972, 35, 756-762 (however it is sleep, and twins are very small - may be self is not developed yet...)
To check your hypothesis it is interesting to contrast EEG of twins joint at somewhere in the body with EEG of twins joined at the head (craniopagus). Then again the effects may be different depending on which part of the brain is shared...
Check please the following link for the popular article and the video on twins joined at the head.
Several years ago we watched British documentary about adult twins (females) joined at the head (if we remember correctly they sheered frontal lobe). Nothing was told in this film about EEG... But what was interesting that they had different hair stiles and very different personalities. Each of them had her own room to rest with different stiles...
If you will find something please share it with us.
Best,
Alex & Andrew
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I have seen several patients who take vitamin B12 as a supplement who have developed insomnia. I am trying to find evidence supporting causality.
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I agree that unnecessary doses of vitamins of B-group may cause insomnia because of the extra-stimulating effect on the CNS.
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Dear all,
I would like to know if there is a proportion in the concentration of any compound to compare iv / ip / icv administration in a mouse model.
Thanks
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I think iv and ip sometimes can be the same. It depends on the solubility of the compound. The icv dose we used was more often 1/100 of the iv one. Again it depend how it passes over the liquor-brain barrier.
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I used to stain with VSD (RH1691 or RH1838) and record from a cortical area of the monkey brain two times a week (the monkey is behaving during the recording).
After about three months from the first staining (and the moment the dura mater is first opened), even if the brain still looks in a good shape, I often fail to record any good signal.
This problem persists even if I carefully remove the new transparent tissue layers that grow on the top of the cortex after the dura mater is chronically opened.
Does anybody know why it happens and how to avoid or recover from this problem?
(More details on the protocol I am using can by found in this paper
Slovin, H., Arieli, A., Hildesheim, R. & Grinvald, A. Long-term voltage-sensitive dye imaging reveals cortical dynamics in behaving monkeys. J. Neurophysiol. 88, 3421–3438 (2002).)
Thank you!
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Hi Giacomo, My guess is that the cortical tissue is undergoing chronic inflammation. We only have experience in rat but if the cortex is "irritated" e.g., touched, the staining becomes poor. Somehow inflammation reduces inter cellular spaces and prevent diffusion of dye molecules.  
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Since all the treatments that have been approved by the US Food and Drug Administration (FDA) for Alzheimer's. For example, cholinesterase inhibitors and memantine can help treat memory and thinking problems. But these drugs just help manage the symptoms and there is currently no cure for AD. I would like to hear from you what makes it that hard to find a cure and are we close to finding a treatment for AD!
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1. If you don't know the cause, you can't find a cure.2. Make sure you aren't adding to the significant misdiagnosis figures by failing to rule out dementia mimics.
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I post fixed rat brains in a 4% formaldehyde solution (10X the volume of the brain) but I don't know the optimal time for this fixation step.
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Dear Sissoeff,
If you perform cardiac perfusion/fixation, your post-fix duration of 4% paraformaldehyde depends on what you are looking for. For example, in our experiments we follow IHC of tight junction proteins, GFAP and c-fos in brain. For this, our postfix time is about overnight.
Best wishes
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It has long been argued that the brain has no sensory receptors, but the smooth muscle controlling blood flow of the intracerebral arteries clearly has sensory and motor innervation. 
Robert A. Hill, Lei Tong, Peng Yuan, Sasidhar Murikinati, Shobhana Gupta, Jaime Grutzendler. Regional Blood Flow in the Normal and Ischemic Brain Is Controlled by Arteriolar Smooth Muscle Cell Contractility and Not by Capillary Pericytes. Neuron, 2015; DOI: 10.1016/j.neuron.2015.06.001
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I would like to highlight that the trigeminovascular reflex mediated via the tracts nucleus solitarii is essential for that, as implied in the current pathophysiological models of migraine. It may explain why a lot of patients receiving Metoprolol, beta-blocker which does penetrate in the brain, have a real benefice nervetheless.
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I am trying to find the best way to measure the blood brain barrier permeability Invivo (Mice),I tried the Evans blue dye with High molecular weight dextran but I'm still looking for a better method to measure the changes in the blood brain barrier permeability with aging.
Your help is much appreciated.
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Hi there,
I am currently drafting a review on this very topic. The available techniques that I have identified for measuring BBB integrity and permeability include: Evans blue, fluorescence, TEER, MRI-Gd, IgG, PAMPA, PET, perfusion CT, horseradish peroxidase, NIR, SPECT, and MRI-ASL.
Regards,
Jerome
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I am trying to remove the blood from the brain capillaries after injection of a dye, I tried intracardial injection of Ice-cold heparinized PBS but I faced high resistance during the injection, so if anyone can help with a detailed protocol  to make sure that whole blood was removed from the brain capillaries this will help a lot.
Your suggestions are much appreciated.
Thanks
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Dear Sweilem,
Intracardiac perfusion is the best way to remove the blood from brain capillaries. You will need to add sodium nitrate and heparin to your PBS solutions to prevent clothing. You will need to use a large needle (blunt, >G18) to reduce the resistance you have mentioned. Basically deeply anesthetise the animal, open the chest cavity, expose the heart and stabilize it with forceps, insert your blunt needle up from the ventricle, start the flow of heprinized PBS solution with a pressure at around 150-200 mmHg, cut the right atrium to let the incoming blood out, run the solution until the outflow is clear of red blood cells (~250 ml). If you need to fix the tissue you can change from PBS to 4%PFA (or whatever fixative you are using). For details of the protocol please see my PhD thesis and JCN publication listed below.
best wishes, Refik
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AIMS Neuroscience is requesting paper submissions for our September issue. Manuscripts will need to be received by 29 August 2016, and decisions on acceptance will be completed by 29 September. The aim of this special issue is to explore the role of the hippocampus in memory. Research on the hippocampus and medial temporal cortex in memory has been extensive. The hippocampus has been proposed as both a storage location and as promoting the gradual integration of newly acquired information into cortical association networks via binding, reactivating, and strengthening connections. What are the current theories and how do these fit with long-term cortical memory storage? Please add your own answers here to stimulate interest and discussion.
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