Questions related to Neurobiology and Brain Physiology
Can we consider consciousness as a type of energy that supplies the brain with energy, given that the brain has very high resistance, up to 60 ohms, and in order to generate small currents within the brain, we would need a very high voltage? Additionally, Newton's first law states that an object at rest remains at rest unless acted upon by an external force. Is it possible that consciousness could be a source of energy for the brain? Could this be a valid possibility?
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
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?
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?
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.
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). The word comes from Latin com- "together" and -siliens "jumping" (as in resilience).
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®ion=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.
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.
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.
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.
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).
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?
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?
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
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!
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
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!
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.
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).
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.
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,
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 ?
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).
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?
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.
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?
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?
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 ?
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?
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?
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.
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.
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!
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!
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.
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!
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?
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.
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.
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?
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?
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!
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.
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.
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 ?
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? :-)
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 ?
can anyone help me about whether excitatory neuron and inhibitory neuron are colocalized or their locations are nearby? especially on drosophila, thanks a lot
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
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).
when we perform brain slice culture of cerebellum parts, should I also include the brain stem together to culture? or just cerebellum? Thanks,
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 !!!
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.
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.
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.
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?
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.
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.
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?
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.
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).)
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!
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.
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
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.
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.
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.