Neurobiology and Brain Physiology - Science topic

Would anyone be able to sent the drivers and software to my email?

@citlali... It wasn't possible.

“Is it possible to consider that consciousness is a kind of energy ?”

- really the question above looks as rather, if too, vague scientifically, since to answer to it, it is necessary before to understand – what are “consciousness” and “energy”; and, at that, it is necessary to understand what are some really fundamental phenomena/notions, first of all in this case “Matter”, “Space”, “Time”, “Information”; and “Consciousness” and “Energy”, which really fundamental phenomena/notions as well;

- whereas all these phenomena/notions are fundamentally completely transcendent/uncertain/irrational in mainstream philosophy and sciences; and for the posters in the thread.

The fundamental phenomena/notions above can be, and are, scientifically defined/understandable only in framework of the philosophical 2007 Shevchenko-Tokarevsky’s “The Information as Absolute” conception, recent version of the basic paper see

https://arxiv.org/abs/1004.3712 , more see at least a couple of dozens of pages in this link.

If briefly – “Matter” – and so any material structure, and any “Consciousness”, including human’s one, are fundamentally different informational systems, which are based on fundamentally different sets of basic laws/links/constants, and so exist and operate, i.e. change their states, say if some Matter’s particle moves, or some consciousness thinks, in fundamentally different spaces, which only a bit partially intercrossed. If Matter’s space, and a motion in the space are well instinctively observable, however nobody saw where some thought is.

Energy fundamentally isn’t something either material or relating to a consciousness, that is – really rather mystic till now even in the SS&VT conception above phenomenon, however about which it is known already that energy is absolutely fundamental phenomenon - a “Quantity”, which isn’t some concrete informational pattern/system, however it is absolutely fundamentally necessary for any pattern/system could change, including be created.

So really “consciousness on Erath” that every living being has, just so Life on Earth exists, though more correctly every, again – fundamentally non-material - consciousness – a bacterium’s of a human’s one, uses fundamentally practically material living beings’ organisms [animals, including humans – body+brain] as stable residence and power supply that provide specific energy consumption by non-material consciousness functional modules.

The practically material brain is only power supply module and an auxiliary functional module at consciousness operation, say, it is used as “mother board” and “hard disk” in the “computer+program” system “consciousness”;

- etc., more see the link above, to read the SS&VT initial functional consciousness model in https://www.researchgate.net/publication/329539892_The_Information_as_Absolute_conception_the_consciousness it is useful as well.

Cheers

Mattes Kappert According to Cho et al., (2021), The phasic activity of the signal represents has been shown to occur in the frequency range of 0.08 Hz to 0.33 Hz while the tonic signal is captured in the frequency range of 0.010 Hz to 0.033 Hz. if 0.33 Hz is phasic, twice that frequency is 0.66 Hz and that exists in the band of data you have.

Here is a link to Cho's article.

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.

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.

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.

Hi Ghulam, indeed if you consider selectivity and sensitivity, HPLC coupled to electrochemical detection would be method of choice for the analysis of neurotransmitters in rat/mice brain. Concentration levels up to 50 pmol/L and lower are achievable with only 5 uL sample volume injected. So it can be used in both micro dialysis experiments as well as the analysis of brain tissue (homogenates). See for example:

Regards, Hendrik

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:

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

Nice Contribution Michael A. Hunter

Caffeine has protective role in neurodegenerative diseases. Please see the following RG links and PDF attachment.

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.

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!

Professor Zeashan Khan,

Thank you very much.

Hi Sean,

Sure, see attached. The readme file has the necessary info to create the ROIs. All the best!

-Ranga

 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 

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: 

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).

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

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.  

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.

What are your end point measurements?

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 !!

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

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

I would say telemetry is for sure better

Dear Ivan,

no, we have never been able to solve this problem. Sorry I cannot help at the moment.

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.

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.

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!

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.

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.

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

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

Dear Nirmala, thanks a lot for your letter and recommended addresses (!)

Sincerely, Leon

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

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

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.

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..

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..

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

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

The answer is "A".  Visual physiology/photometric units use a base 10 log scale. 

Distinct type of  " Purkinje cells " not seen in mammals 

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,

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

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?

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.

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

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:

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

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:

If it helps, the picture you posted is one of Thomas Deerinck's pictures of the cerebellum - see link: 

Hello 

I do really appreciate  your wide contribution to our search!

I will start reading the material.

thanx again!

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

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

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.

extracellular potassium accumulation is modelled as part of the paper:

The Sodium-Potassium Pump Controls the Intrinsic Firing of the Cerebellar Purkinje Neuron

I thick  your slides should be restricted to cerebellum, because the two differ with respect to cellular compositions and functions.

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/

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!

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.

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

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

here's an answer I once posted to another forum:

Great TED clip attached as link

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.

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). 

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

I agree that unnecessary doses of vitamins of B-group may cause insomnia because of the extra-stimulating effect on the CNS.

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.

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.  

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.

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

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.

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

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

The hippocampus via the trisynaptic circuit serves to act as a comparator of old and new data.  Old information travels from the entorhinal cortex (at ECII) via the perforant path to the dentate on to CA3 and final is passed on unchanged to CA1 from which it is sent via the subiculum back to EC.  But, if there is new information then CA3 is inhibited while new information from primary sensory cortices is sent via association cortices to ECIII which projects to CA1 where this new information drives the firing of CA1 pyramidal cells which in turn send this revised input signal back to EC via the subiculum.  The next time the information enters CA3 from EC it will have been modified to reflect what was recently seen or heard.

If the activity of this circuit is dysregulated as occurs with age-related amnestic mild cognitive impairment wherein there is loss of inhibitory control over CA3 subregion then learning and memory function is impaired.  

Check out our paper:

The hyperinsulinemic-euglycemic clamp, or insulin clamp, is the gold standard for assessing insulin action in vivo. You can see how it's done here:

As this is quite complicated, another method would be to do an Insulin Tolerance Test (ITT) by injecting a bolus of insulin and recording blood glucose levels at different time points. Some authors who do not want or cannot do an ITT or insulin clamp use the HOMA-IR (Homeostatic model assessment Insulin Resistance), as it requires only a simple dosage of plasma glucose and insulin. But this test was developed for humans and there is controversy as whether it should be used in mice.

In the CNS, it is not as straightforward, and would require analyzing the phosphorylation state of several proteins involved in the insulin signaling cascade. Plasma to CSF insulin ratio can also be an indicator. See below:

You should send your question to Prof. Harald Sontheimer who is registered on RG.

Best regards

Robert

Visual impressions are converted into and stored as

tuples of symbols. Imagine the view of a cluttered

desktop: from a glance you can only keep a

working memory -ful of items. I'd like to

mention Kim's Game.

Visual working memory is restricted in capacity

to the Miller constant. On the other hand, we

don't have one working memory for auditory

and one for visual items: we only have a single

working memory for items of any modality, in

a neutral currency, the symbols.

Packets stored in long term memory can only

be recalled in a reliable way if any packet fits

entirely into working memory. Bigger data

structures can be made by linking pairs

of tuples by containing the same symbol,

like the equi-join in relational databases.

Literature

Regards,

Joachim

I'd be wary to say there were no differences.

It depends on the brain region and whether you are looking at mRNA or protein expression. Zangenehpour and Chaudhuri (2002) show that mRNA for both is induced along roughly the same time lines though c-fos reaches its maximal level after about 30 minutes compared to 60 minutes for zif268. However, protein translation for zif268 appears to occur faster and is more prolonged, reaching a maximum at around 90 minutes and remaining at a plateau for about 60 min. c-fos instead reaches a peak after approximately 120 min and rapidly declines from there.

However, this data is related to light stimulation and measurements made in the visual cortex and judging from other papers out there, the time courses for different regions and different interventions vary: phencyclidine (non-competitive NMDA-R antagonist) treatment causes a phasic response in zif268 (increase after an hour followed by a suppression 1-2 days later) that was absent in c-fos yet CPP (competitive NMDA-R antagonist) caused similar changes in both zif268 and c-fos (Gao et al., 1998). Learning and memory tasks also show spatial and task-related variations in zif268 and c-fos expression (Barry and Commins, 2011) so you really need to look for any publications relating to the brain region/task you're interested in or to do some control experiments looking at fixed time points after your intervention to get an idea of the time course for certain.