- Fouad Lemtiri-Chlieh added an answer:Has any one had experience with automated whole-cell patch clamp in brain slice, such as ones from AutoMate Scientific?What are your thoughts on improving efficiency/performances using auto patch in slice?
As far as I know. I do not know of any such automated patch clamp for brain slices and Automate Scientific don't have anything like that. Could you please send a link to this system that you are describing?
meanwhile, there are other automated sytems to patch clamp isolated cells (used for high throughput) amongst them is the patchxpress, you get gigaseals with this system because they use glass pipets (the one I saw had 16 amplifiers). There are also the IonWorks quattro and IonWorks Barracuda (you don't get Gigaseals with these, they use special chambers with holes in them...up to 96 I think or probably more with other cahmbers) but they are used to screen large amount of compounds (over hundred thousand chemicals) in ashort amount of time. you need to have a large pocket to buy these (>half a million USD - that was 4 years ago). And you need to have a huge library of these coumpounds to test, otherwise it's not useful. Bottom line, these systems are mostly by pharmaceutical companies or small companies that have the expertise and are hired by the big pharma to test like I said tens of thousands of coumpounds.Following
- Fatiha Chigr added an answer:Which methods are most commonly used to measure (assess) neuroinflammation in the CNS?And neurodegeneration in mice.
Using ELISA, W Blot or IHC, you can assess neuroinflammation by using anti-GFAP (for gliosis) and microglial markers. For better characterization, use anti-cytokines too.Following
- Jennifer Keene added an answer:Does anyone know why Wako Anti-IBA1 (Cat # 019-19741) works in a perfusion fixed rat brain but not in post-fixed?
We've previously had great imaging staining rat frozen rat brain slices with Wako Anti-IBA-1 when the rats were perfused with PFA. Due to some of the other stains on our new experiment we switched to a PBS perfusion and PFA post-fixing after slicing. Most of our stains are having no problem but the IBA-1 isn't working. Anyone else had a similar problem and figured out how to fix it?
We've used antigen retrieval in the past but moved away from it when we were getting good images without antigen retrieval. We can certainly try going back with the IBA-1 specifically, as well as try reducing the fixation concentrationFollowing
- Ulyana B Lushchyk added an answer:Is there any correlation between vascular pathology and psycological disease?Would a decrease blood supply, or an anatomical variant of the arteries predispose someone for psycological "fall out"? Any thoughts?
The mental disorders and vascular pathology have a direct correlation dependence. Cerebrovascular insufficiency develops in cortical areas in zones of vascularisations of a cerebral artery. The psychological and neurological deficit correlated with vascular disorders on topographic criteria. During individual vascular therapy we receive rhe decreasing of psychological disorders:http://angio-veritas.com/technologies/uzd-diahnostyka-sudyn-mozku-v-psyhonevrolohiji/?lang=en and http://angio-veritas.com/technologies/individual-angiotherapy-with-instrumental-monitoring/?lang=en&lang=enFollowing
- What are the mechanisms for secretion of different gliotransmitters such as glutamate, GABA, and ATP by astrocytes? Receptors for all major neurotransmitters seem to be present on the astrocytic plasma membrane (Volterra and Meldolesi,2005), and activation of these receptors (because of neural activities) leads to an intracellular Ca2+ increase and subsequent release of gliotransmitters from glial cells (Perea et al., 2009).
The problem is, how can the astrocyte understand which of the gliotransmitters should be released in different states, according different neural activities?
Dear professor Verkhratsky
Many thanks for your valuable suggestionsFollowing
- Cainositas Cainosito added an answer:What is the meaning of "synaptic puncta"?Could you tell me what does the "Synaptic puncta" mean?
Is it a synonym for synaptic surface?Following
- Karla Kretschmannova added an answer:Does anybody have experience with zirconia ceramic blades for cutting brain slices?How many times can you reuse the blade? Can you use them with Leica Vibratome?
Thank you very much for all answers. We are now using them for about a month (everyday cutting, 1-2 animals) and they really work very well! I can't believe we have not switched earlier....Following
- Alfredo Pereira Junior added an answer:Do astroglial calcium waves support conscious computations - and what kind of computation?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. In the attached powerpoint presentation I present a model that addresses the issue of astroglial contribution to conscious processing, and welcome your critical comments here in RG.
Reference: 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
Terrence Sejnowski and colleagues are advancing our knowledge of the role of astrocytes in brain computational processes:
Proc Natl Acad Sci U S A. 2014 Jul 28. pii: 201410893. [Epub ahead of print]
Astrocytes contribute to gamma oscillations and recognition memory.
Lee HS, Ghetti A, Pinto-Duarte A, Wang X, Dziewczapolski G, Galimi F, Huitron-Resendiz S, Piña-Crespo JC, Roberts AJ, Verma IM, Sejnowski TJ, Heinemann SF.
Glial cells are an integral part of functional communication in the brain. Here we show that astrocytes contribute to the fast dynamics of neural circuits that underlie normal cognitive behaviors. In particular, we found that the selective expression of tetanus neurotoxin (TeNT) in astrocytes significantly reduced the duration of carbachol-induced gamma oscillations in hippocampal slices. These data prompted us to develop a novel transgenic mouse model, specifically with inducible tetanus toxin expression in astrocytes. In this in vivo model, we found evidence of a marked decrease in electroencephalographic (EEG) power in the gamma frequency range in awake-behaving mice, whereas neuronal synaptic activity remained intact. The reduction in cortical gamma oscillations was accompanied by impaired behavioral performance in the novel object recognition test, whereas other forms of memory, including working memory and fear conditioning, remained unchanged. These results support a key role for gamma oscillations in recognition memory. Both EEG alterations and behavioral deficits in novel object recognition were reversed by suppression of tetanus toxin expression. These data reveal an unexpected role for astrocytes as essential contributors to information processing and cognitive behavior.
PMID: 25071179 [PubMed - as supplied by publisher]Following
- Sunil Kumar added an answer:What is the neurobiological basis of subconscious brain?Theories of conscious and subconscious brain have been around for decades, but do we have any neurobiological understanding of the subconscious state of the brain? It’s been said or reported in encyclopedia that about 60 – 80% of the brain remains in subconscious state most of the time and carrying lots of thoughts, emotions and information from past and present, and these thoughts and information can drive and modulate mental content which can affect the behavior when retrieved and processed by the conscious brain. But do we have the molecular, cellular or neurological evidence of the subconscious brain and how the information from subconscious brain transfers to the conscious state?
Thanks to all for for very meaningful comments and sending the related links to understand some neurobiological aspect of subconscious brain. Although we need very intense research to really get close to complete understanding behind subconsciousness, but this really help to improve our understanding about conscious and subconscious state of brain.Following
- What is the physiological or anatomical difference between place cells and grid cells in the hippocampus?
In the medial temporal lobe,there are specific types of neural cells such as place cells, head-direction cells, grid cells, and boundary vector cells which involved in cognitive map and spatial memory. Hippocampal “place cells” encode the rat’s location within an open environment independently of its orientation and fire in the specific position. The complementary encoding of the orientation, independently of location, is done by “head-direction cells” .I think all of them are pyramidal neurons. So Is there any physiological or anatomical difference between these kinds of cell?
Dr. Burgess said:
"The differences between grid cells and place cells may well be due to their inputs, although some of the stellate cells in layer II of medial entorhinal cortex are probably grid cells, and they have some differences to pyramidal cells."Following
- Is there any specifically exclusive to the hippocampal astrocytes property? The Hippocampal astrocytes may have specific property, which other astrocytes in other brain regions do not have it.
Dear professor Verkhratsky
your suggestions are completely right. All cells are important.
But I think astrocytes have tools for managing the neural system that other cells haven't it. Ca signaling ( local, global and spotty) and secretion of variety substances with different effects on function and performance of other cell (eg neuron) activities, are these tools. This is just a scientific sense.Following
- Yu-feng Xie added an answer:Why do I observe a decrease of the evoked field excitatory postsynaptic potentials in time?Good Afternoon, I’m doing in vivo electrophysiology in anesthetized mice. I’m recording evoked field excitatory postsynaptic potentials (fEPSP) in the CA1 stratum radiatum after the electrical stimulation of CA3 axons. Since I moved a couple of weeks ago to a new setup I’m experiencing a weird response. Basically, after setting the electrodes in the place where it is possible to find a clear evoked response, this response tends to decrease over the time without inducing any specific protocol (Recordings of 120 minutes; evoked response corresponds to 1 pulse each 15seconds). In this experiment I use Isoflurane (5% during induction, 1.5-1.25% during the recording, Iso delivered with compressed air at a rate of 1L/min). I use also concentric bipolar stimulation electrodes (I get a clear response with a minimal electrical artifact with an intensity of 300-500μA and duration of 20-40 μseconds). To record I use glass microelectrodes with a tip of 1-2 μm diameter filled with Pontamine sky blue in sodium acetate. Since this is a limitation to my work, I’m trying to find a possible explanation or issue in my procedure/setup. All the possible hints are very welcome. If you need more details I can send right away. Thank you very much.
i agree with Michel G Desarménien, try different ISIFollowing
- Magor Lorincz added an answer:Anyone know of a reliable antibody I can use to label up serotonergic fibers?I'm looking for the equivalent of the Tyrosine Hydroxylase antibody used to visualize dopamine neurons and dopaminergic fibers except for serotonergic fibers. I would like to visualize serotonergic fibers from the dorsal raphe projecting to the SN/ VTA and beyond through the medial forebrain bundle to the striatum in rats. Any ideas?
5-HT antibody from Immunstar, but check the Varga V et al. (2009) Science for the exact details. Good luck!!!Following
- Do hippocampal astrocytes have any effect on spatial memory formation and retrieval? If yes how? According the effects of astrocyte in synaptic plasticity and neural function, it's not out of mind that astrocyte may play an important roles in formation and retrieval of spatial memory. But I’m looking for the related mechanism(s).I'll be appreciate who help me to finding my answer.
Thanks a lot. I had it before. That is a nice paper. please see my paper too and let me know your comments about it.
"Mechanisms of hippocampal astrocytes mediation of spatial memory and theta rhythm by gliotransmitters and growth factors"Following
- Pedro J García-Ruiz added an answer:How the electrical stimulation of the brain works for dopamine and serotonin release in extracellular space and modulate the behavior?It’s been known for decades that electrical stimulation of brain increase the extracellular concentration of dopamine significantly and helps to restore some function of the brain specially in movement disorders like Parkinson disease, dystonia etc. Recent past has also revealed that electrical stimulation of the brodmann area 25 or subgenual cingulate in human cortex help in reducing the depression like symptoms in patient suffering from major depressive disorder. Is their information available about the functional mechanism behind the induction of the dopamine and serotonin release by electrical stimulation of the brain? And, is it works for both dopamine and serotonin release differently or it works on the same principle for both? Also is this process of electrical stimulation help or induce the synthesis of the dopamine and serotonin or it just help in release of available neurotransmitters only? If later is the case what’s the intracellular concentration of the dopamine and serotonin after stimulation? I am trying to find out the mechanism about how cells maintains its equilibrium after stimulation which can increase the extracellular concentration of these neurotransmitters significantly in very short span of time and not warranting the long term integrity of cells. Any suggestion or comments would be highly appreciated.
This is a simple and very good question, and my personal answer is: We don´t know. It is intringuing how deep brain stimulation (DBS) is so effective in Parkinson´s disease….dystonia and other conditions. First it was suggested that DBS might be acting by releasing dopamine….but this is not clear at all. DBS can be excitatory and inhibitory…at the same time depending on what structure is involved (soma or axon) (see Satomi Chiken and Atsushi Nambu Disrupting neuronal transmission: mechanism of DBS? Frontiers in systems Neuroscience 2014). Probably DBS dissociates inputs and outputs, resulting in disruption of abnormal signal transmission. Another interesting approach is suggested by Vinata et al, according to these authors, DBS might act increasing neurogenesis (Vinata Vedam-Mai1 Increased Precursor Cell Proliferation after Deep Brain Stimulation for Parkinson’s Disease: A Human Study. PLOS 2014) or by induction of different gene expression (T. SCHULTE et al Neuroscience 2006; 138: 1377–1385). In any case we often use very effective treatments years (or decades) before we understand the exact mechanism, this is the case of DBS…but also L-Dopa etcFollowing
- Pradip Kumar Kamat added an answer:Which neuronal cell line is best to study toxicity of nanoparticles?I need to study brain neuronal toxicity. In this purpose which NORMAL neuronal cell lines is best to study toxicity and that cells must be related to alzheimer's disease. I need to study the same nano-particles for alzheimer's therapy.
You can use SHSY5Y cell line to strudy Alzhiemers like pathology. Other cell line are also there likeN2A which is also suitable but SHSY5Y is the best one. Good luck.Following
- Aurélie Stephan asked a question:What can we expect from Zolpidem?Hello scientific community,
I've heard about Zolpidem/Ambien a few days ago and what I heard was very promising. It could have a positive effect on a wide range of cerebral disorders (aphasia, acoustic agnosia, alzheimer, and so on... so they said) since it may act on the GABA A system which is easily implicated in a lot of disorders.
So I was hoping it could be of some help for a little kid I know who has a lot of developmental disorders: mental retardation, some autistic behaviors..
But I couldn't find any paper really talking about the perspective of the compound. So I hoped someone here could tell me where we are today concerning that compound, can we expect a lot from it, and especially in the case of that kid, could such a compound help at least improve some of his difficulties?
Thanks in advanceFollowing
- Javad Mirnajafi-Zadeh added an answer:Is there any technique apart from fMRI which enables us to record electric/molecular changes in live animals?fMRI techniques do not work properly if we are studying effect of treatments on stress/fear/anxiety response of animals because for fMRI we have to restrain animals that interferes with the outcome. I need an alternative for fMRI. Maybe combined observations of 2-3 techniques may give a reliable and reproducible outcome?Dear Mehta
I think the best region for recording the electrical activity of brain for "memory dysfunction studies" is "Kippocampal formation". Although it will be interesting to look at the whole brain activity, but is needs expensive thechniques (such as those Maryam mentioned). You can simply record the field potentials from the hippocampus in freely moving animals. Measuring the changes in suynaptic plasticity of this region can give you valuable data on memory dysfunctions. At the same time, EEG recording from this region and analysis of frequency spectrum can be also helpful.Following
- Yasuko KY Kishi added an answer:Can anyone help regarding diagnostic criteria for Polyphrasia?As for polyphrasia, which disease is categorized as a standard?
・Some kind of brain functional disorder
・Pervasive Development Disorder
I usually suppose that the polyphrasia patient is accompanied by a sleep disorder, or fatigue of the brain function (Broca's area).
As a symptom, it resembles narcolepsy or idiopathic sleep disorder.
In my country, there is a symptom called polyphrasia, but there is not the official diagnosis.
I want to take the case of other countries into reference.Dear Mr.Michael Krichbaum
Indeed, we are often blind to clinical symptoms of actually, because we are particular about the disease name. The "logorrhea" seems Greek is the etymology...
I can not judge for me whether 1990s is the old generation in psychiatry and psychology. ( at over the world )
However, research of " logorrhea " and " polyphrasia " is essential in my research (dissociative disorder). Because any comment did not come for a long time, I had almost given up about this question.
Your comment gave me breaking through my one wall.
Thanks so much.
- Jane Drake Brody added an answer:Heroes and Biology - any thoughts?Under the influence of Joseph Campbell, I have been regarding heroes and gods as personified emanations of primal urges to action. Currently, I use the work of Eric Neumann, Jung, Nietzsche and James Hillman in addition to Campbell to support my theory. I'm hoping to find some evidence of this in the neurosciences. Can anyone point me in the right direction?Noe, Thank you! You have clarified it.". . .involves fundamental aspects of social psychology and anthropology, with a neurobiological basis. It is needed an interdisciplinary vision. To discuss it, we must give up some preconceived criteria by our training, and analyze it holistically." That is exactly what I am trying to do. While my research is not about criminals, I have been looking at the work in those areas by Anneliese Pontius to whom another researcher referred me.
I am proposing that the characters in a play represent behaviors, both good and evil, that are driven by neurobiological impulses that emerge due to the stressors imposed by the workings of the plot. In our daily life, we do not generally exhibit such extremes of behavior, but in conflictive situations, such responses to life break through more rational modes of behavior.Following
- Ursula Ehrfeld added an answer:What frequency would be best to get high spatial resolution in the brain structure to detect the waves and coincidences using electrophysiology?Great idea Ursula, thanks for bringing attention to this "partially forgotten" theory of memory.
Indeed, it is time to start testing this theory with wet lab stuff.
One key will be to get spatial resolution high enough in the brain structure to detect the waves and coincidences in action using electrophysiology.
What frequency would work best?Olivier,
Sorry for escaping into a parallel e-mail discussion! Now I'm back again on ResearchGate.
I had been confused by your last question! I did not understand why you need high resolution capability of the theta waves. Thank you for clarification!
As I told you, in my holographic hypothesis I don't need at all high temporal and/or spatial resolution for encoding information. For me, 'information' is not encoded in single cells, not even in small cell assemblies. In the holographic analogy 'information' is represented by a comprehensive pattern of waves and oscillations (w/o) distributed over the whole brain, especially distributed over more than one sensory system. 'Information' is reaching the brain as a 'concerted action' of a huge amount of w/o stemming from the outside world and reaching a variety of sensory systems (visual and auditory and/or olfactory and/or tactile, etc.); these w/o representing the 'information' will be recognized instantaneously AS A WHOLE by a comparably huge amount of neurons. This is the very moment where synchronous impact – high temporal correlation of several inputs – is required. Spatially, they are distributed over the whole brain. For me, 'Binding by Synchrony' is an event which takes place when 'informations' – represented by w/o – are entering the sensory systems. The w/o are bundled to 'informations' by synchrony, i.e., they are characterized and identified by synchronous arrival. To emphasize: w/o do not encode information, they ARE the information! The 'inner representation' of an outside world object is equivalent to the sum of all w/o reaching the brain from this and similar objects.
The holographic storage of the w/o reaching the brain from the outside world requires not only the participation of a variety of sensory systems, it always requires, in addition, the involvement of a variety of subcortical regions which we attribute to the EMOTIONS.
In the German text, I posted on ResearchGate, I made an attempt to explain my view. Unfortunately, I did not translate it up to now. Hopefully a can catch up soon.
- BethAnn McLaughlin added an answer:Does anyone know which growth factors can help in Pontine (PnC pontis caudalis) neuron culture?I am interested in a cell culture of gigantic PnC neurons, but there is little information about growth factors adequate for this neuron type.NS21 media supplement is time intensive to make but very reliable Described by Jonnas Hell and Ben Barres. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2678682/Following
- Valia Rodriguez added an answer:Can anyone advise me in search of software for EEG sources?I'm doing source analysis. Does anyone know a software for source analysis like FD VARETA?Look in here http://www.uzh.ch/keyinst/loreta.htmFollowing
- JingHong Chen added an answer:Opinions on wire types for extracellular recordings and iontophoresisDoes anyone have opinions about the best type of wires to use in glass pipettes for single unit extracellular recording and iontophoresis? We've been using coated platinum, but it's so expensive. Do you know if there's a noticeable difference between the effectiveness of coated silver, bare silver/silverchloride, gold, tungsten and platinum wires?We also use carbon-fiber electrodes of Kation Scientific (Carbostar). Not expensive, youmay use several times if protect well. Recommend.
- Gabriele Scheler added an answer:Intrinsically generated action potentials - any thoughts?It has been said that some neurons have the capability to spontaneously generate an action potential without receiving any kind of synaptic input, in other words the AP is intrinsically generated.
How does the cell do this? Is this a slow depolarization resulting in tonic low frequency firing? Can phasic firing also be intrinsically generated?
Which brain areas and cell types are particularly known for exhibiting this type of behavior?Following
- Milorad Toša Zikic added an answer:Are certain sexually dimorphic features in the brain different in individuals of the same sex but of different sexual orientation?According to DF Swaab (2008: "Sexual orientation and its basis in brain structure and function", PNAS 105 (30): 10273-10274. DOI: 10.1073 / pnas.0805542105. PMC 2,492,513th PMID 18,653,758th"...) neurobiological research on sexual orientation man only gain momentum, and have already shown that people have a number of differences in the brain, not only in terms of gender, but also in relation to sexual orientation ... ". Svab was first announced that sexual orientation in men and biological "clock" located in the hypothalamus, in his suprachiazmatic nucleus.
In Journal of Eng. Proc Natl Acad Sci USA (2008) Ivanka Savic and Per Lindstrom, after conducting brain research of 25 heterosexual men and women and 20 lesbians and gay men, by the application of magnetic resonance volumetry of cerebral and cerebellar hemispheres, showed that the relationship between brain hemispheres, and the form amigdale connectivity, atypical in sexually different gay homosexual persons.
Laura Allen and Simon LeVay showed that two of the four anterior hypothalamic nuclei (INAH 2 and 3) are significantly higher in men than in women on the basis which it is hypothesized that dimorphism of these nuclei might accord to sexual orientation. Le Vayi hypothesized that (INAH 2 and 3) are higher in individuals sexually oriented toward women (heterosexual men and homosexual women) and lower in individuals sexually oriented toward men (heterosexual women and homosexual men).In humans and in animals, there is a drive homosexual patients of both sexes. Biological specificity is homosexual men, but also is present between the number of animals, in particular mammals. Thus, it is likely that homosexual activity a man can be considered as a biological variant of humans sexuality.
In 1990, the Krauts and Hoffman reported that the suprachiasmatic nucleus (SCN) in heterosexual men significantly higher than in women and that in gay significantly lower than in heterosexual men. In the same year, the Krauts and his colleagues investigated the correlation of brain development with his sexual orientation, treating the brain of male rats pre-and postnatally aromatase blocker ATD, and this presentation was produced enlarge SCN, which resulted in bisexual behavior in adult male rats.
Although the study of brain structures observed morphological - dimorphic difference in the persons of different sexual orientation ... maybe they are just a reflection of the observation but no real difference. That is why the researchers homosexuality posed an intriguing question whether perhaps certain sexually dimorphic features in the brain are different sample of individuals of the same sex but different sexual orientation? But whether the observed sex-atypical characteristics result of processes that occur during fetal (prenatal) or neonatal development, as is the case with gender identity and sexual orientation, it is still an open question.
Also, results Simon LeVay research and his discovery of the nucleus differ in size between heterosexual and homosexual men suggest that sexual orientation in humans requires further research on the biological level.
Identifying, on which essentially based the largest number of forwards studies it is not the same as finding the cause. Of course, anatomy is not the etiology, but may offer a starting point for further research in the quest for the ultimate origins of sexual orientation.Following
- Pandi-Perumal Seithikurippu Ratnas added an answer:What is your opinion about using "neuroglia-science" or "glia-science" like neuroscience and establishing new specific fields for studying Glia cells?According to the recent studies about computational power of astrocytes (for review see Min, Rogier 2012) or their role in health and diseases (for review see Philip G. Haydon 2009, Domingues, AMJ M Antonio 2010) and so on (see book of Verkhratsky, A 2009), it seems astrocytes are very important cells in the brain and we are in the astrocytes decade.
In the wake of my questions about astrocytes, I want to know your opinion about using "neuroglia-science" or "glia-science" or "astro-science" like neuroscience for studying glia cells? they are mysterious and powerful cells.Hi Hossein, I appreciate your enthusiasm and passion to classify as a separate discipline for glia.
As you know, most glia are derived from ectodermal tissue of the developing embryo, in particular from the 'neural' tube and crest. What if someone makes an argument that since 'neural tube' or 'neural crests' (and not 'glial tube or glial crests') are involved, still it qualifies to be in the neuroscience? What about if some one argues that the glia in the brain is part of central 'nervous' system (as we don't have a central 'glial' system). What about those who work on the neuron-glial communications? How would you call them? Neurobiologist? Giolioscientists? or Neuroglioscientists? Can you see the points? Can you understand the intricacies in such move?
The fact that you have your collection of papers from leading authors or pioneers in glial biology; have you ever discussed your ideas with them as why such idea might be worthwhile? Any paradigm shift must come from the higher up. Not from you and not from me. We are not pioneers. Additionally, any such move should be proposed in a specialty glia conference and a consensus has to be made among the scientists.
I have proposed my own theory on glia, but never published for various reason. But I am no expert or a pioneer. Do you think, those pioneers in glia, didn't thought about it? Why they haven't done so far? Have you thought about it?
Hypothetically, everyone agrees that the name that you suggested 'glioscientists' is the most appropriate way to call scientists in this research domain. How would you call a basic researcher who is focusing on 'spinal cord neurons'? There are tons of information (basic and clinical) on spinal cord. There are lots of research going on in this domain. What if those researchers felt that they are working on neurons, but in spinal cord - not in the brain. If they say, 'Although we do work in the CNS circuitry, we need to be called in a special name'. Would such argument is acceptable to you? Do you think, either they would ask such manner or would you go ahead and grant one if any such requests arise?Following
- Niels Jensen added an answer:Does arachidonoyl serotonin, an endogenous (supposedly) cannabinoid, have any affinity for 5-HT receptors?N-arachidonoyl-serotonin inhibits FAAH and binds to the TRPV1 receptor, but has it been shown to have any activity regarding its 5-HT moiety at classical serotonin receptors?According to classical 5-HT agonist binding site structure-affinity relationships: a clear no. According to these, a free amine moiety is required for affinity - in arachidonoyl-5-HT the nitrogen is blocked as a neutral amide. Plus the arachidonoyl moiety is way too big to fit into the binding pocket. Because of this, I do not think that anybody has ever actually tested this, but I might be wrong. Check the PDSP database.Following