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SfN 2010 is over, hangovers are subsiding, and - like the rain clouds here in San Diego - post-meeting illness is rolling in.
During the conference, however, the weather was absolutely beautiful! Which made it very easy to go out. Which made it very easy to get distracted. But being from San Diego, I was unfazed by the 70 degree weather in November, and had a pretty productive SfN (day 4 notwithstanding). Some thoughts:
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Anything to add? See y’all next year!
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When I started graduate school a few years back, the plan – like most of my peers – was to pursue a career in academia. But grad school has a way of wringing the enthusiasm out of many who tread the tortuous path. Luckily (and I do think it is just that for most), my excitement and wonder is still going strong over four years in. But there are aspects of the academic job description that I’m having trouble accepting. Mainly, the ridiculous hours and incessant grant writing.
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I guess I’m at the stage where I’m debating the trajectory of my future. And not being particularly interested in any of the science talks offered today, I decided to shun science for the Why Academia? workshop (my first workshop at any SfN). Perhaps it should have been titled “How Academia?” because the majority of the presenters focused on how to succeed at the post-doc and young investigator levels. The consensus: put in work, learn from your inevitable rejections, be persistent (research is a marathon, not a sprint), and drink beer. Seriously, almost every presenter mentioned the importance of decompressing with a few beers. By that metric, I think many of us are well on our way to tenure. Some additional tips I found helpful:
The first speaker (sorry, I never caught his name) also had a pretty good quote when speaking about an investigator’s research progression that my memory only allows me to paraphrase: If what you did last year still looks good, then you haven’t done anything good since. Anyway, that’s all I really got to today, the morning session being a casualty of last night’s party. But I’m here until the bitter end, so let’s see how this thing wraps up…
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If you wanted to see any posters about optogenetics and channelrhodopsin yesterday, I hope you are very patient or very tall. Crowds were ridiculous. Wasn’t any better for the morning symposium, either.
Molecular and Cellular Mechanisms of Memory Allocation Neuronal Circuits = best symposium of SfN 2010 thus far. I believe someone else is going to blog about it on this site, so I’ll let her do the elaborating. But there is some pretty cool stuff going on in the Silva and associated labs.
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UCSD party was rockin. The outdoor roof venue away from all the club music was much appreciated. The $12 mixed drinks, not so much. I also learned that texting in the restroom while drunk is not a good combination – or at least it wasn’t for the a-hole next to me who couldn’t seem to hit the urinal to save his life. Despite that little mishap, it was great to see everyone out there having a good time.
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8am comes a bit too early for this west coast grad student. I think I liked it better yesterday when the conference started around noon. But the sacrificed hours of sleep were worth it as Andrew Jackson shared some rousing data this morning about “artificially” induced cortical plasticity by pairing endogenous presynaptic firing with post synaptic activation via a neural implant. One tid bit I found interesting is that the induced plasticity, given extensive pairings, can last for about one week, max. This obviously poses a problem if your goal is to enduringly remap impaired neural circuits. Then again, is this return to baseline due to disuse of the artificial pathway in lieu of the endogenous circuit - a scenario that probably doesn’t hold when the endogenous circuit is damaged?
Is anyone else consistently mislead by some of the talk titles? I attended Silvia Arber’s “Connecting Motor Circuits” talk expecting to hear about...
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neuronal connectivity in the motor cortex. Instead, I heard all about spinal cord circuits. Yes, I probably would have figured this out had I actually read the abstract ahead of time, but this type of behavior comes at the price of even less sleep. Turned out ok, though, as she gave a good talk with a couple of intriguing findings. Notably, using a modified rabies virus that only labels monosynaptic partners, her group found that spinal interneurons innervating distinct functional groups of muscles (extensors vs flexors) are anatomically segregated, and this separation is dependent on proprioceptors during development(I think Ed Callaway will be talking more about the rabies virus technique tomorrow at…8:30am – Grrr). Didn’t get to catch too many posters, but this one from McCartney and Sutton caught my eye, even though it’s not really related to what I do. A somewhat simple story with very clean data. Nice. Miss A.J. McCartney, if you’re reading this, you should upload your poster to this site, or send a link in the comments so others who missed it can have a look. In fact, anyone with a poster should upload it by either signing up here, or simply emailing it to me and I’ll make sure it gets posted (jbiane@ucsd.edu). UCSD neuro alum Andrew Hires gave what had to be the longest poster walk through I’ve ever witnessed. Arrived when he was 1/3 of the way through the figures. Thirty minutes later, when I left, there was still one figure to go. In his defense, it was not his poster – must have taken over last minute for the absent author. Plus, there was one gentleman in the audience who was quite keen on inquiries. Cool poster, though (a Svoboda lab poster, so of course). Also, did you know that following a lesion to the forelimb region of M1, neurons innervating spinal cord segments far, far away can invade the affected region of the spinal cord, potentially causing neurons that controlled hindlimb muscles to now control forelimb muscles? That’s some pretty hefty remapping, but the anatomical tracing studies of Starkey et al suggest this is the case. Very interested to see if electrophysiology studies show any evidence of functional connectivity in this population. 
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Researchers who study the neural correlates of learning know that long-term potentiation (LTP) between groups of neurons that fire concurrently is tantamount to memory formation [1]. Recently, neuroscientists are starting to realize the extent of their old adage, “Neurons that fire together, wire together.” A more complete maxim might roughly approximate as, “Neurons that fire together, wire together, and the more the better!” This idea continues to garner support from recent work by Lee, Ramineni, Hepler, et al.† (2010) in their PNAS article titled “RGS14 is a natural suppressor of both synaptic plasticity in CA2 neurons and hippocampal-based learning and memory” [2].
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Understanding G-protein signaling is important for appreciating the role of RGS14 in learning and memory. G-proteins are heterotrimeric switches that are involved in regulating an array of cell-signaling pathways [3]. Downstream signaling pathways include: activation or inhibition of adenylyl cyclase, opening or closing of K+ channels, phospholipase C activation, and cGMP phosphodiesterase activation [4] (See original figure 1). Along with calcium and Ras/MAP kinases, G-protein signaling is one of the key regulators of LTP. On one had there are excitatory G-protein signals such as those from the Gs and Gq families of G-proteins that keep voltage-gated M-type K+ channels closed in neurons (n.b. Gs activates adenylyl cyclase and Gq activates phospholipase C) [5, 6]. On the other hand there are inhibitory G-protein signals downstream of the Gi and Go pathways, which include voltage-gated Ca2+ channel inhibition and activation of inwardly rectifying K+ channels [7, 8]. Although the effect of the neuron’s electrochemical gradient by Gi and Go is the opposite of Gs and Gq G-proteins, Gi and Go do not directly regulate the function of Gs and Gq G-proteins. That is to say, they do not put the brakes on each other; they only impose opposite electrical properties onto the neuron. Thus, without brakes, both signaling pathways have the potential to spiral out of control. RGS Proteins (known Regulators of G-protein Signaling) modulate G-protein signaling so this doesn’t happen. Typically RGS proteins do this by limiting G-Protein activation by acting as GTPase activating proteins (GAP). RGS14 is one such RGS protein that is uniquely positioned to decrease G-protein excitatory mechanisms and promote inhibitory mechanisms, making it an ideal for regulation of synaptic plasticity. RGS14 limits the lifetime of the Gα subunit, in this way it suppresses excitatory pathways more so than inhibitory pathways because Gi activity is regulated largely by the Gβγ G-protein subunit. Furthermore, RGS14 can actually act as a scaffold to assemble Gαi subunits. Knowing this, Lee et al., performed a series of experiments aimed at elucidating the role of RGS14 in hippocampal LTP, plasticity, and memory formation. Several forms of learning and memory have been extensively studied as LTP forming at the DG-CA3-CA1 hippocampal sub-region circuit. Oddly, a well defined fourth region, the CA2 sub-region of the hippocampus, has not been shown to be involved in this circuit. The neurons in the CA2 region don’t seem to have LTP abilities. Lee et al., using monoclonal antibodies to select for RGS14 (through immunohistochemical staining) revealed that there were high densities of RGS14 found in CA2 pyramidal neurons. Next, they compared the CA2 LTP abilities of RGS14 knock-out mice to that of wild-type mice. Synaptic stimulation results in sustained LTP in CA1/CA3 neurons of wild-type rodents, however, not in the CA2 region as expected. Interestingly, the RGS14 knock-out mice showed synaptic plasticity in all three hippocampal CA regions! Next, Lee et al. investigated the underlying molecular mechanisms as to how the loss of RGS14 affords the CA2 region the opportunity to form LTP. Along with its GAP activity, RGS14 is known to bind several proteins such as Raf kinases, leading to the inhibition of growth factor-directed MAP kinase signaling. Therefore, they tested whether an inhibitor of ERK/MAP kinase would affect the newly endowed increased capacity for LTP in CA2 neurons caused by the loss of RGS14. The MEK inhibitor used in the study completely eliminated the LTP potential in CA2 neurons (It was also able to eliminate the LPT capacity in the CA1 region). This suggests that MEK/ERK pathways play a key role in regulation of LTP and RGS14 subserves this signaling pathway in the CA2 region of the hippocampus. Finally, the experimenters tested learning and memory performance in the RGS14-KO mice. They found that the loss of RGS14 actually improved the performance of these mice in tests of novel object recognition and spatial memory. Meanwhile it did not enhance the performance of any non-hippocampal-dependent tasks. This suggests that inhibitors of RGS14 could potentially serve as treatments for cognitive deficits associated with various forms of disease/disorders such as Alzheimer’s or Fetal Alcohol Syndrome, which have symptoms known to affect hippocampal learning and memory. One caveat to this notion of trying to increase LTP capacity however, is that unbridled synaptic potentiation is what leads to epileptic seizures. Thus, as another old adage of all scientists goes, “More research is needed.”
2. Lee, S.E., Simons, S.B., Scott, A.H., Zhao, M., Schroeder, J.P., Vellano, C.P., Cowan, D.P., Ramineni, S., Yates, C.K., Feng, Y., Smith, Y., Sweatt, J.D., Weinshenker, D., Ressler, K.J., Dudek, S.M., and Hepler, J.R. (2010). RGS14 is a natural suppressor of both synaptic plasticity in CA2 neurons and hippocampal-based learning and memory. Proceedings of the National Academy of the Sciences, 107(39), 16994-16998. 3. Shu, F-J., Ramineni, S., Hepler, J. R. (2010). RGS14 is a multifunctional scaffold that integrates G protein and Ras/Raf MAPkinase signaling pathways. Cellular Signaling, 22, 366-376. 4. Lodish, Berk, Kaiser, Krieger, Scott, Bretscher, Ploegh, and Matsudaira. Molecular Biology of the Cell, 6th edition, W.H. Freeman (2008). 5. Marrion N. V., Smart T. G., Marsh S. J., and Brown D. A. (1989) Muscarinic suppression of the M-current in the rat sympathetic ganglion is mediated by receptors of the M1-subtype. British Journal of Pharmacology, 98, 557–573. 6. Caulfield, M. P. and Birdsall, N. J. (1998). International Union of Pharmacology. XVII. Classification of Muscarinic Acetylcholine Receptors. Pharmacological Reviews, 50(2), 279-290. 7. Caulfield, M. P. (1993). Muscarinic Receptors-Characterization, coupling and function. Pharmacology and Therapeutics, 58(3), 319-379 8. Heitz, F., Holzwarth, J. A., Geis, J.-P., Pruss, R. M., Trumpp-Kallmeyer, S., Hibert, M. F., Guenet, C. (1999). Site-directed mutagenesis of the putative human muscarinic M2 receptor binding site. European Journal of Pharmacology, 380, 183-195.
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- This experiment deserves comments!
Daryl J. Bem (2010). Feeling the Future: Experimental Evidence for Anomalous Retroactive Influences on Cognition and Affect. Journal of Personality and Social Psychology, in press, DOI: 10.1037/a0021524
"ABSTRACT: The term psi denotes anomalous processes of information or energy transfer that are currently unexplained in terms of known physical or biological mechanisms. Two variants of psi are precognition (conscious cognitive awareness) and premonition (affective apprehension) of a future event that could not otherwise be anticipated through any known inferential process. Precognition and premonition are themselves special cases of a more general phenomenon: the anomalous retroactive influence of some future event on an individual’s current responses, whether those responses are conscious or nonconscious, cognitive or affective. This article reports 9 experiments, involving more than 1,000 participants, that test for retroactive influence by “timereversing” well-established psychological effects so that the individual’s responses are obtained before the putatively causal stimulus events occur. Data are presented for 4 time-reversed effects: precognitive approach to erotic stimuli and precognitive avoidance of negative stimuli; retroactive priming; retroactive habituation; and retroactive facilitation of recall... all but one of them yielded statistically significant results. Skepticism about psi, issues of replication, and theories of psi are also discussed."
- EXPAND FOR EXPERIMENTAL RESULTS PREVIEW
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"Across all 100 sessions, participants correctly identified the future position of the erotic pictures significantly more frequently than the 50% hit rate expected by chance: 53.1%, t(99) = 2.51, p = .01, d = 0.25.3 In contrast, their hit rate on the nonerotic pictures did not differ significantly from chance: 49.8%, t(99) = -0.15, p = .56"
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One of the most prevalent assumptions we make as neuroscientists is that the brain communicates using a binary code. That is, either a neuron fires and action potential and passes along information (1), or it doesn’t (0). Presumably, information is stored and conveyed by the pattern of neurons that are active at any particular time. For example, let’s say we have 10 neurons. Neurons 2,4,6 and 8 represent an apple, while neurons 3,5,6 and 9 represent a banana. If 2,4,6,and 8 are active at one time point, we identify an apple. If only neurons 2,4 and 8 fire, we would probably still identify an apple due to activation of the entire network via pattern completion. But the point is a neuron has to fire an action potential in order to convey information. Right?
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Most computational models build off this ‘all or none’ assumption, and they seem to do a decent job in representing some phenomena. But why would it have to be this way? What is so special about this transient fluctuation in membrane potential, and what about it allows images and events to enter our awareness? Is it the opening of voltage-gated ion channels? Release of neurotransmitter? Rapid movement of ions? Do action potentials that originate at the hillock have different effects than those initiated in the dendrites? I cannot wait for the day when we have the technology to begin to address some of these questions. And I think we’re close. With techniques like 2-photon imaging and calcium uncaging, we could theoretically “excite” neuronal boutons such that neurotransmitters are released (via Ca2+ binding) without an action potential ever taking place in the cell. Conversely, we could block neurotransmitter release and electrically stimulate cells. Granted, information is almost certainly held within vast networks of cells, so experiments like these on the single-cell level are futile. But enormous progress is being made in identifying neuronal ensembles active during a particular behavior or memory (for example, see this week's J Neurosci article from Dombeck et al). And if we can identify the neural correlates of a particular memory, we might be able to apply techniques similar to those mentioned above to this population. But the question still remains: what the hell is so special about action potentials? And can postsynaptic potentials that fail to reach threshold still convey information at the level of awareness? I also need to mention a wonderful review article by Alcino Silva and colleagues in a recent issue of Science, titled Molecular and Cellular Approaches to Memory Allocation in Neural Circuits. In particular, there was one assertion that thoroughly confused me. In the article, a model is presented for how two or more memories closely associated in time might be stored, such that retrieval of one memory enhances the probability of retrieving the other (see figure). To quote the article, “two memories acquired within minutes of each other may be stored How does the proximity of synapses (on the same neuron) have anything to do with the likelihood of co-recall??? Based on the binary action potential assumption above, an information signal is based on whether a neuron fires or not. And if a neuron fires, it should have the same effect on all it's afferent connections. Far as I know, activated spines do not send out retrograde signals that potentiate surrounding synapses on an immediate time scale. So, what am I missing??? Seriously, I’m asking you. YOU, person reading this right now. You’ve read this far, so you must be interested. The only thing I can come up with is that events occurring in close temporal proximity lead to increased probability of potentiating synapses on the same neuron. And if there is large overlap of neurons that make up the networks representing events A and B, then the probability of activating network A will increase the probability of activating network B. But in this scenario the proximity of these synapses should not matter, so long as the synapses reside on the same neuron. WTF???
Comments?Synaptic tagging?Without reading the review, could they not be talking about events after the action potential has fired? When the first memory is triggered by activation of a certain set of synapses, molecular events at these synapses can alter them in some way to modify the probability they will fire next time. If the specificity of these molecular events is not perfect, synapses in close proximity to the activated set, may also get tagged or modified, thus changing their firing probability, which in turn will affect the ability to recall the associated memory. All the synapses are still firing all-or-none (don't worry, the universe didn't just turn upside down!) but events after the initial action potential can influence a local region of dendrite, which will include the synapses of the second memory. This paper from the Svoboda lab talks about how molecular tagging events are sometimes not localized to just the activated synapse but can spread a little way along the dendrite. This may not be what you were getting at Jeremy, but it's the only explanation I could come up with! -Clare
Hmmmmm, still don't see itBloody hell. Just responded via word press, but lost it due to a dang error page. Let's try again. Yeah, I see where you're going with this, and I think it's an excellent explanation of why two events in close temporal proximity (A and B) would be stored in neighboring synapses. But I fail to see how this would affect co-recall of these two memories. In my mind, co-recall is the process where retrieval of memory A increases the probability of activation of memory B, and this takes place on the scale of sub-seconds. However, the passive diffusion of agents that Svoboda discusses takes place on order of seconds, yes? Now, I could see how retrieval of memory A could facilitate retrieval of memory B at some point in the future, but co-recall? Maybe I'm misinterpreting their definition of co-recall (or your response)? But even if the diffusion and influence of these potentiating agents were instantaneous, would that really matter? In this case, activation of memory A might make it easier to independently recall memory B, but it wouldn't activate memory B, and thus no co-recall. I suppose I could find some scenario using reverberating loops or something where this might work, but I don't think that's what the authors had in mind. Something ain't right. Either I'm totally missing something, my base assumptions of how the brain operates are fundamentally flawed, or the review is mistaken. I suspect it's the first. Comment on Qualitative InformationBradley Monakhos 23:16, 9 November 2009 (UTC)  Everything in our environment comes to us through waves of energy. When a wave contacts a surface, two piece of information can be coded temporally - Frequency and Amplitude. Coding the frequency and amplitude is enough to transmit qualitative information about a stimulus. In the visual system for example, qualitative information must somehow be transmitted through modulation of neuron firing patterns because of the quick convergence of stimuli information passed from photoreceptors to ganglion cells (see Fig 1). Although, spatial information is stored retinotopically, qualitative information must some how be conveyed by information stored in the frequency of neuronal firing patterns. This is the same for light, sound, touch, pain, etc. --- Dees Noodle Need Sauce I know, you need a source right. Here's a little snip from a researcher at the RIKEN Institute. If you don't know what RIKEN is, it's the MIT of Japan. In fact, many of the faculty at MIT and RIKEN have joint appointments at both institutes. Be sure to check out the RIKEN-MIT Center for Neural Circuit Genetics. Enter Toshihiko Hosoya: “It has been believed that a single neuron usually transmits a single piece of information. However, doesn’t that seem wasteful?” says Hosoya. “Information will be transmitted more efficiently if multiple pieces of information are carried in one signal. This also forms the fundamental basis of information processing theory.” Therefore Hosoya decided to investigate extensively what information is transmitted by the retinal neurons. He used the neuron that responds to OFF, which ‘fires’ (generates an electrical signal) when it becomes dark. First, he repeatedly stimulated the retina using an image with changing dark areas, and examined the timing of the firing of the neuron that responds to OFF. It used to be thought that the responses of the retinal neurons involved a wide temporal fluctuation, with the timing of the firing differing between events, even in response to the same stimulation. In recent years, however, it has become evident that firing occurs with high reproducibility in terms of time in response to the same stimulation. Hosoya showed experimentally that the firing events in response to the same stimulation occurred with only a small fluctuation of several thousandths of a second. “This is quite an intriguing feature,” says Hosoya. “Because the retinal neurons fire with high reproducibility in response to the same stimulation, it has become easy to analyze what kind of information is conveyed when the neuron fires.”  The retina neurons that respond to OFF fire more frequently as the image input becomes darker and darker. “It has long been known that the firing frequency changes depending on ‘how dark it has become,’ or on the amplitude of the intensity change. Extensive examination shows, however, that both the firing frequency and the time interval are quite accurate (Fig. 3). This seems to carry some information.” Hosoya theorizes as follows. “The neurons may transmit information on ‘how it has become dark’ as well as on ‘how dark it has become’.” It has also been demonstrated that accurate firing patterns are transmitted from the retina to the brain through the optic nerve. Upsetting conventional common sense, it may be shown that a single neuron transmits multiple pieces of information by using an accurate firing pattern.
Commnet on 'Comment on Qualitative Information'Ok, good foundational argument for your rate-encoding system. The conclusion of Hosoya seem quite intuitive to me, so I don't know what they're talking about when they say 'upsetting conventional common sense.' (Maybe I possess uncommon common sense?) It's easy to see how onset of firing encodes when a stimulus is present, while firing rate encodes amplitude. But I find it harder to relate this to internal circuits that code for something like a memory. No, wait, maybe I can. Ok, in 'my' system where each neuron in the circuit encodes a particular aspect of the memory, firing rate could simply encode amplitude of that aspect. For instance, with our black neuron (see discussion below), rate of firing would encode the amplitude of black of the object. This scenario would be interesting in that you'd have neurons belonging to the same memory circuit firing at vastly different rates, each encoding for the amplitude of their respective representation. Ok, so there. Now we have a testable hypothesis. Go prove me wrong :)
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Circa 1948 Wilder Penfield suggested that certain aspects of human memory can be stored in descrete brain regions. Penfield, a neurosurgeon specializing in focal epilepsy treatment, developed a technique for removing epileptic tissue while avoiding/minimizing damage to areas involved in patients mental processing. Applying local anasthetic to various brain regions of conscious patients, he determined that areas of the medial temporal lobes seemed to be important for memory. Although this idea was met with controversy, a number of neurosurgeons were inspired by Penfield’s work, among them were William Scoville and Brenda Milner. The duo of Scoville an Milner report the extraordanary story of the patient H.M. (His name is Henry Molaison. Only in death will we have our own names since only in death are we no longer part of the effort. In death we become heroes).
If HM ever played guitar, he would have been the only living member of the Forever-27 Club. His tragic accident that lead to the bilateral removal of his medial temporal lobes at the age of 27 would inform the field of neuroscience at a level deserving of a Nobel Prize. First HM showed us that the medial temporal lobe was important for converting short term memories into long term memories. He then showed us that there was various other types of learning and memory that did not include the hippocampus. At 1:00 pm tomorrow (Wednesday, 11.17.2010), Suzanne Corkin, Ph.D. is presenting a special lecture on how HM shaped the science of memory. Do not miss out!
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OneSci is pleased to announce that we have begun to publish our own open source empirical research findings which include open user comments and commentary.
Local increase in cortical ACh signaling during performance of a motor skill learning task.
Biane, J. (2010). The OneSci Journal 1(A), e1-e4.
- We have new conference posters up!
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From the OneSci Wordpress Blog
- Cryostat Protocol (March 02, 2011 19:45)
- Expert (December 02, 2010 15:51)
- SfN Blitz: Postgame Analysis (November 19, 2010 10:41)
- SfN Blitz: Day 4 (November 16, 2010 23:06)
- Henry Molaison HM (November 16, 2010 17:04)
- SfN Blitz: Day 3 (November 16, 2010 12:22)
- SfN Blitz: Day 2 (November 14, 2010 22:10)
- Local increase in cortical ACh signaling during performance of a motor skill learning task. (November 09, 2010 16:37)
- RGS14 is a natural suppressor of both synaptic plasticity in CA2 neurons and hippocampal-based learning and memory (November 02, 2010 12:15)
- Feeling the Future Experimental Evidence for Anomalous Retroactive Influences on Cognition and Affect (October 23, 2010 17:11)
Habenular Nuclei comprise a small group of nuclei that are part of the epithalamus of the diencephalon, situated at the posterior end of the thalamus, on its upper surface. The habenular nuclei are typically divided into the lateral and medial habenular nucleus. The pineal gland is attached to the brain in this region. Nerve impulses from the habenular nuclei are transmitted to the septal nuclei via the stria medullaris, which is found on the medial surface of the thalamus.
The medial habenular nucleus is a major cholinergic pathway, expressing the choline transporter gene Slc5a7 more densely than any other brain region. The high affinity choline transporter is responsible for taking up choline into the presynaptic terminal of cholinergic neurons, where it can be synthesized into the neurotransmitter acetylcholine.
Open the tab below to view Slc5a7 expression in the medial Habenula (MH) in the mouse brain. The MH is located just below the hippocampus.
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An Electrophoretic Mobility Shift Assay (EMSA) is a common affinity electrophoresis technique used to study protein-DNA or protein-RNA interactions. This procedure can determine if a protein or mixture of proteins is capable of binding to a given DNA or RNA sequence, and can sometimes indicate if more than one protein molecule is involved in the binding complex. A mobility shift assay is electrophoretic separation of a protein-DNA or protein-RNA mixture on a polyacrylamide or agarose gel for a short period (circa 2 hr). The speed at which different molecules (and combinations thereof) move through the gel is determined by their size and charge, and to a lesser extent, their shape.
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The control lane (DNA probe without protein present) will contain a single band corresponding to the unbound DNA or RNA fragment. However, assuming that the protein is capable of binding to the fragment, the lane with protein present will contain another band that represents the larger, less mobile complex of nucleic acid probe bound to protein which is 'shifted' up on the gel (since it has moved more slowly).
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