tag:blogger.com,1999:blog-46778960996991253192024-03-19T03:40:08.557+01:00NerdoscienceA blog about all new exciting things in Neuroscience, Biology and Science in general.
The focus will be on my major interest fields: Electrophysiology and the CerebellumNeuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.comBlogger26125tag:blogger.com,1999:blog-4677896099699125319.post-76836174744942530052013-01-28T17:55:00.001+01:002013-01-28T17:55:21.575+01:00No pain no gain, lots of pain little gain?Done. That is the final verdict. My manuscript is finally done and I am submitting.<br><br>
Of course there were a lot of things that needed fixing today:<br>
References didn't look right in Mendeley. The Journal of Neuroscience wants all journal titles to be the official abbreviations, something Mendeley doesn't support out of the box. This means adding and editing several .txt files to get everything working together. After several hours of frustration I decided to tweet to @mendeleysupport and they helped me with my problems. Turned out I am not so smart (d'uh), default.txt actually means default.txt.txt. Meaning that when windows explorer says default.txt it is actually .txt.txt. Silly silly me....<br>
Then all figures should be in RGB and all text as outlines. Of course a quick fix to do, but also needed some attention.<br>
And then of course there is the problem of all authors who need to make small smaller smallest adjustments to the text. At a certain moment I think we arrived at "not better, just different", which signals we're done with it.
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Good thing is that it all looks great now. Figures are also done, text is done, ready to submit.
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All these problems meant that I have spent yet another day on this paper. Time that was actually meant to go into an awesome experiment today. I still need a few cells in vivo from the cerebellar nuclei; hard experiments that need some time and attention. Both of which are in short supply lately.
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So, there you have it. The mad scramble to the finish is already turning into a hectic mad scramble to the finish. I have only five weeks left..... Two papers to finish and a discussion to write.
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I'll keep you all posted!
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Best, Lau
Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0tag:blogger.com,1999:blog-4677896099699125319.post-36657735393271554872013-01-15T22:21:00.000+01:002013-01-15T22:21:17.848+01:00Finish line set! Now for the mad scrambleWeeks, no months ago, I wrote about the "whirlwind that is called finishing your thesis". It has been very quiet here, and now you know why.<br>
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Good news is that I did finish one manuscript. It is now on the desk of my professor who is of course tearing it apart again... Still, I do not despair, since the date for my graduation ceremony is set at the end of May (yes, ceremony. PhD-getting in The Netherlands is <a href="https://www.google.com/search?um=1&hl=nl&tbo=d&tbm=isch&q=promoveren+ceremony&oq=promoveren+ceremony&gs_l=img.3...4280.9209.1.9791.13.11.2.0.0.0.267.1286.7j3j1.11.0...0.0...1c.1.RcubTrgCLek&bav=on.2,or.r_gc.r_pw.r_cp.r_qf.&bvm=bv.41018144,d.d2k&biw=1440&bih=785&emsg=NCSR&noj=1&ei=usf1UI7iO8Pa0QXw54CYCQ">a piece of theater</a> for the whole family to enjoy!). There's only two more chapters to finish, which will be done (no, really urgently need to be done) in two months or so. To complicate things a little bit I got sick this weekend, which caused me not to work for two days. A complete disaster when on a tight schedule I might say.<br><br>
So, my dear readers, now you know why I am so quiet lately. I hope to pick up blogging on interesting stuff again when my thesis has left my desk.Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0tag:blogger.com,1999:blog-4677896099699125319.post-58107031304252263982012-11-29T16:24:00.001+01:002012-11-29T16:24:16.332+01:00Grant application from hellToday is the deadline for my grant, or rather: the deadline is in less than seven hours. And I am freaking out!<br>
The grant application is done, looking great and shiny as a pdf on my computer. It has been read by several people, who all had remarks and wise advice. So, why would I freak out you ask?<br><br>
The Dutch funding agency asks for an acceptance form stating that the host institute accepts the candidate and the grant if the grant is awarded. So far so good you would say, but the form has been on a desk for a week and now needs to be run by several offices in one day. Extra complicating the story is that I am at GMT+1 time, the host institute is at EST time and the deadline is midnight GMT+1. So, it is now past four in the afternoon, people at NWO will probably leave around five, which leaves me only forty-five minutes to fix things here......<br><br>
Extra complicated is the fact why it is taking so long at the other side of the pond. They need to check the terms and conditions on the grant. One problem there is the Dutch code on animal experiments. The Netherlands has some strict regulations, and the universities have agreed on a code to be open about animal research. Although the document does not have legal value like a law, research funded by NWO still has to adhere to it. And here begin the problems. It states all research should adhere to Dutch animal law. Of course the document was drafted in Dutch and the possibility of non-dutch research applying to the code was not incorporated in the code. So, in principle the strange situation could arise that by agreeing to adhere to the code, Dutch law should take effect when my research is concerned, also abroad. This then causes the Dutch law openbaarheid van bestuur (Openness of Governance) to be applicable to all experiments I do abroad. Something the University probably won't agree to.<br><br>
I asked NWO, they didn't know directly so I had to email them. They will get back to me today with an answer. Then, hopefully, this answer is 'good enough' for the host institute and they sign the form and email it to me. Then I can send in the grant tonight. When they are not happy, then I have to get back to NWO, if they are still there to answer the phone of course.
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That's why I'm freaking out.....
Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0tag:blogger.com,1999:blog-4677896099699125319.post-90123484716277574562012-11-13T22:10:00.000+01:002012-11-13T22:10:41.038+01:00They're moving the finishing line!!!Dear reader,
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it's been a while (again) since I last posted here. I have been caught up in the whirlwind that is called "finishing your thesis". I hoped the storm would have died down a little bit, but if anything, the gale has been growing stronger.
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Last week I finished the one manuscript that was supposedly between me and a thesis. Unfortunately, it turns out non-finished manuscript #2 also needs to become a finished manuscript. So, my assumption that I would go back to more normal, less frantic, working was false. At the moment I'm in full swing getting insane electrophysiology done. I'm talking 'whole cell in-vivo at 2mm depth with a perfusion electrode nearby' crazy electrophysiology. It's an unpublished thing we developed, so I can't be too specific. But, needless to say these experiments suck b*lls when you're in a hurry finishing things.
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Then there's a lot of histology that needs to be done. Some simple recovery of patched neurons and testing a new antibody that we need for immuno-EM. I heard it's always wise to learn a new technique during the last weeks or months of your thesis work (not), so I'm going to do EM now as well (Jeeeej!!!!).
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On the bright side, I have been looking for good estimations of the number or density of cells in the cerebellar cortex. After some cries for help and google scholar searched I have come to the conclusion that no-one ever put all things together. So, I compiled an estimate based on a collection of literature. It all seems to point (roughly) to the same estimation: (in cells per cubic millimeter mouse cerebellum)<br>
Purkinje cells: 20,000<br>
Granule cells: 2.63 million<br>
Mol. Layer Intern: 100,000<br>
Golgi cells: 4,500<br>
I was quite surprised with the Golgi cells being so low. Still, they have an amazing axonal branching pattern, so they can provide a large number of granule cells with inhibition. Also, the high number of interneurons in the molecular layer surprised me. So, the ration MLI:PC seem to be 2:1, quite surprising....<br>
Where did I get this knowledge you ask?<br><br>
<b>References:</b><br>
Lange (1974) Cell and Tissue Research 153:219-26<br>
Woodruff-Pak (2006) Neuroscience 141:233-43<br>
Dugue (2009) Neuron 61:126-39<br>
Sturrock (1989) Journal fur Hirnforschung 30(4):499-503<br>
Altman (1977) Exp Brain Res 29:265-74<br>
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ps. I still love science, don't be alarmed ;-)
Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0tag:blogger.com,1999:blog-4677896099699125319.post-61111891190336383492012-10-25T21:44:00.000+02:002012-10-25T21:44:21.512+02:00Troubles of a grant virgin....I am writing, or rather trying to write, a grant application. It is very difficult and quite different from writing a paper. (So I decided to write a blogpost instead first)<br> I know what is expected from me in a paper. Introduce the study, present your results in a clear way, discuss the results in the context of the scientific field. Also, when appropriate give credit to previous work (references).<br>
But, how does that work in a grant application? There are no results, only plans. So, that means writing an introduction and then present the plans. How far should I take this? The committee is multidisciplinary, so too much details will not help, but maybe there will be some specialists there who would appreciate details. Still, I really wouldn't want to bore any members of the committee. AAAAAARGH!!!!!<br>
Should I use references in the same way as in a paper? I guess not since the grantcommittee will not be interested in all the details. Still, it is good to show that my plans are based in reality and not too outrageously far-fetched.<br><br>
One thing I picked up from a grant I could use as an example from my boss is that every figure should have a very clear, exciting and colorful message. Maybe I should include some figures from my present work, combined with some figures from papers the lab has published I'm going to work......
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Decisions, decisions.....
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There must be some people here who have written grants before. What are the do's and don'ts??? I would be eternally grateful ;-)Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0tag:blogger.com,1999:blog-4677896099699125319.post-38258985586955266712012-10-06T18:08:00.002+02:002012-10-14T14:13:13.648+02:00People hang on his every word, even the prepositions...Okay, so that was another embarrassingly long absence from blogging.
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The last months have been hectic, both professionally and on a personal level. I have a postdoc (jeej!), so I have to finish my PhD in time. This means: finish my book in November, graduate in April, get to Boston in May.
Two papers... two papers is the only thing in between me and my thesis. Two papers to analyse all the data for, two papers to write and then two papers to send off. I know it's ambitious, too ambitious maybe, but I don't really seem to have a choice.
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Meanwhile there was a great little conference here in Amsterdam the last few days. The Cerebnet and C7 consortia had a joint meeting right here in our institute. Today was the final day with a few workshops. Together with a colleague I demonstrated in-vivo patch recordings in the cerebellar nuclei. Now I'm waiting for a PCR gel to settle and I can go home and crash. Next week, an old student will visit the lab, so that's another week out of my schedule. Two papers.....
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There is one great thing though from the conference I have to share with you. The keynote lectures were done by two emiritus professors: Professor Nieuwenhuys and Professor Voogd.<br>
Rudolph Nieuwenhuys spoke about the evolution of the brain and what that tells us about its function. He is an unbelievable speaker, with his 80+ years he still captures the audience; I never heard our colloquiumroom so quiet. A very clear lecture with clear takehome messages after every few slides.
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Jan Voogd then took the audience home, back to the cerebellum. Why is the cerebellum so big in humans? Which zones got bigger? Is this only in primates or also in other mammals? Dolphins for example show a big cerebellum, but this is mainly due to skeletomuscle zones that increased in size. In primates however, the increase is in the non-skeletomuscle parts of the cerebellum.
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They must be the two most interesting men in the world!
<iframe width="420" height="315" src="http://www.youtube.com/embed/fYdwe3ArFWA" frameborder="0" allowfullscreen></iframe>
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The best part actually might have been that they both refused to operate the computer, so someone else was advancing the slides for them. This took the pace out of the presentation and it all came across very calm and controlled. Maybe there is a lesson to be learned here for presentation skills!
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If you want to learn more about these two absolute legends in neuro-anatomy, you can buy their <a href="http://www.amazon.com/The-Human-Central-Nervous-System/dp/3540346848/ref=sr_1_1?ie=UTF8&qid=1349539022&sr=8-1&keywords=the+human+central+nervous+system">book</a>! It's a great bargain, just under $100 for about a thousand pages of wonderful diagrams and clear explanations.
Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0tag:blogger.com,1999:blog-4677896099699125319.post-73560382737106667062012-07-05T22:17:00.000+02:002012-07-05T22:17:06.682+02:00Easy Come, Easy GoMy newspaper has a section called 'Next Question' which contains intriguing questions from readers. This time the question was "How come we never 'forget' how to ride a bike?" The answer was complicated, convoluted and -at best- incomplete. The answer came from a Dutch Neuropsychology professor who explained that when learning to ride a bike you need to couple correct movements to what you see and feel on a bike.
<blockquote>(Not a literal translation, paraphrased)<br><i>If you learn it a little bit you are motivated to get better and better. That is why you keep on making the correct movements fitting to the perceptions. This way you produce robust connections between so-called perception cells and action cells. He makes a reference to Hebb: "Cells that fire together wire together". The more you do it, the more ingrained it becomes. Because every bike works (almost) the same, the relation between perception and action is stable. You never experience something completely different on a bike, that's why you never unlearn it.</i></blockquote><br>
So, you might think, that's not such a bad answer. And no, it's not. It's a bit unclear on which parts of the brain are involved. What are perception cells and action cells, but other that that it sort of makes sense. But in the last section it goes off a bit:<br>
<blockquote>(again paraphrased)<br><i>Less consequent experiences are more susceptible to forgetting. That's why we have problems forgetting what we ate last week for every day. This is because we eat something different almost every day, the memories interfere and we are not able to form strong memorytraces.</blockquote></i><br>
Right, so riding a bike is part of declarative memory? It seems that the answer here is solely built on the principle that if a trace is enforced every time in a constant way it becomes stronger. Though true, it doesn't tell you why you never <i>unlearn</i> to ride a bike, even though you haven't done it for years, while you do forget what you ate yesterday!<br><br>
What about those pesky Dutch spelling rules? We got drilled in school to know where to put <i>d</i>, <i>t</i> or <i>dt</i>. But sometimes I forget.... Why do we forget numbers so easily, but are always able to thump in our pin at an ATM machine? (Honestly, sometimes I can't remember the digits, but when I see a keyboard I can type it!). The same goes with passwords at your computer, sometimes you can't remember, but your fingers can!<br><br>
The answer of course lies within the cerebellum. If you say coordinated movements, such as riding a bike, you say cerebellar involvement. On the other hand, riding a bike is also very much a sequence that you have learned, so you would expect striatal involvement. It's probably a bit of both; maybe first cerebellar coordination to get the movements right, then striatal consolidation? Why then don't you unlearn how to ride a bike, while you do forget other things? Although we do not know the cellular and molecular mechanisms, this question can be answered via a different route.<br><br>
Imagine what would happen if you would learn and unlearn movements in the same vivid and thorough way as you remember your lunch. You would step onto the greens of a golfcourse and you would be able to swing the perfect ball within a few trials. Sounds perfect, doesn't it. But a quick learning implies a quick unlearning as well. You would not be able to make that perfect swing again in one go. And that's what you don't want for your movements. You would forget how to walk after sitting for an hour. So, movements are learned very slowly, so they are also unlearned or forgotten very slowly. Why don't you forget how to learn to ride a bike? Because it took long to learn.Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0tag:blogger.com,1999:blog-4677896099699125319.post-44155004335454537932012-06-28T23:02:00.000+02:002012-07-05T22:28:07.322+02:00Astrocytic regulation of Up- and Downstates<span style="float: left; padding: 5px;"><a href="http://www.researchblogging.org"><img alt="ResearchBlogging.org" src="http://www.researchblogging.org/public/citation_icons/rb2_large_white.png" style="border:0;"/></a></span>
Last week we discussed the paper from <a href="http://www.pnas.org/content/early/2012/04/27/1120380109.short">Wang <I>et al</I></a> (From Maiken Nedergaards lab) in our journalclub. Since our lab has <a href="http://www.nature.com/neuro/journal/v9/n4/full/nn0406-459.html">healthy interest</a> in up- and downstates in Purkinje cells, it was a good choice I think.<br><br>
The authors show that by stimulating the Bergmann glia via a transgenic receptor bistability is reduced and the Purkinje cells show more up- than downstates. During the stimulation, the Bergmann glia cells show a calciumtransient and the extracellular potassium concentration decreases. Interestingly, when the Bergman glia cells were hyperpolarized, Purkinje cells spent more time in the upstate.
Now of course the question is "What causes what?" And that's where the paper goes off the rails for a bit. It claims a causal relation: calcium transients cause the extracellular potassium concentration decrease by uptake by Bergmann glia. This in turn causes a reduction in bistability. But a critical experiment, buffering calcium in Bergmann Glia, was not done. Also, there is no proof that the potassium is taken up by Bergmann glia cells. Still, the paper is interesting. It raises a lot of questions, but firmly establishes a role for glia in Purkinje cell modulation.
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Another puzzling aspect is the exact mechanism of regulation. How does hyperpolarization of Bergmann glia induce calcium transients? Then, how does the calcium transient cause a reduction in extracellular potassium? Would the presumed uptake of potassium by Bergmann glia cells not depolarize the glia cells again? And how does this decrease in extracellular potassium influence the up- and downstates in Purkinje cells. Actually, the last question can be somewhat answered from the paper. It seems that by reducing the external concentration of potassium, the membrane potential for the upstate drops while the membrane potential for the downstate increases. Also, from the paper of <a href="http://jn.physiology.org/content/98/1/278">Fernando Fernandez <I>et al.</I></a> it seems that potassium conductances play a large role in the generation and control of bistability.<br><br>
A possibility that can be excluded is the <a href="http://www.sciencemag.org/content/330/6005/790.abstract">hyperpolarization-induced release of GABA via the Best1 channel</a> found in Bergmann glia. It seemed a very likely candidate: hyperpolarization forces anionic GABA out of the cell and the calcium transient opens the channel. However, bistability during Bergmann glia stimulation was not affected, thus excluding the possibility that GABA release plays a role here.<br><br>
So, it seems that bistability in Purkinje cells can be controlled (somewhat) by Bergmann glia, it is influenced via extracellular potassium and the mechanism is hyperpolarization of the upstate, bringing the states closer together. <a href="http://jp.physoc.org/content/539/2/469.full">Serotonin also does this by acting directly on Ih channels.</a> But this is contested already by Fernandez <I>et al.</I> who didn't find any involvement for Ih channels in bistability. They show that potassium plays a big role in bistability, which is in line with the current study. Then, finally there is the possibility of GABA release from Bergmann glia. But that didn't play a role here....<br><br>
The discussion on Purkinje cell bistability is here to stay. Not only the discussion whether it is really there during waking, but also how it works. Now we probably have to wait for someone to come up with the solution that will connect the pieces rather than introducing a new set of factors. I will stay on top of this, exciting times!<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=PNAS&rft_id=info%3Adoi%2F10.1073%2Fpnas.1120380109&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Bergmann+glia+modulate+cerebellar+Purkinje+cell+bistability+via+Ca2%2B-dependent+K%2B+uptake&rft.issn=&rft.date=2012&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=&rft.au=Fushun+Wang%2C+Qiwu+Xu%2C+Weishan+Wang%2C+Takahiro+Takano%2C+and+Maiken+Nedergaard&rfe_dat=bpr3.included=1;bpr3.tags=Neuroscience">Fushun Wang, Qiwu Xu, Weishan Wang, Takahiro Takano, and Maiken Nedergaard (2012). Bergmann glia modulate cerebellar Purkinje cell bistability via Ca2+-dependent K+ uptake <span style="font-style: italic;">PNAS</span> DOI: <a rev="review" href="http://dx.doi.org/10.1073/pnas.1120380109">10.1073/pnas.1120380109</a></span>Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0tag:blogger.com,1999:blog-4677896099699125319.post-62071335022319357202012-06-12T12:56:00.001+02:002012-06-12T12:56:27.524+02:00Some changes...I want to make a better blog. A blog that is easier to interpret than it is now. Clearer and easier to read.<Br><br>
So, there going to be some changes around here. Posts will be classified into categories, for example: "Research", "PhD life" and "Science related". This way it is easier for you, my dear readers, to navigate to the bits and pieces you find interesting. And of course, you already noticed, the layout and colorscheme have been changed.<br><br>
Content will stay roughly the same of course!Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0tag:blogger.com,1999:blog-4677896099699125319.post-90770866358830919092012-06-12T12:56:00.000+02:002012-07-05T22:34:19.057+02:00Clustering VN cell types<span style="float: left; padding: 5px;"><a href="http://www.researchblogging.org"><img alt="ResearchBlogging.org" src="http://www.researchblogging.org/public/citation_icons/rb2_large_white.png" style="border:0;"/></a></span>
A while ago, during SfN, <a href="http://nerdoscience.blogspot.nl/2011/11/yesterday-i-met-my-heroine-in.html">I wrote about an interesting poster</a> on clustering cell types by single cell RT PCR. The paper is out and I just wanted to share some details with you (In case you're too lazy to read it yourself ;-)).
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The cells in the vestibular nuclei (and in the cerebellar nuclei I can tell you) are hard, if not impossible to distinguish electrophysiologically. So, if you want to find out what different cell types are doing during behavior you're going to have a hard time. No way to distinguish the glutamatergic projection neurons from the glycinergic ones and no way of telling if you're listening to an interneuron or to a GABAergic projection neuron. But <a href="http://www.jneurosci.org/content/32/23/7819.abstract">Kodama et al</a> used expression profiles of transmitter-related genes, ion channels and marker genes based on the <a href="http://www.brain-map.org/">allen brain atlas</a>.
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To be able to compare the results to previous studies they used three mouselines characterized before: YFP-16 (excitatory neurons), GIN (somatostatin, inhibitory neurons), GlyT2 (glycine transporter 2). Only five genes for neurotransmitters and genes related to neurotransmitters were used (VGluT1/2, glycine transporter 2 and Gad1/2). These genes clustered nicely on the different mouselines. Interestingly, the clusters are not perfect, proving that you always have some sort incompleteness and bleed-through with transgenetic animals.
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Now the interesting part is if you can match the expression profile of ion-channel related genes to the <a href="http://www.jneurosci.org/content/27/9/2318.long">physiology</a>. For example: fluorescent neurons in YFP-16 animals have narrow action potentials. And GIN neurons show less rebound firing than YFP-16 neurons do. So, you would expect differences in ion-channels mediating action potential shape and differences in T-type calcium channels and H-channels. Indeed, these differences are reflected in the expression profiles. Genes for NaV1.1 and NaV1.6 are upregulated in YFP-16 neurons as compared to GIN and GlyT2 neurons. The same goes for the hyperpolarizing currents: Kcnc1, 2 and Kcnc3 were all upregulated in YFP-16 neurons. Also the differences seen in postinhibitory rebound firing were reflected in the expression profiles. HCN and combined T-type channel expression were upregulated in YFP-16 neurons.
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Now six classes of neurons can be distinguished by marker genes.<br>
Exc1: Vglut2/ Secreted phosphoprotein 1<br>
Exc2: Vlugt1/ Corticotropin releasing hormone<br>
Exc3: Adcyap1<br>
Inh1: Nav beta4/ GlyT2<br>
Inh2: Coagulation factor C homolog<br>
Inh3: Corticotropin-releasing factor-binding protein<br>
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By doing in-situ hybridization combined with tracer injections, the authors were able to pinpoint the roles of some of the classes. <a href="http://jn.physiology.org/content/95/5/3012.long">Exc1 neurons</a> project to the motor nuclei, Exc2 neurons project to the cerebellar cortex as mossy fibers, <a href="http://www.jneurosci.org/content/29/32/10104.long">Inh1 neurons</a> project to the motor nuclei as well, Inh3 neurons project to the vestibular nuclei and Exc3 and Inh2 neurons could not be traced. (Nucleo-olivary?)<br>
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The tactic used here to classify neurons has some clear advantages. Even neurons that cannot be clustered (easily) on the basis of electrophysiology alone can be identified using genetic expression clustering. Also, if specific markers are known, transgenic mouselines can be generated specifically for each cluster.<br>
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There are also a few things that worry me a bit about the paper. The spike-in RNAs used to quantify the expression profiles do not show the linear relationship that you would expect (fig 1E). In other words, it is not clear whether the results from the genetic profiles are compared to the linear fit and how the outlier is handled. Another concern is that only the MVN was used and only the central part of the MVN. What about the other nuclei and the periphery of the MVN? This is especially a concern since different neuronal morphologies are not uniformly present throughout the nucleus. So, maybe there is only a subsampling of the neurons in the present study.<br>
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Some more research is needed to address these issues. Still, I think the paper is a big leap forwards for cerebellar research.<br><br>
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=The+Journal+of+neuroscience+%3A+the+official+journal+of+the+Society+for+Neuroscience&rft_id=info%3Apmid%2F22674258&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Neuronal+Classification+and+Marker+Gene+Identification+via+Single-Cell+Expression+Profiling+of+Brainstem+Vestibular+Neurons+Subserving+Cerebellar+Learning.&rft.issn=0270-6474&rft.date=2012&rft.volume=32&rft.issue=23&rft.spage=7819&rft.epage=31&rft.artnum=&rft.au=Kodama+T&rft.au=Guerrero+S&rft.au=Shin+M&rft.au=Moghadam+S&rft.au=Faulstich+M&rft.au=du+Lac+S&rfe_dat=bpr3.included=1;bpr3.tags=Neuroscience">Kodama T, Guerrero S, Shin M, Moghadam S, Faulstich M, & du Lac S (2012). Neuronal Classification and Marker Gene Identification via Single-Cell Expression Profiling of Brainstem Vestibular Neurons Subserving Cerebellar Learning. <span style="font-style: italic;">The Journal of neuroscience : the official journal of the Society for Neuroscience, 32</span> (23), 7819-31 PMID: <a rev="review" href="http://www.ncbi.nlm.nih.gov/pubmed/22674258">22674258</a></span>Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0tag:blogger.com,1999:blog-4677896099699125319.post-85066686996850363082012-06-04T20:29:00.000+02:002012-06-04T20:29:46.506+02:00Brains!!! Brains!!!A surprising message from the CDC: 'There is no zombie apocalypse' and 'CDC does not know of a virus or condition that would reanimate the dead (or one that would present zombie-like symptoms)'.
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Of course the evidence is crystal clear and shows the opposite! There are zombie killings all over the world!<br>
<a href="http://www.sfgate.com/cgi-bin/article.cgi?f=/n/a/2012/06/03/national/a082650D25.DTL&tsp=1">San Fransisco Chronicle</a><BR>
<a href="http://www.heraldsun.com.au/technology/sci-tech/cdc-declares-there-is-no-zombie-apocalypse-after-spate-of-cannibal-killings/story-fn5iztw3-1226382746704">Herald Sun</a><br>
<a href="http://www.nydailynews.com/news/national/zombie-apocalypse-horror-movie-genre-twisted-real-life-news-headlines-article-1.1089108?localLinksEnabled=false">NY Daily News</a><br>
<a href="http://www.theonion.com/articles/study-reveals-pittsburgh-unprepared-for-fullscale,1815/">The Onion</a><br>
Clearly, CDC is getting people accustomed to the idea that zombies exist and are going to take over the world, why else all the <a href="http://www.l4d.com/blog/">video games</a> and <a href="http://www.imdb.com/title/tt0365748/">horror movies</a>? It's a conspiracy I tell you!<br>
There are even <a href="http://zombieresearchsociety.com/advisory-board">serious scientists researching this</a>! Do they get the attention they deserve??? NO!
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<b>*Sane Mode Activated*</b><br>
Of course there's no zombie apocalypse, but it's amazing the CDC thought it necessary to comment on this. The existence of zombies should not be a question, let alone an apocalypse. Still, zombies amaze us. Why? Is it something to do with the fact we all like control and we all like to live our lives as we choose? So, a disease that would turn you or others into man-eating brainless undead freaks people out? I guess all people are control freaks up to a certain level.<br><a href="http://www.popcap.com/games/plants-vs-zombies/home" imageanchor="1" style="clear:right; float:right; margin-left:1em; margin-bottom:1em"><img border="0" width="200" src="http://screenshots.en.sftcdn.net/en/scrn/130000/130220/plants-vs-zombies-wallpaper-pack-14.png" /></a>
Good thing I know I've already turned half-zombie by my cat! Yes, cat-lovers, you have a good chance of being infected by Toxoplasmosis, a parasite that lodges itself in your brain and could cause <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=toxoplasmosis%20behavior">behavioral changes</a> in the host.<br>
Fortunately the changes are mild and...... Hmpfff...... Braaaaaainnnns! Brains!!!!! Brains!!!!!Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com1tag:blogger.com,1999:blog-4677896099699125319.post-12376189187529925562012-06-01T00:18:00.001+02:002012-06-01T00:35:25.023+02:00Not a landmark, just 'a thing'Today was a bad day at the lab for me (<a href="http://brainteresting.org/?p=163">'typical', according to Danielle</a>). Experiments didn't work, I freaked out (again) over my results, got depressed about my chances of publishing a paper and I didn't see my PhD ending this year.
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My experiments stopped working about a month ago. I've had it before; it seems to be an up and down motion of productive weeks and unproductive weeks. I think in-vivo patching is a precarious interplay between lots of factors. Get one wrong and your experiment will fail. Get them all right and you have a chance at results, provided you work hard.
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I aim at patching in the cerebellar nuclei, but recently I often overshoot them and get vestibular nuclei instead (which seem to be very easy to patch for some reason). Also, the patches I get in the cerebellar nuclei are of bad quality. I get to 100-200 MOhms of seal and then they drop off. Or they just don't open nicely and I have to dump the recording because nothing can be learned from it. It's probably something to do with slight differences between mice and a slow drift of the stereotaxic location of the nuclei between generations of mice. Why the patching is so hard, I don't know. Tomorrow I will have freshly polished and flamed electrodes. I will throw out my internal solution and make some new. Hopefully this will solve some of the problems.
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I freaked out over my results because I feared I might have patched a lot of vestibular nuclei cells. By inspecting my data closely, this turned out not to be the case. Thank god, I might have been forced to throw out months of work... This of course caused my slight panic attack over my chances of publishing a paper and finishing my PhD. When the attack was gone I decided to take matters into my own hands and have another try at an experiment (for the result, see above).
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Fortunately I have very considerate and wise colleagues. One particular in-vitro patch clamp colleague (who always plays <a href="http://www.youtube.com/results?search_query=creationism+vs+evolution&oq=creatio&aq=2&aqi=g10&aql=&gs_l=youtube.3.2.0l10.130.3096.0.5840.11.9.2.0.0.0.121.365.8j1.9.0...0.0.ZSsxp4eXs2Y">creationism vs evolution</a> or <a href="http://www.youtube.com/results?search_query=religion+vs+atheism+debate&oq=religion+vs+a&aq=1&aqi=g6&aql=&gs_l=youtube.3.1.0l6.88759.93860.0.95451.19.14.3.2.2.0.31.403.14.14.0...0.0.471DplY3hNs">religion vs atheism debates</a> for the lab, which we all thank him for ;-)) had very helpfull insights: A PhD defence shouldn't be too much a landmark event. It doesn't define you as a scientist, it's merely a thing that you need to do to make life easier. It's something you need to pass to get to the next level, but it doesn't define your expertise or you being a scientist. It's just 'a thing'. The most important issue here is to publish thorough papers that you can always defend. So, my PhD book will be more of a 'booklet' with one or two papers and unpublished chapters. Which might end up as published work someday. Don't get me wrong, I would be very happy to get the definite proof on some of the things I've been working on, but it's just not going to stand in the way of me moving on.
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So, tomorrow I'm going to talk to 'my boss' to talk about a PhD defence date for this year (2012, remind me if I missed the mark ;-)). I will continue work on my cerebellar nuclei and cerebellar cortex stuff. If it all works out, it will be submitted or published when I'm finished. If not, so be it.Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0tag:blogger.com,1999:blog-4677896099699125319.post-57368544211304697112012-03-21T23:10:00.000+01:002012-03-21T23:10:56.646+01:00Art of Neuroscience - AmsterdamSo far my idea for consistent posting after my return from SfN. No messages from my side. None whatsoever, my apologies. <br>
I have a new idea though, inspired by an email from <a href="http://brainteresting.org/">my lovely girlfriend</a> about efficient writing. Tips included: 'Forget the idea you're ever going to finish' and 'Forget a generalized audience, ... in writing, your audience is one single reader'. So, armed with some new energy I have to tell you about the wonderful initiative we have in Amsterdam.<br><br>
Science and art have always been friends, since <a href="http://en.wikipedia.org/wiki/Benjamin_Franklin">art can inspire scientists</a> and <a href="http://en.wikipedia.org/wiki/File:Studies_of_the_Arm_showing_the_Movements_made_by_the_Biceps.jpg">science can look pretty darn good too</a>. Everyone must have been amazed by the pictures taken with the <a href="http://en.wikipedia.org/wiki/File:Hubble_ultra_deep_field_high_rez_edit1.jpg">Hubble space telescope</a>, the <a href="http://en.wikipedia.org/wiki/File:FluorescentCells.jpg">pictures taken daily</a> through microscopes in every lab on the globe and <a href="http://en.wikipedia.org/wiki/China_Central_Television_Headquarters">buildings no-one thought were possible</a>, made possible by science.<br><br>
To deliberately make art from science takes more effort, but can have great results. The Amsterdam 'Art of Neuroscience' competition challenges scientists to take their science from the lab, make it pretty and then present it to a general audience. The event took place at <a href="http://www.e-nemo.nl/">NEMO</a>, the Amsterdam science museum, during the <a href="https://www.hersenstichting.nl/activiteiten/alle-activiteiten/brain-awareness-week.html">brain awareness week</a> and received considerable media attention. The entries were from the fields of human fMRI, electrophysiology and imaging to name a few.<br><br>
It's best not to talk (write) too much about it. Better to just direct you to the pictures!<br>
<a href="http://aon.nin.knaw.nl/">The winner - M. Steenwijk</a><br>
Honorable mentions - J. Winnubst, S. Hoyng, C.P.J. De Kock and R. Meredith<br><br>
See all submissions <a href="http://aon.nin.knaw.nl/index.php/submissions">here</a>.Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0tag:blogger.com,1999:blog-4677896099699125319.post-89068311724701407972011-11-20T06:09:00.001+01:002011-11-20T22:39:19.681+01:00Granule cells in awake animals - Strange resultsSfN seems a distant past. Two days in Boston have seemed to eradicated all memory about Washington. Now, after one day in New York even Boston begins to fade. There is however, still so much to tell about the SfN.
Especially the last afternoon poster session was very interesting for cerebellar physiologists. There were two sessions at the same time dedicated to the cerebellar cortex and nuclei. Unfortunately, I was presenting my own poster at the opposite side of the hall, which resulted in me sprinting across the whole thing twice to catch a glimpse of cerebellar research. Nice....
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Mossy fibers seem to be much more active in awake animals than in anesthetized animals. This off course has two effects: granule cells receive both stronger excitatory input and stronger feedforward inhibitory input via Golgi cells. This causes granule cells on average to be more active, especially during movement when they could spike at sustained rates as high as ~5Hz! But, in my opinion, here are some serious concerns with the study as it is now. Clapping resulted in a strong excitatory response in all cells. The authors claimed this was a direct auditory response. This seem strange since in that case all granule cells should receive auditory information. And with only ~4 mossy fiber inputs per granule celll, this seems strange. The auditory input could of course evoke a startle response, which activated granule cells via movement.
<br>Also, the firing rate during movements seems very high for granule cells. This was never recorded extracellularly with for example vestibular stimulation during rotation, where the average maximum firing rate was only 0.7Hz. There is a more scary interpretation of the results. It would be very interesting to see for how long after startle responses or after movement the cells could be recorded and with what quality. Maybe the movement is just too much for such a little cell, and it begins to leak during movement.
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I wrote a long time ago a blogpost about patching in awake and getting your article in Science. I think this study would need a great deal of improvements before it can be published. Still, it is very exciting that some people can patch granule cells on a daily basis in awake animals. Much respect...Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0tag:blogger.com,1999:blog-4677896099699125319.post-76821084867705701052011-11-16T17:18:00.001+01:002011-11-17T14:59:18.760+01:00Bias of the agesYesterday I had an interesting exchange at the optogenetics social (which by the way was the best social I've attended, thank you Ed Boyden!). Someone there was upset with how neuroscience works at the moment (or rather doesn't) and I guess he has a point.
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Jerry Simpson is also saying this to me all the time, although in a different way. Yesterday I ran into him at the posters (like I do five times a day). When he said goodbye he said: "<i>I'm going to have a look what things are presented that have already been done in the 60's!</i>"
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The current focus on optogenetics brings back memories doesn't it? In the early 2000's the human genome project was officially finished. The predictions for the results and benefits of the project were huge. Francis Collins, the director of the human genome project actually said that in ten years there would be genetic tests for many common conditions. Some more enthousiastic people even stated that cancer would be eradicated within the next ten years or so. How wrong has history proven them to be.
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Now in the optogenetics era we have the risk of falling for the same false ideas. Like I wrote in a previous post, science is not about techniques, it should always be about questions.
<br>There probably is much redundant research. People compete for the hottest, newest results in the most high-impact journals. The people who arrive at the same conclusions, but just a month later have big problems to publish the data while their study might actually be better! Also, people tend to repeat older studies with new techniques without any clear reasons to do so. Then the newest study is marked as new results and older material is lost in the ages. Google and Pubmed also play a role in this novelty-bias. Which results do these search engines show? Indeed, the newest ones.
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If anyone has a good idea how to avoid redundancy in research, how to convince people to take into account all those older studies, how to convince journals that 'new' does not mean 'good', please tell me. We should all be able to work out a solution.Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com2tag:blogger.com,1999:blog-4677896099699125319.post-72988244651234759362011-11-16T16:35:00.001+01:002011-11-16T17:04:12.979+01:00Cell-specific markers in the Vestibular Nuclei!Yesterday I met my heroine in Cerebellar electrophysiology. <a href="http://www.snl-d.salk.edu/">Sacha Du Lac</a> runs a lab at SALK that has basically done all identification of cell types in the vestibular nuclei. This started back in the early 2000's and is continuing since. They used the GIN, YFP-16 and GlyT2 mouse lines to label three neuronal classes in the vestibular nuclei. These mouselines have been used before and provide labeling of (putative) GABAergic, glutamatergic and glycinergic neurons. However from early morphological work in the 1960's from Chan-Palay it is clear that there are more than three classes of neurons, probably five or six classes. How to resolve this discrepancy? Electrophysiology is not the way to go since the classes show a continuum of electrophysiological parameters. In other words, there are no clear electrophysiological markers for these cells.
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The people at SALK used a different approach: they used single cell RT PCR to construct single cell cDNA libraries of ~100 genes for ~150 individual cells. This library was then used to construct a clustering of cell types and genes. From this analysis six clear subtypes emerged. All six subtypes can be easily described by the exclusive expression of one or two genes. Of course this is awesome news since it seems possible to make cell-specific transgenic lines (Did I hear anyone scream optogenetics again?). Unfortunately, since the mouselines are not available yet, they didn't have any electrophysiology or morphological data on the subclasses, let alone a wiring diagram of the nuclei.
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It goes to show that things are often more complicated than we thought. Or, just as complicated as people suspected decades ago.Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0tag:blogger.com,1999:blog-4677896099699125319.post-45552418282935071732011-11-15T03:28:00.001+01:002011-11-15T03:39:31.244+01:00There's no such thing as a free pen!I've got a pen. I don't know what company gave it to me, but I got a pen. It's already broken and I didn't need the pen to start with, but that's probably not that important. What is important is that I got something for free. Also I've tried to win an Ipad a few times. I didn't win it, I got another pen.
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As you've already probably guessed, I've been visiting the exhibit today. I wanted to check out a few companies and see some products. The danger is in the people with the badge-scanners. They will hunt you down and in return for a pen they scan your badge so they can spam you and make money off of you. Or as someone once cleverly put it: <i>If you’re not paying for it, you’re not the customer. You’re the product being sold.</i>Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com1tag:blogger.com,1999:blog-4677896099699125319.post-67342481055075230242011-11-14T16:24:00.001+01:002011-11-14T16:54:22.887+01:00Undergrads are like a supercomputerYesterday I saw the talk from Winfried Denk. Why is Winfried Denk awesome? He practically invented the two photon microscope. He now invented a technique to image large brain volumes and trace all neurites in it. How he does it is as interesting as the results. Computer tracing did not provide the results he wanted. There were a lot of misses, partially traced neurites, wrong combinations, etc. Manual tracing performs much better, but is very time consuming since all tracing at the ultrastructural level is done by outlining the neurites in every slice. This is slow, as Winfried showed us by playing a movie of someone outlining neurites section by section. Or as Winfried put it: "This is so slow, I can't look at it!". His new tracing methods only involves clicking every few slices in the neurite you're tracing. This results in a 'skeleton' trace of the neurons. By having a small army of undergrads every neuron is traced multiple times after which the computer can evaluate the differences in tracing and by a 'democratic' process selects the correct 'skeleton'. The really cool part is where the automatic segmentation is overlaid on each skeleton. Now each neuron has a volumetric model. For a small piece of retina it cost ~30.000 hours to trace 1m of neurite from a few hundred of cells.
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So, by combining a sloppy computer segmentation with the awesomeness of the paid undergrad brain you can reconstruct sections or a whole brain at the ultrastructure level. He is some sort of scientific Chuck Norris!Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0tag:blogger.com,1999:blog-4677896099699125319.post-77630094804433203982011-11-14T15:09:00.001+01:002011-11-14T16:28:59.813+01:00Why cheap techniques are not always goodYesterday there was a whole alley of posters about optogenetics here at the SfN meeting. Of course this technique is very hot, easy and cheap to use. So, it was to be expected that a lot of labs would jump on the bandwagon. Unfortunately, most research was not very interesting. Or rather, very not interesting: "We used optogenetics to look at attention", "We made a new virus that performs slightly worse than what is available", "We introduced optogenetics into the common hedgehog, and guess what; it does what it's supposed to do!", "We used optogenetics to...". You get what I mean....
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Fortunately, among all this nonsense there were a few gems.
One poster finally solved convincingly the debate how many cerebellar molecular layer interneurons provide input to one Purkinje cell. This question is more complicated than it seems since molecular layer interneurons are electrotonically coupled. When coupling is strong you can have indirect effects of multiple cells through other interneurons. The lab of G.J. Augustine from Duke University used ChR2 expression in interneurons to map the spatial extent of inputs from molecular layer interneurons to one patched Purkinje cell. First they mapped the spatial extent of one interneuron by patching it and scanning the slice looking for direct activation. The spatial extent of one neuron turned out to be ~5500um2. Then, by mapping the input to one Purkinje cell they estimated that five to six interneurons are involved in providing inhibitory input to one Purkinje cell. After blocking gap junctions this number reduced to ~2 interneurons. Interestingly, this effect completely disappeared when coronal slices were used. This confirms that interneurons are coupled in the sagittal plane and interneurons can influence distant Purkinje cells in the same zone.
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An other poster was about the difference between somatostatin and parvalbumin positive interneurons in the visual cortex. M. Sur's lab from MIT used celltype specific virus-driven expression of ChR2 to probe the functional impact of interneurons in vivo. Tuning curves for Pyramidal cells were determined by providing moving gratings and imaging the pyramidal cell's responses using calcium imaging. When PV neurons were activated, the pyramidal cell's response showed a scaling of the response. In contrast, SOM interneurons provided a subtractive operation. Clearly the two neuron classes have different functional implications. Since PV interneurons project mainly to the soma of cells and SOM interneurons mainly to the dendrites, it would be interesting to see whether this effect would hold for other brain areas as well where inhibitory input is differentially provided to somata and dendrites.
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Clearly, optogenetics is a powerful tool when used correctly. It's always been the same: techniques should never be leading in research, questions should.Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0tag:blogger.com,1999:blog-4677896099699125319.post-85241973220918189182011-11-13T02:45:00.001+01:002011-11-13T03:27:57.918+01:00The Cerebellar-Cerebro connectionIt's been too long. Still, another attempt to revive the blog. I am at the SfN at this moment and I have to say that the environment is very inspiring. Inspiring for my research and inspiring for blogging.
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There are a lot of gaps in our current understanding of the neurosystem. One particular issue concerning the cerebellum is how it fits into the rest of the nervous system. Just ask any cerebellar scientist what the cerebellum does and how it does that. You'll get very diverse answers. Also, nobody knows exactly how the cerebellum codes signals and how the code is composed coming from the cerebellar nuclei. What is the influence of the cerebellar nuclei on the thalamus, on the red nucleus, on motor nuclei in the brainstem? Are there projections from the cerebellar nuclei directly to the cerebral cortex, or to the hippocampus? All these questions have only been very slightly touched upon in the sixties and seventies of the twentieth century using tracing techniques and some basic electrophysiology. Only recently a few papers came out from David McCormick's lab and Dieter Jaeger's lab on how the cerebellar neurons relate to EEG signals from the cerebral cortex. Many scientists I have spoken to are anxious to start and discover how the cerebellum ties in with the rest of the nervous system.
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Today I saw three posters from the Detlef Heck's lab that shed some light on how the dentate influences the thalamic and the reticulo-tegmental nuclear pathways to the prefrontal cortex. Apparently, when Purkinje cell input to the dentate nucleus stops (for example due to PC loss in Lurcher mice) the balance between RTN and thalamic pathways shift towards more input from the thalamus to the prefrontal cortex. This shift is probably only visible on longer timescales, so acute pharmacological interventions won't show this shift. The posters were written from the standpoint of an autism model. I find that a bit of a long shot; I had never considered Lurcher mice an autism model. However, the same effects were seen in Fragile X mice making the claim somewhat more believable. Still, all mutants used were global mutants, so no cell specificity here, so the results are quite hard to interpret.
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It seems that the cerebellar cortex has a direct effect on the cerebral cortex, but how and what influence this is, is completely unknown. We know the pathways, we know a bit about coding in the cerebellum and frontal neocortex. Let's hope we can find answers to these questions in the coming years. The first steps have been taken, now we need to find the details.Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0tag:blogger.com,1999:blog-4677896099699125319.post-50205975840058288112010-07-04T17:49:00.002+02:002010-07-04T17:52:48.914+02:00Forum European NeuroscienceHey all,<br /><br />It's been too long since I posted here. The main reason being the preparation for FENS (Forum of European Neuroscience). Today is the second day of the conference and the debate on a few things is clearly on:<br />* Is there rebound in CN neurons under invivo awake conditions?<br />* If there is rebound in CN neurons, what would it do?<br />* Up- and downstates in the cerebellum, are they real, or an artifact? (Yes, I hear you! Not again!!!!!!)<br />* Up- and downstates in the cerebrum: an effect of anesthesia and sleep?<br /><br />So, expect me to post a few things about these subjects the coming time. I think these questions will keep me occupied for a while.Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0tag:blogger.com,1999:blog-4677896099699125319.post-70547965481747131762010-05-13T18:31:00.003+02:002010-05-13T18:34:02.949+02:00Understanding Animal ResearchIt's been a while since I posted something here. I found a very good website with balanced views on animal research: <a href="http://www.understandinganimalresearch.org.uk/">Understanding Animal Research</a>. And they're on facebook as well! Unfortunately we don't have anything like this in The Netherlands.Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0tag:blogger.com,1999:blog-4677896099699125319.post-83424810434382887922010-02-24T22:16:00.002+01:002010-02-24T22:21:18.287+01:00Animal rights terroristsThe reason I only call myself 'Neuronerd' is simple. I don't want my appartment to be set on fire, or my family harassed.<br />The situation is outrageous!<br /><a href="http://negotiationisover.com/2010/02/07/ucla-theatre-presents-dario-ringach-cant-answer-an-email-but-hes-perfect-for-the-pretend-debate/">Terrorist website</a> (Warning caps-lock key is stuck on this blogger's keyboard)<br /><a href="http://scienceblogs.com/ethicsandscience/2010/02/time_to_get_mad_time_to_speak.php">It's time to get mad</a> I agree, we should not let these nutcases win.Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0tag:blogger.com,1999:blog-4677896099699125319.post-75324820626951734782010-02-24T11:23:00.002+01:002010-02-24T11:26:33.688+01:00Brain development<a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj6pw2LlJpA4xkUeyyD-DMjoZlqdXYkqES5Ggj5JLCXEGUoGQLWqPVr8GJZ5Tbj-RykIO2q4ZPFm2vm7E4sJo6jth60d6_T0JT93cSqwAr-d7Zky-fHVLvH_S4cie9CU8N6pUz1a5vLgxdu/s1600-h/brain_dev.jpg"><img style="display:block; margin:0px auto 10px; text-align:center;cursor:pointer; cursor:hand;width: 400px; height: 259px;" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj6pw2LlJpA4xkUeyyD-DMjoZlqdXYkqES5Ggj5JLCXEGUoGQLWqPVr8GJZ5Tbj-RykIO2q4ZPFm2vm7E4sJo6jth60d6_T0JT93cSqwAr-d7Zky-fHVLvH_S4cie9CU8N6pUz1a5vLgxdu/s400/brain_dev.jpg" border="0" alt=""id="BLOGGER_PHOTO_ID_5441753863167768274" /></a><br />Here's an awesome cartoon from Jorge Cham, artist behind "PhD Comics". Check out his website: <a href="http://www.phdcomics.com/">Piled Higher and Deeper</a><br />(WARNING!!! Procrastination awaits you!)Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0tag:blogger.com,1999:blog-4677896099699125319.post-64782579856646109362010-02-08T21:27:00.004+01:002010-02-08T22:22:36.533+01:00Patching in awake animals gets you into Science!Navigation activates the hippocampus. For each location we visit, specific place cells are activated. Conventionally, place cells are recorded by using chronic single- or multi unit recordings. The biggest drawback of these techniques is the lack of information about what is happening inside the cell. This part of information has been lacking for a long time. Whole cell, or sharp electrode recordings can provide this information, but are very challenging in awake behaving animals. The group of Michael Brecht (who else) have taken the challenge and recorded from a number of hippocampal neurons in awake navigating animals (<a href="http://www.sciencemag.org/cgi/content/abstract/327/5964/474">Epsztein et al. Science, 2010</a>).<br /><br />The most interesting finding is the occurence of spikelets in these neurons. These spikelets are different from spikes and EPSPs, but still they are correlated with navigation. Of course this all sounds very interesting, but is it actually? What are we learning here? The spikelets probably do not transmit down the axon because they reflect subthreshold activity. They can, like EPSPs, be underlying spikes in these neurons. But, these spikes could have been detected by extracellular means as well.<br /><br />Then there must be some exciting story at the input site! Of course there must be a cool story here, otherwise 'Science' would never consider it for publishing. Unfortunately, the authors have no clue what they are looking at. They propose axo-axonal coupling, dendritic spikes or extopic axonal spikes. But none of these explanations have been tested here. So, the input side of this story has not been investigated properly yet.<br /><br />Now, what did we learn from this? 1. There are spikelets in hippocampal principal cells. 2. These spikelets can be underlying spike firing. 3. spikelets are correlated with navigation in a similar way as spikes.<br />So it seems that using a fancy technique is enough to get into science. Let's all go for patching in free-flying zebra finches. Not because we might actually learn something from it, but because we can and it gets us into 'Science'.Neuro Nerdhttp://www.blogger.com/profile/01166415732502224710noreply@blogger.com0