Neuroscience posts

February 13, 2012
08:19 AM
5 views

Neurons tuned like the strings of a harp

by TheCellularScale in The Cellular Scale

The auditory brainstem of the boring-old-chicken is actually home to some fascinating neurons.Key West rooster, taken by me.The Nucleus Laminaris (NL) is a group of coincidence-detecting neurons which receive indirect input from both ears and is located in the bird auditory brainstem. NL neurons show a peculiar dendrite pattern. These bipolar neurons fall into the particular category of football shaped cells which have dendrites coming out the top and bottom of their cell body. The cell body (soma) of these neurons are about the same size, but depending on where they are in the NL, the cells have either short, medium or long dendrites. The ones near the midline have a bunch of short stubby little dendrites.Figure 2B from Smith and Rubel, 1979If they are a little further out from the midline, they have longer dendrites.Figure 3B from Smith and Rubel, 1979and finally if they are furthest from the middle, they have fewer and much longer dendrites.Figure 10A Smith and Rubel 1979all together this makes a gradient from short to long dendrites. From Figure6 Smith and Rubel 1979The big question here is "Why?"What is the purpose of having stubby or extended dendrites like this? Well, even in 1979 when Smith and Rubel reconstructed these neurons, they knew that these neurons had a special answer to the "form and function" question. The amazing thing about these neurons is that they are 'tuned' to respond maximally to specific frequencies (sound waves). And just like strings on an instrument, the cells with shorter dendrites respond to higher frequencies and the cells with longer dendrites respond to lower frequencies. Why is this? Dendrites don't actually vibrate like strings, but there must be some reason for a cell with short dendrites to respond to higher frquencies and a cell with long dendrites to respond to low frequencies. The answer lies in what the Nucleus Laminaris actually does. In the next post we'll venture into the wilds of computational neuroscience and explore the reason behind this strange connection between dendrite shape and cell function. © TheCellularScaleSmith DJ, & Rubel EW (1979). Organization and development of brain stem auditory nuclei of the chicken: dendritic gradients in nucleus laminaris. The Journal of comparative neurology, 186 (2), 213-39 PMID: 447882... Read more »

Smith DJ, & Rubel EW. (1979) Organization and development of brain stem auditory nuclei of the chicken: dendritic gradients in nucleus laminaris. The Journal of comparative neurology, 186(2), 213-39. PMID: 447882

February 13, 2012
07:00 AM
5 views

February 13, 2012

by Erin Campbell in HighMag Blog

Our nervous system would be in trouble without myelin sheaths and nodes of Ranvier. No, those two things do not refer to some kind of Lord of the Rings-type silliness. They are very important components of our nervous system that ensure fast and efficient signal conduction.Myelin sheaths are membranes that insulate the axons of many neurons. Myelin sheaths have distinct domains of ion channels and proteins, such as the nodes of Ranvier, along the axon that are required for the high speed and efficiency of signal conduction along the axon. The nodes of Ranvier, for example, are especially important for swift movement of an axon’s action potential, which jumps from node to node in a process termed staltatory conduction. A recent paper describes the importance of a cytoskeletal adaptor protein called 4.1G in regulating the localization of proteins along the axon-sheath interface. Ivanovic and colleagues found that in mice without 4.1G, adhesion proteins and neuronal proteins were mislocalized. Images above show localization of 4.1G at the same sites as two other periaxonal membrane proteins (MAG on left, Necl4 on right) in adult mouse sciatic nerves.Ivanovic, A., Horresh, I., Golan, N., Spiegel, I., Sabanay, H., Frechter, S., Ohno, S., Terada, N., Mobius, W., Rosenbluth, J., Brose, N., & Peles, E. (2012). The cytoskeletal adapter protein 4.1G organizes the internodes in peripheral myelinated nerves originally published in the Journal of Cell Biology, 196 (3), 337-344 DOI: 10.1083/jcb.201111127... Read more »

Ivanovic, A., Horresh, I., Golan, N., Spiegel, I., Sabanay, H., Frechter, S., Ohno, S., Terada, N., Mobius, W., Rosenbluth, J.... (2012) The cytoskeletal adapter protein 4.1G organizes the internodes in peripheral myelinated nerves. originally published in the Journal of Cell Biology, 196(3), 337-344. DOI: 10.1083/jcb.201111127

February 13, 2012
12:12 AM
24 views

Just ONE Copy of The Daily Mail Could Ruin Your Life

by Neurobonkers in Neurobonkers

A comprehensive debunking of the Daily Mail's reporting of science.... Read more »

The Poynter Institute. (2006) Eyetracking the news. A study of print and online reading. Poynter. info:/

February 12, 2012
03:28 PM
33 views

Big Brains in Evolutionary History

by Matt & Cris in Originus

In 1985 I visited the Soviet Union with a small group of Austrian tourists (I was studying in Vienna at …Continue reading »... Read more »

Gross, C. (1993) Huxley versus Owen: the hippocampus minor and evolution. Trends in Neurosciences, 16(12), 493-498. DOI: 10.1016/0166-2236(93)90190-W

February 12, 2012
01:30 PM
17 views

The Role of experience in flight behaviour of Drosophila

by Sathishk in neuro JC

This study illustrates the requirement of training and exercise in executing successful fine motor skills in the invertebrates.Fruit fly Drosophila groups reared and grown in two different fly chambers ,one allows free flight movement and other restricted flight movement were tested for various flight kinematics in free flight arena and tethered flight simulator.Overall performance [...]... Read more »

Hesselberg, T., & Lehmann, F. (2009) The role of experience in flight behaviour of Drosophila. Journal of Experimental Biology, 212(20), 3377-3386. DOI: 10.1242/jeb.025221

February 12, 2012
01:21 PM
23 views

Cell Phone Use and Risk of Brain Cancer

by William Yates, M.D. in Brain Posts

In my last post I examined the epidemiology of brain tumors using a summary of the latest data from the United States. The summary noted the slight decline in the number of malignant brain cancers over the last twenty years.One area of concern that is receiving increased attention is the potential for cell phone risk to raise the risk of brain cancers.Obviously if cell phone use was a very large effect one might have expected an increase in the rates of brain tumors and cancer over the last twenty years. This corresponding to the time when cell phone use has increased dramatically in the U.S. and around the world. Multiple case control studies have been completed examining this possible association and the majority of studies have not demonstrated a significant effect. One recent study from Frei in Denmark along with colleagues in France and Switzerland adds to the apparent safety of cell phones.The key design elements of the Frei study included:Study type: Cohort study using all individuals born in Denmark from April 1, 1968Study groups: Cell phone subscribers status (subscribers versus non-subscribers) was identified via phone records and linked to centralized health records containing health registry information including presence or central nervous system tumors.Confounding variables controlled: age, gender, education level, incomeOutcome variable: incidence rates ratio with 95% confidence interalThis data set included over 300,000 individuals with a cell phone subscription and a larger group of control individuals. The researchers grouped brain tumors into malignant gliomas, meningiomas (largely benign brain tumors) and a residual group of other brain tumor and cancer types.The analysis showed the incidence rates for cell phones subscribers did not statistically differ from those who did not differ from those without cell phone subscriptions in any brain tumor or cancer group.This is an important study. It represents a very large data set with comprehensive registry data that would be difficult to replicate in the United States health care system. The authors noted no specific increase in temporal lobe gliomas in the cell phone user group. This region of the brain would be the closest region to cell phone placement during calls and theoretically most likely to be affected if an association was present.The authors concluded: "a small to moderate increase in risk for subgroups of heavy users or after even longer induction periods than 10-15 years cannot be ruled out". Nevertheless, this study should reduce worry that cell phones users are significantly increasing their risk for brain tumors or cancer.Photo of male and female chachalaca pair from Bentsen Birding Center in Texas from the author's files.Frei, P., Poulsen, A., Johansen, C., Olsen, J., Steding-Jessen, M., & Schuz, J. (2011). Use of mobile phones and risk of brain tumours: update of Danish cohort study BMJ, 343 (oct19 4) DOI: 10.1136/bmj.d6387... Read more »

Frei, P., Poulsen, A., Johansen, C., Olsen, J., Steding-Jessen, M., & Schuz, J. (2011) Use of mobile phones and risk of brain tumours: update of Danish cohort study. BMJ, 343(oct19 4). DOI: 10.1136/bmj.d6387

February 10, 2012
03:06 PM
1 view

Wrap your brain around precursor cells

by Erin Campbell in the Node

A fully differentiated cell took a fascinating journey to become its present self. For every cell, a precursor cell existed that gave rise to it. And for every precursor cell, a stem cell existed that gave rise to it. Understanding precursor cells is an important part in understanding stem cell biology. Today’s image is from [...]... Read more »

Mairet-Coello, G., Tury, A., Van Buskirk, E., Robinson, K., Genestine, M., & DiCicco-Bloom, E. (2012) p57KIP2 regulates radial glia and intermediate precursor cell cycle dynamics and lower layer neurogenesis in developing cerebral cortex. Development, 139(3), 475-487. DOI: 10.1242/dev.067314

February 9, 2012
09:42 AM
47 views

LTP and LTD at the same time? Adventures in Functional Compartmentalization

by TheCellularScale in The Cellular Scale

On Monday we talked about LTP and LTD on a basic level, today we are discussing how they interact with each other. In a recent Open Access paper, Pavlowsky and Alarcon ask the question: Can some synapses on a neuron strengthen while at the same time others weaken? And if so, how do the two processes interact with each other? neurons firing (source)First let's get some background. Synapse strengthening (LTP) and synapse weakening (LTD) both require new proteins to be synthesized at the soma* (*in this particular situation, sometimes they don't require it, but those details are too deep to dive into here). So what happens if LTP is induced at some synapses and LTD is induced at others on the same neuron? There are three possibilities:They compete for protein synthesis at the soma, one using up all the precious protein synthesis machinery and impairing the development of the otherThey cooperate, one starting up the protein synthesis engine at the soma so it's ready to go, helping the other. They don't interact and just do their own thing like normal. To determine which of these possibilities actually happen in a neuron, Pavlowsky and Alarcon induce LTP and LTD on the same cells, but in different places. Showing stimulation on the same side of the somaFrom Figure 2 Pavlowsky and Alarcon 2012 They induced LTP in one spot (S2) and then induced LTD in another (S1). And lo and behold! the LTP happening first prevented the LTD (favoring the compete hypothesis above). So this shows that LTP and LTD compete in the neuron. But what are they competing for?There are two steps in protein synthesis where LTP and LTD might compete: translation (getting a protein from an mRNA) and transcription (creating more mRNA from the DNA). To test whether translation or transcription is important for this competition, the researchers induced LTP at S2 in the presence of either a translation blocker (anisomycin) or a transcription blocker (actinomycin-D). Then they washed away the blocker and induced LTD at S2.From Figure 6 Pavlowsky and Alarcon 2012 The translation blocker allowed for subsequent LTD at S1 (top left of figure), while the transcription blocker didn't (top right of figure), even though both prevented the initial LTP at S2 (bottom panels of figure). This is evidence that the translation phase of protein synthesis is important for determining which form of plasticity gets induced (LTP or LTD). So what does all this mean? The results support the compete hypothesis, that the first plasticity induction (LTP or LTD) gets dibs on most of the plasticity-related protein synthesis machinery and prevents the other from happening. However, if the first induction can't access the protein translation machinery (because it is blocked with anisomycin), then the second induction is able to use it just as it normally would. The authors do a thorough job investigating this phenomenon, testing different time intervals between LTP and LTD induction, testing location of the stimuli, and have some interesting discussion about what this might mean for learning and memory. If you are interested in the details, I highly recommend this paper, it's in PLoS One, so it is open access. Pavlowsky A, & Alarcon JM (2012). Interaction between Long-Term Potentiation and Depression in CA1 Synapses: Temporal Constrains, Functional Compartmentalization and Protein Synthesis. PloS one, 7 (1) PMID: 22272255... Read more »

Pavlowsky A, & Alarcon JM. (2012) Interaction between Long-Term Potentiation and Depression in CA1 Synapses: Temporal Constrains, Functional Compartmentalization and Protein Synthesis. PloS one, 7(1). PMID: 22272255

February 9, 2012
05:36 AM
66 views

Why parkin has scientists backing the future of Parkinson's research

by Andrew Watt in A Hippo on Campus

Back in the '80s the name Michael J. Fox was more or less interchangeable with that of Marty McFly, the effortlessly cool protagonist from the Back to the Future trilogy who introduced an entire generation of kids to hoverboards, self-lacing shoes and flux capacitors. Not to mention 'Johnny B Goode'. These days however Fox's name is more likely to have us thinking of his fight with Parkinson's disease, which he was diagnosed with back in 1991, or the advocacy work he does for his aptly named Michael J. Fox Foundation for Parkinson's Research. Looking at their mission statement you can't help but get the feeling that Fox has brought a little of Marty "nobody calls me chicken" McFly's fighting spirit to the Foundation as it dedicates itself to "finding a cure for Parkinson's disease through an aggressively funded research agenda". Whilst a cure remains allusive, recent research funded by the Foundation has resulted in a giant leap forward in our understanding of Parkinson's disease and suggests that the cure which Fox hopes will one day put him out of business may not be as far off as once thought.It all starts in the basal gangliaClinically, Parkinson's disease (PD) is characterised by an array of motor symptoms including tremors, rigidity, slowness of movement (or bradykinesia) and gait and walking difficulties. Symptoms which are thought to result from neuronal degeneration within the substantia nigra, a small region of the basal ganglia which acts to produce and release the neurotransmitter dopamine. The basal ganglia is a highly organised group of structures located at the base of the forebrain which exerts a constant inhibitory effect on our various motor systems. An effect which helps to prevent our bodies from becoming inappropriately active. And that's where dopamine comes in. The dopamine, produced by the substantia nigra, acts to facilitate the release of the basal ganglia's inhibitory influence, and thus allows movement to occur. It might be easier to think of the motor system as a somewhat fused set of gears attached to a small motor. Despite the motor (motor system) being active the friction (basal ganglia) is too great to allow the gears to turn. The friction can however be overcome by spraying a small amount of lubricant (our dopamine in this analogy) onto the gears, thus whilst the dopamine doesn't actively turn the gears it acts to reduce the constant friction between the gears thus allowing the motor to initiate movement. Our brains work in much the same way, everything is able to work smoothly in the presence of our personal lubricant, dopamine (sounds wrong I know but stick with me here), however when sufficient levels of dopamine are not available, such as in Parkinson's disease, our ability to initiate and control our movements slowly grinds to a halt.Like most neurodegenerative conditions, the neuronal loss associated with Parkinson's disease occurs due to a variety of factors, some of which are environmental whilst others are genetic. However, as is often the case, it is the rarer genetic forms of the disease which offer the greatest promise for therapeutic advancement in the field. Approximately one in 10 Parkinson's cases result from mutations in the parkin gene, a gene on chromosome six which encodes a component of the E3 ubiquitin ligase complex (for those of you playing at home). Normally this knowledge would result in the use of a mouse model of the disease, however parkin knockout mice show no signs of Parkinson's disease suggesting that parkin mutations act selectively on human nigral dopaminergic neurons. The selective nature of the parkin gene was, until recently, a major hurdle in Parkinson's research as the complexity of neuronal networks in the human brain make it incredibly difficult to study the genetic form of the disease. After all parkin-affected dopaminergic human neurons aren't something you can just grow in a lab. Or at least they weren't, until now.Test tube neuronsThat's right for the first time ever scientists have managed to generate human dopaminergic neurons from Parkinson's disease patients with parkin mutations. And what's more they made them from skin. Ok so to be more specific the researchers generated human induced pluripotent stem cells from dermal fibroblasts (skin cells), collected from two Parkinson's patients (both with parkin mutations) and two controls. The stem cells were subsequently used to generate the dopaminergic neurons some of which contained the parkin mutations and some of which did not. The generation of these mutant neurons allowed the researchers to finally observe parkin in action in its native habitat, and enabled them to see just how mutations in the gene were leading to neuronal damage. As it would turn out normal parkin acts to control the production of monoamine oxidase, or MAO for short, an enzyme which acts to catalyse dopamine oxidation. The production of MAO is normally tightly controlled to ensure that adequate levels of dopamine are being oxidised and our movements are able to all run smoothly. However when parkin mutations occur, the tight control of MAO production is lost and MAO is expressed at much higher levels. But what's the big deal? Surely there's nothing wrong with a bit of extra MAO floating around the place. After all it just means we'll have some MAO for a rainy day, right? Wrong. As it would happen MAO production is generally tightly controlled for a very good reason. It's toxic! Yep, at high levels MAO leads to the degeneration of our dopaminergic neurons as a result of oxidative stress. And no amount of shiraz-based anti-oxidants can do anything about it. But whilst shiraz may not work, it turns out that restoring control over MAO production does, as lead author Houbo Jiang and his team found that the early-stage damage could be reversed by delivering normal parkin back into the cells. As well as providing insight into the role parkin plays in genetic forms of the disease, these findings also provide a novel target for future Parkinson's treatments. MAO production. Whilst one of the drugs currently on the market acts to inhibit MAO activity, there are no therapies which attempt to restore control over MAO production. At least not for the time being. So with the hope these findings seem to be injecting into the field of Parkinson's research, you can't help but get the feeling that if Marty McFly were reading this now he'd smile and say 'if only they knew, there's just a few short years to go'. And I for one am hoping he's right. SourcesJiang, H., Ren, Y., Yuen, E., Zhong, P., Ghaedi, M., Hu, Z., Azabdaftari, G., Nakaso, K., Yan, Z., & Feng, J. (2012). Parkin controls dopamine utilization in human midbrain dopaminergic neurons derived from induced pluripotent stem cells Nature Communications, 3 DOI: 10.1038/ncomms1669... Read more »

Obeso JA, Rodríguez-Oroz MC, Benitez-Temino B, Blesa FJ, Guridi J, Marin C, & Rodriguez M. (2008) Functional organization of the basal ganglia: therapeutic implications for Parkinson's disease. Movement disorders : official journal of the Movement Disorder Society. PMID: 18781672

February 9, 2012
12:02 AM
54 views

Baseline Neurocognitive Test Performance and Symptoms may be Influenced by Depression

by Jane McDevitt in Sports Medicine Research (SMR): In the Lab & In the Field

The objective of this study was to examine depression and baseline neurocognitive function and concussion symptoms in male and female high school and college athletes.... Read more »

Covassin T, Elbin RJ 3rd, Larson E, & Kontos AP. (2012) Sex and Age Differences in Depression and Baseline Sport-Related Concussion Neurocognitive Performance and Symptoms. Clinical Journal of Sport Medicine. PMID: 22246342

February 8, 2012
03:33 AM
72 views

Visualizing The Connected Brain

by Neuroskeptic in Neuroskeptic

So it seems as though the "connectome" is the latest big thing in neuroscience. This is the brain's wiring diagram, in terms of the connections between neurons and on a larger scale, between brain regions.We certainly won't understand the brain without getting to grips with the connections but equally, it's not the whole story. I previously emphasised that the brain is not made of soup; it's not made of spaghetti, either.Connectomics does however unquestionably provide some of the prettiest images in neuroscience. And they just got prettier, with a new technique for visualizing connections, just revealed in Neuroimage: Circular representation of human cortical networks for subject and population-level connectomic visualization.See above. It's a rather lovely vista (for which the authors Irimia et al share credit with the folks behind the Circos visualization tool they used).All you need are some MRI scans, and a lot of image processing, and you can produce one of these "Connectograms". But what does it mean? Here's the authors' description:The outermost ring shows the various brain regions arranged by lobe (fr — frontal; ins — insula; lim — limbic; tem — temporal; par — parietal; occ — occipital; nc — non-cortical; bs — brain stem; CeB — cerebellum) and further ordered anterior-to-posterior. The color map of each region is lobe-speciﬁc and maps to the color of each regional parcellation.In other words, the outer ring is just a list of brain regions, each with an assigned colour. The inner rings tell us about those regions: Proceeding inward towards the center of the circle, these measures are: total GM volume, total area of the surface associated with the GM–WM interface (at the base of the cortical ribbon), mean cortical thickness, mean curvature and connectivity per unit volume. For non-cortical regions, only average regional volume is shown.So each of the five inner rings displays data about one aspect of brain anatomy, for each of the regions. The colors are a heat map of the numbers.Finally, the lines between regions represent the degrees of connectivity between regions via white matter tracts, as measured with diffusion tensor imaging:The links represent the computed degrees of connectivity between segmented brain regions. Links shaded in blue represent DTI tractography pathways in the lower third of the distribution of FA, green lines the middle third, and red lines the top third (see text for details). You can also make a pooled connectogram of the average neuroanatomy across a group of people. Still, it remains to be seen whether these are as useful as they are beautiful.Irimia A, Chambers MC, Torgerson CM, and Van Horn JD (2012). Circular representation of human cortical networks for subject and population-level connectomic visualization. NeuroImage PMID: 22305988... Read more »

Irimia A, Chambers MC, Torgerson CM, & Van Horn JD. (2012) Circular representation of human cortical networks for subject and population-level connectomic visualization. NeuroImage. PMID: 22305988

February 8, 2012
02:07 AM
41 views

a human and a monkey walk into an fMRI scanner…

by Tal Yarkoni in citation needed

Tor Wager and I have a “news and views” piece in Nature Methods this week; we discuss a paper by Mantini and colleagues (in the same issue) introducing a new method for identifying functional brain homologies across different species–essentially, identifying brain regions in humans and monkeys that seem to do roughly the same thing even if they’re [...]... Read more »

Mantini D, Hasson U, Betti V, Perrucci MG, Romani GL, Corbetta M, Orban GA, & Vanduffel W. (2012) Interspecies activity correlations reveal functional correspondence between monkey and human brain areas. Nature methods. PMID: 22306809

Wager, T., & Yarkoni, T. (2012) Establishing homology between monkey and human brains. Nature Methods. DOI: 10.1038/nmeth.1869

February 8, 2012
01:13 AM
33 views

Deaf hearing

by Janet Kwasniak in Thoughts on thoughts

A recent paper examined a patient with deaf-hearing, analogous to blind-sight, where there can be detection of a signal without conscious awareness of it. (citation below) For example, a person with blind-sight may avoid an obstacle without awareness of it; and, a deaf-hearing person may be startled and orient towards a noise without consciously hearing [...]... Read more »

Cavinato, M., Rigon, J., Volpato, C., Semenza, C., & Piccione, F. (2012) Preservation of Auditory P300-Like Potentials in Cortical Deafness. PLoS ONE, 7(1). DOI: 10.1371/journal.pone.0029909

February 7, 2012
09:10 AM
56 views

Military Use of Neuroscience Should Be Regulated, Report Warns

by Jaime Menchen in United Academics

tDCS is a form of neurostimulation that, in the case of the research mentioned above, led to a better detection of concealed objects, based on the fact that the brain detects things before the subject is consciously aware of them. The results also showed that it may improve learning abilities, thus decreasing “the time required to attain expertise in a variety of settings,” according to the study.... Read more »

Clark, V., Coffman, B., Mayer, A., Weisend, M., Lane, T., Calhoun, V., Raybourn, E., Garcia, C., & Wassermann, E. (2012) TDCS guided using fMRI significantly accelerates learning to identify concealed objects. NeuroImage, 59(1), 117-128. DOI: 10.1016/j.neuroimage.2010.11.036

February 6, 2012
08:44 AM
80 views

the synapse: where the magic happens

by TheCellularScale in The Cellular Scale

What is a synapse?The synapse is the junction between two neurons, usually between an axon, which gives the signal, and a dendrite, which receives the signal. This meeting of neurons is absolutely essential to how the brain works. It is where the information gets passed on from one neuron to the next. The 'magic' at the synapseWhen someone talks about neuronal pathways being strengthened, they usually mean a strengthening of this synaptic connection. This strengthening (or weakening) is referred to as "synaptic plasticity." Specifically, when the connection between two neurons is strengthened, it is often referred to as Long Term Potentiation (LTP) and when it is weakened it is is often called Long Term Depression (LTD). Synaptic plasticity is so exciting because it is a feasible biological mechanism for memory formation and storage. How this 'magic' was discoveredThe first paper to show that the connections between neurons could be strengthened was Bliss and Lomo 1973. They were studying the hippocampus, the region that underlies episodic memory and spatial learning.Bliss and Lomo, 1973 Fig1aThey found that when you stimulated the nerve fibers with certain frequencies (100 Hz is now a commonly used frequency for this), the signal from the group of neurons grew, and stayed large for hours. (They tracked at least one experiment for 10 hours!) Bliss and Lomo, 1973 Fig4cIn this figure, the dots represent the size of the signal at each point in time. The arrows represent the high frequency stimulation (here they stimulated 4 times). After each stimulation, the signal grows. The black dots are the pathway that was stimulated and the open circles are an unstimulated pathway that they used as a control. The concept that activity patterns between cells could strengthen the connection between them fundamentally changed the way people thought about information processing in the brain. Now there is a huge branch of neuroscience devoted to connecting LTP and LTD to behavior and investigating the mechanisms which underlie synaptic plasticity. In a retrospective paper, Lomo describes how the discovery came about. I found this quote particularly interesting:"Why did I not pursue and publish a fuller account of my findings in 1966? Because I was overcome by the complexity of the system and my lack of understanding of what was behind the findings. There was also no sense of urgency. Thus, when Tim and I published a full account in 1973 (Bliss & Lømo 1973), it still took years for the significance of the findings to be generally appreciated. "It's hard to imagine 'no rush' to publish something like this and it is refreshing to see a scientist who is hesitant about publishing something that s/he does not fully understand.Bliss TV, & Lomo T (1973). Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path. The Journal of physiology, 232 (2), 331-56 PMID: 4727084Lømo T (2003). The discovery of long-term potentiation. Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 358 (1432), 617-20 PMID: 12740104... Read more »

Bliss TV, & Lomo T. (1973) Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path. The Journal of physiology, 232(2), 331-56. PMID: 4727084

Lømo T. (2003) The discovery of long-term potentiation. Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 358(1432), 617-20. PMID: 12740104

February 5, 2012
04:32 AM
64 views

Psychiatry's True Blood? Pt 1.

by Neuroskeptic in Neuroskeptic

Imagine that there was a blood test that could detect depression. Wouldn't that be useful?It depends.Ridge Diagnostics are a US company who offer such a test. They've just published some results of the technology in Molecular Psychiatry. In two samples of patients with major depressive disorder (MDD), they report differences in the"MDDScore", between the patients and healthy controls.The MDDScore is an aggregate value, calculated from the levels of 9 metabolites in blood serum. They're all well-known molecules, including hormones, such as cortisol and prolactin. The novelty is in how they're put together to make the MDDScore. We're given equations - but the key variables are not provided, because they're proprietary:Long-term Neuroskeptic readers will recall that this "secret ingredients" approach to publishing science was also adopted by another company offering a different depression test.Anyway, the performance of the test was impressive. In both the pilot and the replication samples, the MDDScore was significantly higher in the depressed people than in the controls. In both cases, the test had a sensitivity of over 91% and a specificity of over 81%, which is pretty good. Ridge Diagnostics are already offering the MDDScore clinically. For $745 a pop.However...Although there were two depressed patient groups (n=36 and 34), there was only one set of controls (n=43); both patient samples were compared to it. This means the second, "replication", test was not fully independent of the first one. If the first finding was a fluke caused by the control group having weird results by chance, for instance, then the second study would just repeat the fluke.The patients were significantly older, and with a higher BMI, than the controls. They did control for these variables, which is good, but this raises the question of whether these folks differed in other ways, that they didn't measure, and hence couldn't control for.In both samples, the patients had a very significantly higher MDDScore than the controls (p less than 0.0001, both times). But in both cases, the difference in levels of EGF (epidermal growth factor) was almost as strong: p=0.0003 and p less than 0.0001, respectively. Other metabolites weren't far behind. Testing for EGF would almost certainly be cheaper than getting an MDDScore.Finally, all these data demonstrate is that the test can distinguish between people with MDD and entirely healthy people. But how often are doctors going to need to do that? More likely, they'll want to distinguish depression from other things that are often confused with it, such as: bipolar disorder, anxiety disorders, chronic fatigue syndrome, bereavement, "stress", and all manner of physical illnesses e.g. thyroid problems. Daniel Carlat said last year that If the test cannot distinguish different psychiatric problems, then the MDDScore is simply a non-specific "biomarker" for emotional difficulties of all stripes, and would be essentially useless. How disorder-specific is the MDDScore? This paper doesn't tell us. And to date, this is the only published paper mentioning the MDDScore. The website mentions some conference presentations, but none have yet appeared in a peer reviewed journal.Ridge Diagnostics have an interesting history. But that's another story - stay tuned for Part 2.Papakostas, G., Shelton, R., Kinrys, G., Henry, M., Bakow, B., Lipkin, S., Pi, B., Thurmond, L., and Bilello, J. (2011). Assessment of a multi-assay, serum-based biological diagnostic test for major depressive disorder: a Pilot and Replication Study Molecular Psychiatry DOI: 10.1038/mp.2011.166... Read more »

Papakostas, G., Shelton, R., Kinrys, G., Henry, M., Bakow, B., Lipkin, S., Pi, B., Thurmond, L., & Bilello, J. (2011) Assessment of a multi-assay, serum-based biological diagnostic test for major depressive disorder: a Pilot and Replication Study. Molecular Psychiatry. DOI: 10.1038/mp.2011.166

February 4, 2012
09:47 AM
59 views

Critical role for protein kinase A in the acquisition of gregarious behavior in the desert locust

by Björn Brembs in neuro JC

Posted on behalf of Hans-Joachim Pflüger:
In the article by Ott et al. the role of two protein kinases (PK) in the population density dependent transition from solitarious to gregarious animals is investigated. Only gregarious locusts form large swarms that are harmful for agriculture. The foraging gene product, a cGMP-dependent PK (PKG), implicated in foraging, and [...]... Read more »

Ott, S., Verlinden, H., Rogers, S., Brighton, C., Quah, P., Vleugels, R., Verdonck, R., & Vanden Broeck, J. (2011) Critical role for protein kinase A in the acquisition of gregarious behavior in the desert locust. Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.1114990109

February 3, 2012
02:05 AM
73 views

A gene for trauma

by Suzanne Elvidge in Genome Engineering

Why do some people go through some really traumatic experiences and emerge unscathed, and others end up traumatised? It might be down to coping strategies, but genes might influence it too, according to research from Rutgers University.... Read more »

Martel, G., Hevi, C., Wong, A., Zushida, K., Uchida, S., & Shumyatsky, G. (2012) Murine GRPR and Stathmin Control in Opposite Directions both Cued Fear Extinction and Neural Activities of the Amygdala and Prefrontal Cortex. PLoS ONE, 7(2). DOI: 10.1371/journal.pone.0030942

February 2, 2012
09:17 AM
95 views

You can't trust your receptors: Smell

by TheCellularScale in The Cellular Scale

Food smells better when you're hungry, right? This is a common phenomenon that everyone I've ever talked to on the subject has experienced. For a long time, I assumed that the entire process underlying this phenomenon is in the brain proper, and not in the olfactory epithelium (that is, the smell receptors themselves). However, a study on the adorable (and totally weird) salamander known as the 'Axolotl' suggests that the brain proper can actually modulate how sensitive those smell receptors are.Axolotls (source) yes, it does make a good pokemon characterBefore I start explaining, let it be known that I am not saying the brain proper doesn't contribute to the 'food-smells-better-when-you're-hungry' phenomenon, in fact I would be very surprised if it didn't involve modulation of the ventral tegmental area, nucleus accumbens, and hypothalamus. Mousley et al. (2006) use a technique called electro-olfactogram (EOG) to record the signals from smell receptors. When the cells are excited by an odor, the size of the response can be recorded. They are using this technique in Axolotls, but it can be used in humans too:EOG recording in humans (source)Using this technique, Mousley et al. tested whether the size of the smell cells' signal could be modulated by a neuropeptide that is found in the terminal nerve (the nerve that connects the brain proper to the smell-sensing cells). Chemicals that 'act like' this peptide can have confounding side effects, so the experimentors went to a lot of trouble to make sure they were using the peptide that is actually expressed in these animals. They copied and synthesized this peptide from the genome of the axolotl. So what did they find? The found that this peptide (NPY) could modulate the size of the EOG response in hungry axolotls. They applied the same amount of odor molecule and the same amount of NPY for each recording, so the increase in response is not due to more odor molecules or more NPY being present. They suggest that it might be due to mory NPY receptors on the smell cells themselves, indicating that when hungry, the smell cells change in these animals. Mousley et al., 2006 Fig4So what does that mean? It means that when the animal is hungry, the brain proper has the ability to change the excitability of the smell receptors by dropping some NPY on them (through the terminal nerve). This study showed the one specific peptide had an effect, but the principle that the brain can actually change the way the peripheral receptors sense things really struck me. I had always thought that the receptors were pretty much stable, and pretty much always sent the same signal to the brain, but that the way the brain interpreted that signal could be different. It fundamentally changed my view of sensory cells to learn that the smell receptors don't always send the same signals to the brain. source It made me rethink the studies that show expectation of taste changes the interpretation. The north dakota wine studies, and the wine-taste evaluation studies show that people rate things differently depending on what they are expecting. A common response is 'ha, what idiots to be influenced by the label of the wine and not trust their own tastebuds' when one reads about studies that show people evaluate white wines with red food coloring as if they were red wines and the like.However, now I give these wine tasters more credit. Perhaps the untrustworthy smell cells were actually altered by the brain's expectation. I haven't seen any study testing this idea with EOGs on humans, but I think it would make a great experiment. ... Read more »

Mousley A, Polese G, Marks NJ, & Eisthen HL. (2006) Terminal nerve-derived neuropeptide y modulates physiological responses in the olfactory epithelium of hungry axolotls (Ambystoma mexicanum). The Journal of neuroscience : the official journal of the Society for Neuroscience, 26(29), 7707-17. PMID: 16855098

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