What was bright and shiny this week? 04.10.09

11 April 2009 by Noah Gray, posted in Uncategorized

Looking back over what caught my eye, I was a little light on neuro this week. But perhaps you’ll understand when you realize that competing for my attention were polls examining the understanding of evolution in Muslim schools, the steady rise of ‘shit’ in the Guardian, the NYT threatening to close the Boston Globe, and the potential break-up of an ice shelf the size of CT. Nevertheless, let’s check out the neuro: (cont.)


Less than half of postdocs considering a future in academia
Okay, so right out of the gate I lead with a non-neuro story, but of course this is significant. When a journal as prominent as Science discusses the concept of “leaving science”, it catches all of our attention. This editorial sparked a blog post from me, as well as some decent discussion. I’m still waiting for someone to find me the primary data from that poll…
The mechanism underlying scratching as itch relief
This story was picked up by the NYT_, who made up for a lame fluffy piece on memory editing?r=1&partner=rss&emc=rss&pagewanted=all with this more balanced informative piece describing the latest research from Nature Neuroscience. Although we already knew that there were a class of spinal neurons dedicated to broadcasting itch signals, we did not know how these signals were ceased through the action of scratching. The NN paper found something slightly predictable, namely that scratching produces an inhibition of STT neuron activity only during histamine-evoked activity, but not during spontaneous activity or pain-evoked firing. In other words, a state-dependent inhibition.
Schizophrenics see through hollow-mask illusion
The New Scientist covered a fascinating finding building upon our knowledge that schizophrenics are immune to certain visual illusions. Specifically, the “hollow-mask illusion” failed to confuse or fool those with schizophrenia while control subjects were fooled 99% of the time. This could be quite a diagnostic tool, as concluded by the authors. The finding also underscores a pet theory of a few prominent schizophrenia researchers, which goes a little like his: those suffering from the illness have increased perceptual, sensory or other superior basic traits that when translated through faulty circuitry, cause the psychosis. Although advantageous for detecting certain environmental stimuli, these same heightened abilities become a liability when too much information is passed on to suboptimal higher-order processing centers. Just theory.
Specific neotenic changes in human cortical mRNA expression could underlie increase in brain size
Developmental retardation, or neoteny, has been proposed as a possible mechanism contributing to the rise of many human-specific features, including an increase in brain size and the emergence of human-specific cognitive traits. These authors compared the transcriptomes of chimps and humans and found significant differences in the levels of a particular subclass of the transcripts, ones that are known to influence brain development. They believe that increased activity by these genes while the progression of neural development is slowed down in time leads to the increase in brain size observed in humans.
Social isolation reduces post-stroke survival rate
In rats, those animals that were housed individually following transient intraluminal middle cerebral artery occlusion (a surgically-induced stroke) had a decreased poststroke survival rate and enhanced infarct size and edema development as compared to those animals socially housed following the stroke. There was also an altered neuroinflammatory response, with IL-6 levels centrally down-regulated (but peripherally up-regulated) in the isolated animals. Since IL-6 antibody injection neutralized the socially-induced differences, the authors even had a molecular link between the housing situation and the stroke outcome.
Connectomics and the future of understanding the brain’s wiring diagram
The Economist had a pretty nice piece on connectomics in last week’s edition. For the uninitiated, connectomics aims to map all of the connections between neurons in the brain. This piece also reminded Mo Costandi of how cool this field is (and how pretty the data are) and he dug up two blog posts: one on brainbow and the other on retrograde-traveling rabies tracing viruses
Increased membrane cholesterol might initiate a death cascade in mature hippocampal neurons
Using neuronal cultures, researchers found that older neurons tend to aggregate more cholesterol in their plasma membranes. Cholesterol tends to make membranes more fluid and this change could potentially lead to increased Ca2+ influx into those cells, and subsequent activation of proteases like calpain. Continuing along this trajectory, enhanced calpain activity may cut and produce more toxic fragments of tau, causing greater cell death in these older cells. So cholesterol may be at the root of the strong link between Alzheimer’s pathology and aging.
Increased maternal grooming leads to a decrease in dendritic complexity, spine density & mini currents
Mouse mothers exhibit a wide range of attentive and nurturing behavior when it comes to taking care of their pups. The authors here found mothers that were at the two extremes of “licking and grooming” (LG) display and subsequently examined the morphological and functional traits of cortical neurons in those pups after they became adults. Interestingly, those pups subject to high LG actually had decreased dendritic complexity, a reduced spine density and reduced amplitudes when miniature currents were measured. Since these measures were taken in the somatosensory cortex, these differences could reflect a desensitization to the constant touch the pups experienced, but it must be more complicated than that since these changes persisted for at least 2 months, well into adulthood. I initiated some discussion on the paper to try to get to the bottom of this. I would like to know what the developmental time course of these changes are, and I’d also like to dissociate social behavior from the changes by mixing up the housing environment in the intervening months between weaning and the measurements. Your views are welcome here, but more appropriately on the paper itself.


One Response to “What was bright and shiny this week? 04.10.09”

  1. Eric Michael Johnson | Permalink

    That’s very interesting about the high LG behavior resulting in less dendritic complexity in the somatosensory cortex. The authors report an earlier study in their lab showing exactly the opposite in the hippocampus:

    “it was shown that hippocampal CA1 pyramidal neurons of adult offspring from high LG mothers exhibited longer dendrites and increased spine density as compared to offspring of low LG mothers.”

    Would this suggest that reelin acts as a promoter in one region and an inhibitor in another?

    I was very excited by the work of Meaney and colleagues a few years ago that showed epigenetic affects resulting in increased affiliative behavior in high LG pups (and reduced glucocorticoid levels). Like you, I’d be curious to know what occurs when low LG pups are introduced to a group of high LG pups. Do they adapt to the new “culture” as Rutte and Taborsky found with generalized reciprocity or are their neural pathways, and the associated behaviors that result, fixed after exposure to a low LG maternal style?

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