Encephalon Celebrates its Emerald Anniversary

Welcome to a landmark edition of Encephalon, the cream of the crop of brain science blog carnivals. This is the 55th edition of Encephalon, an anniversary achieved by less than 5% of married couples. Thus, this edition is a testament to the dedication of neuroscience bloggers: they don’t even take vows, yet they still stay committed to providing their readers with scintillating perspectives on developments in brain science. While more than 95% of married couples give up before their emerald anniversary, brain bloggers keep typing away, upholding their pledge to inform. (We will conveniently disregard the fact that Encephalon occurs biweekly, not annually, which, if considered, would make the analogy to marriage somewhat ridiculous.) Anyway, on to a selection of the best and brightest neuroscience blogs from the last couple of weeks.

Jeremy, a contributor to SharpBrains, provides a superbly written piece about assessing the affects of video games on adolescents. The rational perspective is greatly appreciated.

Greg from Neuroanthropology discusses neuroplasticity, and why the process has been oversimplified, the term overused, and the hype a little unjustified (hmmmm...this reminds me of mirror neurons).

The Neurocritic applies his caustic wit to the sensationalism that surrounds studies of the underlying personality traits of liberals and conservatives.

Cognitive Daily looks at a study of teenagers' sexual behavior. Listen up, abstinence-only advocates...

Dr. Shock MD reviews targets in the brain for deep brain stimulation, an intriguing treatment for highly resistant depression.

Mo at Neurophilosophy has an excellent and thorough discussion of a fascinating disorder: developmental topographagnosia.

Brain Blogger contributes its usual group of insightful posts. One discusses the potential antipsychotics may have in reducing the risk of suicide in depressed patients, something that current antidepressants fail at doing (they sometimes actually increase it). Another examines a little-known treatment for diabetes: the ketogenic diet.

Neuronism continues to impress with well-written contributions to Encephalon. This one is an overview of computational neuroscience, a little-understood but increasingly important field.

Dan at Sports are 80 Percent Mental is exceptional at getting us to consider the neuroscience of sports. This time he describes the success of different cognitive strategies in golf.

The Mouse Trap has two interesting postings about 8 common adaptive problems that drive evolution across species, they are here and here. Another post discusses a suggested expansion of the big five personality traits.

That's it for the emerald edition of Encephalon. Thanks for all your submissions! The next edition will be hosted by Combining Cognits on October 13th. Send your submissions to encephalon {dot} host {at} gmail {dot} com.

Encephalon #55 Call For Submissions

Encephalon #55 will be hosted here next Monday--I may be too lazy to post original material, but I'm not too lazy to post links to other people's stuff! Please send potential postings to encephalon {dot} host {at} gmail {dot} com.

A Brief Hiatus

Anyone who reads this blog regularly will have noticed that the frequency of posts has slowed quite a bit over the past few weeks. The truth is, between two jobs, an assistantship, classes, and my thesis I've occasionally had trouble finding time to eat and sleep, much less blog. So, I'm taking a brief hiatus to get my priorities under control. I'm definitely not closing up shop, and will still be hosting the 55th edition of Encephalon here on September 29th. Check back occasionally until then...thanks!

Have a Face Only a Mother Could Love? Without Serotonin She Thinks You're Just as Ugly as Everyone Else Does

As the popularity of antidepressant medication has burgeoned over the past few decades, serotonin has become one of the more publicly recognized neurotransmitters. Along with that popularity has come a trend of attributing a wide variety of behaviors (especially depression) to “serotonin imbalances”. While this is a gross simplification in most cases, it does seem to be clear that there is a correlation between serotonin transmission and behavior.

A group of researchers at Case Western Reserve University has recently shown that the disruption of serotonergic function in mice is powerful enough to inhibit one of their strongest instincts: caring for their young. They used female mice with a mutation that causes a reduction in the expression of serotonergic genes and in the synthesis of the neurotransmitter, and monitored the survival of their young after they gave birth.

99% of the pups of the wild-type (normal) mice lived past the nurturing period of youth, but none of the pups of the serotonin-inhibited mothers survived. In fact, most of them were dead after 3-4 days. When the researchers took pups born to the serotonin-deficient mothers and gave them to the wild-type mothers to raise, the pups survived. The serotonin-deficient mothers failed to nurse their pups, didn't build nests for them, and didn't organize them near her in a huddle (which is necessary for their warmth and survival).

The serotonin-inhibited mothers did not seem to exhibit deficiencies in any other behavioral assay, such as maze-running or olfaction. They were not deemed to be overly anxious as measured by locomotor tasks, but instead of mothering they often simply paced the cage and engaged in repetitive digging. The authors suggest that anxiety behaviors may have been more prominent if not for the relaxing effect lactating has on rodents.

How applicable these findings are to humans is, of course, completely unclear. Postpartum depression is often treated with selective serotonin reuptake inhibitors, but even if untreated doesn’t generally lead to abandonment of one’s children. Regardless, finding a neurochemical substrate for an instinct like caring for one's young is notable, as it is a behavior essential to what is widely considered the goal of existence: high reproductive fitness.

Reference:

Lerch-Haner, J.K., Frierson, D., Crawford, L.K., Beck, S.G., Deneris, E.S. (2008). Serotonergic transcriptional programming determines maternal behavior and offspring survival. Nature Neuroscience, 11(9), 1001-1003. DOI: 10.1038/nn.2176

Cocaine and Glutamate, Part Two

Ten years ago, if you had asked a neuroscientist what neurotransmitter is most important to the development of an addiction, nine out of ten times they would have said “dopamine”. Ask the same question today, however, and you’ll probably be told that it is impossible to pin such a complex process on one neurotransmitter, as clearly (at least) both dopamine and glutamate are integral to the addiction process.

In hindsight, it is not surprising that glutamate be involved in addiction. Glutamate is the most abundant excitatory neurotransmitter in the brain. It is utilized in a number of cognitive processes, but essential to synaptic plasticity, and thus to learning and memory. And addiction is really just a type of learning—perhaps learning gone haywire, but learning nonetheless. It involves the association of a positive experience with the drug that was taken to induce it, resulting in a seeking of the drug to reproduce the experience. In addiction, however, unlike other learning processes, this seeking becomes obsessive and compulsive.

It is now thought that cocaine use causes glutamatergic synapses on dopamine neurons in the ventral tegmental area (VTA), a midbrain region of the reward system, to become stronger—even after just a single use. This makes the dopamine neurons there more sensitive to glutamate, causing a hyper-sensitivity to cocaine that results in addiction. It is believed the strengthening of these glutamatergic synapses involves changes in the composition of subunits of glutamate receptors.

In order to shed more light on the specifics of this subunit restructuring, a study published last week in the journal Neuron investigates the behavioral results of changes in glutamate receptor structure. The authors created genetically engineered mice that lacked one of three types of glutamate receptor subunits: GluR1, GluR2, or NR1.

As expected, they found that cocaine-induced strengthening of synapses on dopamine neurons was dependent on the functionality of glutamate receptor subunits, specifically the GluR1 and Nr1 subunits. They also, however, made two major discoveries. First, deletion of the GluR1 subunit caused the extinction of cocaine-seeking behavior to be slowed. Thus, these mice continued to seek cocaine long after cocaine had been withheld from them, when normal mice had already “forgotten” about the drug. By extension, this might mean that pharmacological stimulation of this receptor could have potential as a treatment for addiction.

Additionally, they found that the NR1 receptor subunit was necessary for the reinstatement of drug-seeking behavior after extinction. This is analogous to relapse behavior in humans. Once again, this could have pharmacological potential in addiction treatment.

Of course, these pharmacological applications, if viable, will take some time to work out. As you can imagine, it will not be easy to create a treatment that can selectively inhibit specific subunits on glutamate receptors in a particular brain region (although this can and has been done with other receptor subunits). And, with how important glutamate is to learning in general, there is potential that a treatment aimed at glutamate receptors could disrupt other cognitive processes. So, if you’re waiting for a pill to solve your cocaine problem, you may have to wait a while longer. A cocaine vaccine (see here) may be available first.

Reference:

ENGBLOM, D., BILBAO, A., SANCHISSEGURA, C., DAHAN, L., PERREAULENZ, S., BALLAND, B., PARKITNA, J., LUJAN, R., HALBOUT, B., MAMELI, M. (2008). Glutamate Receptors on Dopamine Neurons Control the Persistence of Cocaine Seeking. Neuron, 59(3), 497-508. DOI: 10.1016/j.neuron.2008.07.010