donderdag, 31 mei 2012

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others should give careful consideration to these risks and uncertainties.

Again, we're behind on blogging you guys are keeping us busy with great neuroscience but here is the story of apair of papers that appeared back to back in last week's issue and a continuation of the discussion started here by Noah about the process of joint publication. The two papers by Tobias Boeckers and colleagues and by Eunjoon Kim and colleagues were independently submitted and both describe autism like phenotypes of mice with mutations in the geneShank2. Shank2 is a scaffolding protein that regulatesexcitatory synapsefunction by holding together various molecules such as neurotransmitter receptors and signaling proteins. Mutations in another member of the samegenefamily, SHANK3, are also associated with human autism, and mutant mice display behaviors reminiscent of ASD symptoms, such as social deficits and obsessive behavior. So this protein family, and more generally, glutamatergic transmission, is potentially one promising line of investigation.

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Each of today Saucony Blue And White papers describe mice with striking Saucony Cohesion 10

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behavior (hyperactivity and social deficits) and alterations in excitatory neuronal activity. And that's where things start to get (even more) interesting. The mice carry very similar genetic mutations, and have similar behavior, yet are opposite in some aspects of electrophysiology. A lot of science we could discuss here but on to editorial .

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