Culling through the SFN abstract browser is an imperfect process. Keyword searches can be helpful, particularly if you’re interested in a fairly specific topic, like, say, “1-bromopropane” (1 hit). But if you’re interested in “postnatal neurogenesis” (292 hits) or “hippocampus memory” (1118 hits), make sure your scrolling finger is rested and well-fed. Because there will be scrolling. Or you might try searching by name. You’ll avoid delayed-onset finger soreness, but you’ll inevitably forget about so-and-so and that other guy, and -worse- you’re certain not to discover anyone new.
So you end up supplementing your name searches with some combinatorial keyword strategy. You find some cool posters. And then you discover that your blogging partner already found the same posters and posted about them two days ago. So you ice your scrolling finger and post about a few cool abstracts he didn’t already mention.
|Title:||Adult hippocampal neurogenesis regulates the response to stress|
|Presentation Time:||Saturday, Nov 13, 2010, 4:00 PM – 5:00 PM|
|Authors:||*J. S. SNYDER1, M. BREWER2, L. GLOVER2, K. SANZONE2, H. CAMERON2;
1UNP, NIMH/NIH, BETHESDA, MD; 2NIMH, NIH, BETHESDA, MD
JSS, our very own functional neurogenista (neurogenisto?) extraordinaire, has a doozy this year, implicating adult-born neurons in feedback regulation of the HPA axis stress response. Glucocorticoids released by the adrenals in response to stress activate receptors in the hippocampus (and other regions), which, in turn, suppress further glucocorticoid release. Jason shows that this hippocampal feedback regulation is impaired when adult hippocampal neurogenesis is blocked by either of two different methods. The convergent results with two different methods constitutes strong evidence that the impairment was caused by the arrest of neurogenesis rather than side-effects of either method of arresting neurogenesis. This is exciting because it may be the best evidence yet linking adult hippocampal neurogenesis to a specific physiologic function. The finding could also provide important insights into the still-poorly-understood role of adult hippocampal neurogenesis in depression and in the therapeutic effects of antidepressant drugs. For instance, previous work suggests that increased neurogenesis may mediate some anxiolytic effects of antidepressant drugs. Jason’s result suggests a potential mechanism: the antidepressant-induced increase in neurogenesis moderates stress-induced HPA activity.
|Title:||Unique gene expression profiles of neural stem cells and their progeny in the adult brain|
|Presentation Time:||Wednesday, Nov 17, 2010, 11:00 AM -12:00 PM|
|Authors:||*O. BRACKO1, T. SINGER2, S. AIGNER2, M. KNOBLOCH1, B. WINNER2, J. RAY2, G. D. CLEMENSON2, H. SUH2, S. COUILLARD-DESPRES3, L. AIGNER3, F. H. GAGE2, S. JESSBERGER1;
1Inst. of Cell Biology, Swiss Federal Inst. of Technol. (ETH), Zurich, Switzerland; 2Lab. of Genet., The Salk Inst. for Biol. Studies, La Jolla, USA, CA; 3Inst. for Mol. Regenerative Med., Paracelsus Univ., Salzburg, Austria
It sure would be nice to know more about the gene expression profiles of neural progenitors and immature neurons in the adult brain. With this information, you could devise new, more precise strategies for targeting genetic manipulations to these populations. You could potentially identify gene networks that make immature neurons more excitable and plastic than their mature counterparts. You could identify genes that cause some neural stem cells to divide while others remain quiescent, or that cause some progenitors to produce neurons while others produce glia or another copy of themselves. Looks like someone is onto this.
|Title:||Time-dependent brain-wide reorganization of functional networks supporting contextual fear memory|
|Presentation Time:||Sunday, Nov 14, 2010, 11:00 AM -12:00 PM|
|Authors:||*A. L. WHEELER1,2, C. M. TEIXEIRA1, A. R. MCINTOSH5,3, N. KOVACEVIC5, P. W. FRANKLAND1,2,4;
1Hosp Sick Children, Toronto, ON, Canada; 2Inst. of Med. Sci., 3Psychology, 4Physiol., Univ. of Toronto, Toronto, ON, Canada; 5Rotman Res. Inst., Toronto, ON, Canada
Contextual fear memories are initially stored in the hippocampus. But over time, they appear to migrate elsewhere. We believe this because of experiments demonstrating that lesions to the hippocampus shortly after acquisition of contextual fear conditioning impair recall of the memory, whereas lesions made several weeks after acquisition usually do not impair recall. So, where do the memories go and how do they get there? Using immediate early genes, Paul Frankland’s lab has analyzed brain activity in response to recall of recent versus remote memories. According to the abstract, the remote memories evoke activity in a broad swath of cortical and subcortical space, suggesting that remote memories have a highly distributed neural representation. I am looking forward to visiting the poster and finding out what the recent memory representation looks like. Is it exclusively hippocampal, meaning that memories migrate over time from the hippocampus to a highly distributed extrahippocampal network? (Doubt it.) Or is the recent memory also highly extrahippocampal? Perhaps the extrahippocampal network is involved all along, with its strength increasing over time so that the hippocampus is eventually rendered superfluous.