[Todos] Seminarios conjuntos DFBMC-IFIByNE- Çagla Eroglu- lunes 21 de diciembre, 13 hs- RECORDATORIO

Paula Felman pfelman en fbmc.fcen.uba.ar
Lun Dic 21 11:01:02 ART 2009


Seminario lunes 21 de diciembre, 13 hs. Aula de seminarios del LFBM

Title: How do Astrocytes Induce CNS Synaptogenesis?

by Çagla Eroglu
Stanford University Medical Center, Department of Neurobiology, Stanford, 
CA 94305, USA, Current address: Duke University Medical Center, Cell 
Biology Department, Durham, NC, 27705, USA.

Abstract:
Synapses are asymmetric cellular adhesions that are critical for nervous 
system development and function, but the mechanisms that induce their 
formation are not well understood.  Thrombospondin (TSP) is a large 
oligomeric astrocyte-secreted extracellular matrix protein that is 
sufficient to induce synapse formation in the central nervous system and is 
necessary for astrocyte-enhanced synaptogenesis in vitro. We identified the 
thrombospondin receptor involved in synapse formation as the calcium 
channel subunit alpha2delta1, which is also the receptor for the 
anti-epileptic and analgesic drug gabapentin. We show that alpha2delta1 
interacts with the epidermal growth factor-like repeats common to all 
thrombospondins. alpha2delta1 overexpression increases synaptogenesis in 
vitro and in vivo and alpha2delta1 is required for thrombospondin and 
astrocyte-induced synapse formation in vitro. We found that gabapentin is a 
potent inhibitor of excitatory CNS synapse formation in vitro and in 
vivo.  These findings identify alpha2delta1 as a novel signaling receptor 
that induces synapse formation and suggest that gabapentin may mediate its 
therapeutic function by blocking new synapse formation.

Host: Dr. Osvaldo D. Uchitel/Dr. Francisco J. Urbano
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