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<br>
Seminario <b>lunes 21 de diciembre</b>, <b>13 hs</b>. Aula de seminarios
del LFBM <br>
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Title: How do Astrocytes Induce CNS Synaptogenesis? <br>
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by Çagla Eroglu<br>
Stanford University Medical Center, Department of Neurobiology, Stanford,
CA 94305, USA, Current address: Duke University Medical Center, Cell
Biology Department, Durham, NC, 27705, USA.<br>
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Abstract:<br>
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. <br>
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Host: Dr. Osvaldo D. Uchitel/Dr. Francisco J. Urbano<br>
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