Synapse formation, pruning and epileptogenesis.
Abstract number :
IW.12
Submission category :
Year :
2010
Submission ID :
12990
Source :
www.aesnet.org
Presentation date :
12/3/2010 12:00:00 AM
Published date :
Dec 2, 2010, 06:00 AM
Authors :
David Prince, Beth Stevens and Cagla Eroglu
Summary: The expression of several key molecules critical for synapse formation and removal during development may be altered after injury and in CNS disease states, resulting in functionally abnormal, epileptogenic brain. Beth Stevens will discuss the role of members of the classical complement cascade, C1q and C3, and microglia in synapse elimination during development and during the early stages of neurodegenerative disease. Absence of these molecules leads to a hyper-connected brain. Cagla Eroglu will review the role of astrocyte-secreted extracellular matrix proteins, thrombospondins, in synapse formation and show that the calcium channel subunit, ?2?-1, is the receptor for both thrombospondin and the anticonvulsant and analgesic drug gabapentin. Overexpression of ?2?-1 may lead enhanced to synaptogenesis and gabapentin is a potent inhibitor of excitatory synapse formation. David Prince will describe results of experiments in genetically altered mice in which either elimination of C1q or overexpression of ?2?-1 results in epilepsy. He will present recent data suggesting that gabapentin is an effective antiepileptogenic agent after neocortical injury.