Purkinje cell dysfunction and alteration of long-term synaptic plasticity in fetal alcohol syndrome.

ABSTRACT: In cerebellum and other brain regions, neuronal cell death because of ethanol consumption by the mother is thought to be the leading cause of neurological deficits in the offspring. However, little is known about how surviving cells function. We studied cerebellar Purkinje cells in vivo and in vitro to determine whether function of these cells was altered after prenatal ethanol exposure. We observed that Purkinje cells that were prenatally exposed to ethanol presented decreased voltage-gated calcium currents because of a decreased expression of the gamma-isoform of protein kinase C. Long-term depression at the parallel fiber-Purkinje cell synapse in the cerebellum was converted into long-term potentiation. This likely explains the dramatic increase in Purkinje cell firing and the rapid osc

SUBMITTER: Servais L 

PROVIDER: S-EPMC1887541 | biostudies-literature | 2007 Jun

REPOSITORIES: biostudies-literature