Ethanol Decreases Purkinje Neuron Excitability by Increasing GABA Release in Rat Cerebellar Slices
Ethanol
Miniature Postsynaptic Potentials
Action Potentials
Excitatory Postsynaptic Potentials
Synaptic Potentials
Rats
Electrophysiology
Purkinje Cells
03 medical and health sciences
0302 clinical medicine
Inhibitory Postsynaptic Potentials
Cerebellum
Animals
gamma-Aminobutyric Acid
DOI:
10.1124/jpet.108.144865
Publication Date:
2008-08-29T01:39:28Z
AUTHORS (5)
ABSTRACT
Cerebellar Purkinje neurons (PNs) receive inhibitory GABAergic input from stellate and basket cells, which are located in the outer inner portions of molecular layer, respectively. Ethanol (EtOH) was recently shown to increase transmission at PNs via a mechanism that involves enhanced calcium release presynaptic internal stores (<i>J Pharmacol Exp Ther</i> 323:356–364, 2007). Here, we further characterized effect EtOH on GABA assessed its impact PN excitability. Using whole-cell patch-clamp electrophysiological techniques cerebellar vermis parasagittal slices, found acutely increases frequency but not amplitude or half-width miniature spontaneous postsynaptic currents (IPSCs). significantly increased decreased paired pulse ratio IPSCs evoked by stimulation layer. In current clamp, both excitatory potentials granule cell axon number action triggered these events; effects depended GABA<sub>A</sub> receptor activation because they were observed presence bicuculline. Loose-patch cell-attached recordings revealed neither potential firing nor coefficient variation interspike interval altered acute exposure. These findings suggest differentially affects cell- cell-to-PN synapses it modulates axonal input. could be part responsible for impairments associated with intoxication.
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