A potassium channel blocker induces a long-lasting enhancement of corticostriatal responses.

Norman ED, Egli RE, Colbran RJ, Winder DG
Neuropharmacology. 2005 48 (2): 311-21

PMID: 15695170 · DOI:10.1016/j.neuropharm.2004.09.018

Disruptions in synaptic plasticity in the dorsal striatum may contribute to the pathophysiology underlying Parkinson's disease. Here we report a novel, chemically-induced form of plasticity induced by application of the potassium channel blocker tetraethylammonium (TEA) in the dorsolateral striatum of the adult rat. Transient application of TEA persistently increased synaptically-evoked extracellularly-recorded corticostriatal responses in an activity-, concentration- and time-dependent manner. Pharmacological experiments suggest that this plasticity is dependent on L-type calcium channel and protein kinase C (PKC) activation. Striatal dopamine depletion induced by nigrostriatal dopamine lesions with 6-hydroxydopamine significantly reduced, but did not abolish, TEA-mediated enhancement of the corticostriatal response. Intracellular recordings demonstrate that this TEA-mediated plasticity is associated with an increase in EPSP size and slope, as well as input resistance. Collectively, these findings demonstrate a novel form of L-type calcium channel-dependent plasticity in the adult dorsal striatum that is induced in the absence of dopaminergic input.

MeSH Terms (11)

Animals Cerebral Cortex Corpus Striatum Dose-Response Relationship, Drug Excitatory Postsynaptic Potentials In Vitro Techniques Potassium Channel Blockers Rats Rats, Sprague-Dawley Tetraethylammonium Time Factors

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