Referenced in: none

Automatically associated channels: Kv1.4 , Kv3.1 , Kv4.3 , Slo1

Title: Long-term K+ channel-mediated dampening of dopamine neuron excitability by the antipsychotic drug haloperidol.

Authors: Junghyun Hahn, Tonia E Tse, Edwin S Levitan

Journal, date & volume: J. Neurosci., 2003 Nov 26 , 23, 10859-66

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/14645479

Abstract
Antipsychotic drugs require days of treatment to begin to produce therapeutic effects. We report that in vivo treatment with the antipsychotic drug haloperidol acts with a delay of days to slow spontaneous repetitive firing by isolated midbrain dopamine neurons. The decreased excitability is caused by an increased number of functional A-type K+ channels without any change in gating properties. Upregulation of dopamine neuron Kv4.3 mRNA accounts for this effect, demonstrating a role for channel gene expression in this delayed drug action. The resultant long-term dampening of dopamine neuron excitability may serve to tone down the dopamine system.