Abstract
Intracellular recordings made in vitro from rat midbrain dopamine neurons showed that apamin (100 nM) did not alter the regular spontaneous firing of the neurons, but it increased the occurrence of bursts of action potentials in N-methyl-D-aspartate. Apamin appeared to facilitate burst-firing induced by NMDA because, by blocking an outward calcium-activated potassium current, it increased the depolarizing action of NMDA.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Action Potentials / drug effects
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Animals
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Apamin / pharmacology*
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Dopamine / analysis
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Male
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N-Methylaspartate / pharmacology*
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Neurons / chemistry
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Neurons / drug effects*
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Potassium Channels / drug effects
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Rats
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Rats, Sprague-Dawley
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Ventral Tegmental Area / drug effects*
Substances
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Potassium Channels
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Apamin
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N-Methylaspartate
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Dopamine