Halothane decreases impulse-dependent but not cytoplasmic release of dopamine from rat striatal slices

Abstract

Using in vitro superfusion techniques and electrical field stimulation, a volatile anesthetic, halothane, decreased impulse-dependent vesicular release, but did not affect amphetamine-induced cytoplasmic release of dopamine (DA) from the rat striatal slice preparations loaded with [3H]-DA. Contrary to previous in vivo studies, halothane at concentrations applied (1% to 4%) did not enhance the release of DA from slice preparation in which the cell bodies were absent, and therefore, the possible site of action was located on the axon terminals. In this in vitro experiment, halothane decreased the fractional release of DA in a concentration-dependent manner and attenuated the increase of impulse-dependent DA release when amphetamine or nomifensine administration was combined with electrical stimulation. D2-receptor agonists (quinpirole and apomorphine) reduced the release, and antagonists (sulpiride and haloperidol) enhanced the release of DA. In the presence of halothane, D2-receptor antagonists had no effect on DA release. It is concluded that halothane may have some modulatory effect on D2-receptor mediated presynaptic control of DA release.