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Vol. 290, Issue 1, 325-333, July 1999
Departments of Physiology and Biophysics (M.S.B., M.A.M., S.B.A.)
and Emergency Medicine (E.B.B.), University of Illinois at Chicago,
College of Medicine, Chicago, Illinois
Dopaminergic neurons in the ventral tegmental area (VTA) are important
for the rewarding properties of drugs of abuse, including ethanol. We
previously demonstrated that ethanol excites VTA neurons and that
ethanol reduces the amplitude of the after hyperpolarization (AHP) that
follows spontaneous action potentials. Because the small conductance
calcium-activated potassium current (SK) is a component of the
AHP of VTA neurons, we assessed the effect of the SK blockers apamin
and d-tubocurarine (d-TC) on the action of ethanol on dopaminergic VTA neurons with intracellular and extracellular recording in rat brain slices. Apamin (1-200 nM) and
d-TC (100 and 400 µM) caused concentration-dependent
reductions in the AHP amplitude. Ethanol (80 mM) caused a small
reduction in the AHP. In the presence of apamin (40 nM), ethanol (80 mM) caused a much larger reduction in AHP amplitude. Extracellular studies showed that apamin (20, 40, and 100 nM) and d-TC
(400 µM) had no significant effect on the spontaneous firing rate of dopaminergic VTA neurons but enhanced the potency of ethanol to increase their firing rate. These results indicate that the
ethanol-induced reduction of the AHP and excitation of VTA neurons is
not due to a reduction in SK current. Furthermore, blockade of SK
current by apamin or d-TC enhances the excitatory effect
of ethanol on dopaminergic VTA neurons. These data suggest that the
amount of SK current present affects the sensitivity of dopaminergic
VTA neurons to ethanol excitation and that neurotransmitters that reduce SK current may increase the reward potency of ethanol.
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