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Journal of Neuroscience, Vol 15, 3065-3074, Copyright © 1995 by Society for Neuroscience
Putative pre- and postsynaptic ATP-sensitive potassium channels in the rat substantia nigra in vitro
AE Watts, GA Hicks and G Henderson
Pharmacology Department, School of Medical Sciences, University of Bristol, UK.
Pre- and postsynaptic adenosine 5'-triphosphate-sensitive potassium
(ATP-K+) currents were studied using whole-cell recordings from substantia
nigra zona compacta "principal" neurons in midbrain slices. The GABAA and
GABAB receptor-mediated synaptic potentials were unaffected by the ATP-K+
channel inhibitor glibenclamide (30 microM) or by the opener diazoxide (500
microM), indicating that ATP-K+ channels on GABA-ergic terminals are not
active, nor can they be activated pharmacologically, under control
conditions. However, application of a glucose-free solution to reduce
intracellular ATP levels caused a reduction of the GABAB IPSP in all
neurons. This was substantially reversed by the sulfonylurea inhibitor
tolbutamide (300 microM) in 50% of the neurons tested. The reduction of the
GABAB IPSP was a presynaptic effect since postsynaptic hyperpolarizations
induced by the GABAB receptor agonist baclofen (10 microM) were unaffected
by glucose- free solutions. Diazoxide (500 microM) induced a slowly
developing hyperpolarization or outward current in 64% of principal
neurons, which was tolbutamide- (100-300 microM) or glibenclamide- (30
microM) sensitive. In contrast, the GABAB receptor agonist baclofen (30
microM) induced a rapid hyperpolarization or outward current in all neurons
tested that was unaffected by tolbutamide (300 microM). Although both the
diazoxide-induced current and the baclofen-induced current were inhibited
by Ba2+ (300 microM), the currents elicited by diazoxide and baclofen
summated. The reversal potential for the diazoxide-induced current was also
less negative than that for baclofen, which was close to EK. In the
presence of intracellular cesium, diazoxide induced a tolbutamide-sensitive
inward current in a proportion of neurons, indicating that it has other
actions in addition to activating a potassium current. Our results suggest
that functional ATP-K+ channels exist both pre- and postsynaptically in the
SN, where they modulate the activity of principal neurons. They are
different to the potassium channels activated by the GABAB receptor agonist
baclofen.
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