K(ATP)-dependent neurotransmitter release in the neuronal network of the rat caudate nucleus.
K(ATP) channels can couple the bioenergetic metabolism of the cell to membrane excitability. Here, we show gamma-aminobutyric acid (GABA) mediated inhibition of dopamine outflow from slices of the rat caudate nucleus that is regulated by extracellular glucose via high- and low-affinity K(ATP) channels. During glucose reduction, a biphasic dopamine effect could be observed with first a dopamine increase followed by a decline at low glucose concentrations. Both phases were inhibited by glibenclamide. Pinacidil decreased DA outflow without an effect of glucose reduction implying an overall activation of K(ATP) channels. The first phase with dopamine increase was related to reduced GABAergic activity and could be blocked by bicuculline. Our results may be explained by different types of K(ATP) channels with low affinity of ATP and glibenclamide on inhibitory GABAergic and high-affinity on excitatory DAergic neurons. This led us to suggest a biological principle through which neuronal networks are functioning.
Steinkamp
Mirja
M
Neurochemical Research Group, Department of Neurology, University of Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany.
Li
Tianlang
T
Fuellgraf
Henriette
H
Moser
Andreas
A
D000818:Animals; D002421:Caudate Nucleus / Q000166:cytology / Q000378:metabolism*; D004298:Dopamine / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000378:metabolism; D009474:Neurons / Q000378:metabolism*; D018377:Neurotransmitter Agents / Q000378:metabolism*; D015221:Potassium Channels / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D018377:Neurotransmitter Agents; D015221:Potassium Channels; C117780:mitochondrial K(ATP) channel; D005680:gamma-Aminobutyric Acid; D005947:Glucose; D004298:Dopamine