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The Journal of Neurophysiology Vol. 87 No. 2 February 2002, pp. 1046-1056
Copyright ©2002 by the American Physiological Society
Départements de Pharmacologie et de Psychiatrie, Centre de Recherche en Sciences Neurologiques, Centre de Recherche Fernand Seguin, Université de Montréal, Quebec H3C 3J7, Canada
Congar, Patrice,
Annie Bergevin, and
Louis-Eric Trudeau.
D2 Receptors Inhibit the Secretory Process Downstream From
Calcium Influx in Dopaminergic Neurons: Implication of
K+ Channels. J. Neurophysiol. 87: 1046-1056, 2002. Dopaminergic (DAergic) neurons possess D2-like somatodendritic
and terminal autoreceptors that modulate cellular excitability and
dopamine (DA) release. The cellular and molecular processes underlying
the rapid presynaptic inhibition of DA release by D2 receptors remain
unclear. Using a culture system in which isolated DAergic neurons
establish self-innervating synapses ("autapses") that release both
DA and glutamate, we studied the mechanism by which presynaptic D2
receptors inhibit glutamate-mediated excitatory postsynaptic currents
(EPSCs). Action-potential evoked EPSCs were reversibly inhibited by
quinpirole, a selective D2 receptor agonist. This inhibition was
slightly reduced by the inward rectifier K+ channel blocker
barium, largely prevented by the voltage-dependent K+
channel blocker 4-aminopyridine, and completely blocked by their combined application. The lack of a residual inhibition of EPSCs under
these conditions argues against the implication of a direct inhibition
of presynaptic Ca2+ channels. To evaluate the possibility
of a direct inhibition of the secretory process, spontaneous miniature
EPSCs were evoked by the Ca2+ ionophore ionomycin.
Ionomycin-evoked release was insensitive to cadmium and dramatically
reduced by quinpirole, providing evidence for a direct inhibition of
quantal release at a step downstream to Ca2+ influx through
voltage-dependent Ca2+ channels. Surprisingly, this effect
of quinpirole on ionomycin-evoked release was blocked by
4-aminopyridine. These results suggest that D2 receptor activation
decreases neurotransmitter release from DAergic neurons through a
presynaptic mechanism in which K+ channels directly inhibit
the secretory process.
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