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The Journal of Neurophysiology Vol. 85 No. 1 January 2001, pp. 468-471
Copyright ©2001 by the American Physiological Society
RAPID COMMUNICATION
1Department of Pharmacology and 2Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37212-0615
Gerdeman, Gregory and
David M. Lovinger.
CB1 Cannabinoid Receptor Inhibits Synaptic Release of
Glutamate in Rat Dorsolateral Striatum. J. Neurophysiol. 85: 468-471, 2001. CB1 cannabinoid receptors in the
neostriatum mediate profound motor deficits induced when cannabinoid
drugs are administered to rodents. Because the CB1 receptor has been
shown to inhibit neurotransmitter release in various brain areas, we
investigated the effects of CB1 activation on glutamatergic synaptic
transmission in the dorsolateral striatum of the rat where the CB1
receptor is highly expressed. We performed whole cell voltage-clamp
experiments in striatal brain slices and applied the CB1 agonists
HU-210 or WIN 55,212-2 during measurement of synaptic transmission.
Excitatory postsynaptic currents (EPSCs), evoked by electrical
stimulation of afferent fibers, were significantly reduced in a
dose-dependent manner by CB1 agonist application. EPSC inhibition was
accompanied by an increase in two separate indices of presynaptic
release, the paired-pulse response ratio and the coefficient of
variation, suggesting a decrease in neurotransmitter release. These
effects were prevented by application of the CB1 antagonist SR141716A. When Sr2+ was substituted for Ca2+ in the
extracellular solution, application of HU-210 (1 µM) significantly reduced the frequency, but not amplitude, of evoked, asynchronous quantal release events. Spontaneous release events were similarly decreased in frequency with no change in amplitude. These findings further support the interpretation that CB1 activation leads to a
decrease of glutamate release from afferent terminals in the striatum.
These results reveal a novel potential role for cannabinoids in
regulating striatal function and thus basal ganglia output and may
suggest CB1-targeted drugs as potential therapeutic agents in the
treatment of Parkinson's disease and other basal ganglia disorders.
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