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The Journal of Neurophysiology Vol. 88 No. 1 July 2002, pp. 534-539
Copyright ©2002 by the American Physiological Society
RAPID COMMUNICATION
Department of Pharmacology and Program in Neuroscience, University of Connecticut Health Center, Farmington, Connecticut 06030
Trettel, Joseph and
Eric S. Levine.
Cannabinoids Depress Inhibitory Synaptic Inputs Received by Layer
2/3 Pyramidal Neurons of the Neocortex. J. Neurophysiol. 88: 534-539, 2002. Using whole cell
voltage-clamp recordings we investigated the effects of a synthetic
cannabinoid (WIN55,212-2) on inhibitory inputs received by layer 2/3
pyramidal neurons in slices of the mouse auditory cortex. Activation of
the type 1 cannabinoid receptor (CB1R) with WIN55,212-2 reliably
reduced the amplitude of GABAergic inhibitory postsynaptic currents
evoked by extracellular stimulation within layer 2/3. The suppression
of this inhibition was blocked and reversed by the highly selective
CB1R antagonist AM251, confirming a CB1R-mediated inhibition. Pairing
evoked inhibitory postsynaptic currents (IPSCs) at short interstimulus
intervals while applying WIN55,212-2 resulted in an increase in
paired-pulse facilitation suggesting that the probability of GABA
release was reduced. A presynaptic site of cannabinoid action was
verified by an observed decrease in the frequency with no change in the
amplitude or kinetics of action potential-independent postsynaptic
currents (mIPSCs). When Cd2+ was added or
Ca2+ was omitted from the recording solution, the
remaining fraction of Ca2+-independent mIPSCs did
not respond to WIN55,212-2. These data suggest that cannabinoids are
capable of suppressing the inhibition of neocortical pyramidal neurons
by depressing Ca2+-dependent GABA release from
local interneurons.
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