Activation of the cannabinoid receptor type 1 decreases glutamatergic and GABAergic synaptic transmission in the lateral amygdala of the mouse.

S. C. Azad
Learning & Memory. 2003-03-01; 10(2): 116-128
DOI: 10.1101/lm.53303

PubMed
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1. Learn Mem. 2003 Mar-Apr;10(2):116-28.

Activation of the cannabinoid receptor type 1 decreases glutamatergic and
GABAergic synaptic transmission in the lateral amygdala of the mouse.

Azad SC(1), Eder M, Marsicano G, Lutz B, Zieglgänsberger W, Rammes G.

Author information:
(1)Max-Planck-Institute of Psychiatry, Clinical Neuropharmacology,
Kraepelinstrasse 2-10, 80804 Munich, Germany.

The endogenous cannabinoid system has been shown recently to play a crucial role
in the extinction of aversive memories. As the amygdala is presumably involved in
this process, we investigated the effects of the cannabinoid receptor agonist WIN
55,212-2 (WIN-2) on synaptic transmission in the lateral amygdala (LA) of
wild-type and cannabinoid receptor type 1 (CB1)-deficient mice. Extracellular
field potential recordings and patch-clamp experiments were performed in an in
vitro slice preparation. We found that WIN-2 reduces basal synaptic transmission
and pharmacologically isolated AMPA receptor- and GABA(A) receptor-mediated
postsynaptic currents in wild-type, but not in CB1-deficient mice. These results
indicate that, in the LA, cannabinoids modulate both excitatory and inhibitory
synaptic transmission via CB1. WIN-2-induced changes of paired-pulse ratio and of
spontaneous and miniature postsynaptic currents suggest a presynaptic site of
action. Inhibition of G(i/o) proteins and blockade of voltage-dependent and G
protein-gated inwardly rectifying K(+) channels inhibited WIN-2 action on basal
synaptic transmission. In contrast, modulation of the adenylyl cyclase-protein
kinase A pathway, and blockade of presynaptic N- and P/Q- or of postsynaptic L-
and R/T-type voltage-gated Ca(2+) channels did not affect WIN-2 effects. Our
results indicate that the mechanisms underlying cannabinoid action in the LA
partly resemble those observed in the nucleus accumbens and differ from those
described for the hippocampus.

DOI: 10.1101/lm.53303
PMCID: PMC196665
PMID: 12663750 [Indexed for MEDLINE]

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