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Vol. 10, No. 2, pp. 116-128, March/April 2003
1 Max-Planck-Institute of Psychiatry, Clinical
Neuropharmacology, Kraepelinstraße 2-10, 80804 Munich, Germany;
2 Clinic for Anaesthesiology, Pain Treatment Unit,
Ludwig-Maximilians-University, Klinikum Grosshadern,
Marchioninistraße, 15, 81377 Munich, Germany;
3 Max-Planck-Institute of Psychiatry, Molecular Genetics of
Behaviour, 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
GABAA 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 Gi/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 Ca2+ 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.
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