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Endocannabinoids contribute to short‐term but not long‐term mGluR‐induced depression in the hippocampus
Author(s) -
Rouach Nathalie,
Nicoll Roger A.
Publication year - 2003
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2003.02823.x
Subject(s) - cannabinoid receptor , metabotropic glutamate receptor , endocannabinoid system , long term depression , neuroscience , hippocampus , cannabinoid , excitatory postsynaptic potential , neurotransmission , postsynaptic potential , agonist , metabotropic receptor , glutamate receptor , chemistry , receptor , psychology , medicine , ampa receptor , inhibitory postsynaptic potential
Activation of postsynaptic group 1 metabotropic glutamate receptors (mGluRs) by the agonist DHPG causes a long‐term depression (DHPG‐LTD) of excitatory transmission in the CA1 region of the hippocampus, as well as causing the release of endocannabinoids from pyramidal cells. As cannabinoid agonists cause a presynaptic inhibition at these synapses and DHPG‐LTD is thought to be expressed, at least in part, by a presynaptic mechanism, we examined the possibility that endocannabinoids mediated DHPG‐LTD. We find that antagonists of cannabinoid receptors reduce the acute depression induced by DHPG, but have no effect on the lasting depression. Furthermore, both the acute and the lasting effects of DHPG were unaffected in the CB1 knockout mouse. These findings suggest that endocannabinoids, acting on a non‐CB1 cannabinoid receptor, contribute to the acute depression but not to DHPG‐LTD. Presumably some other retrograde signalling mechanism is responsible for DHPG‐LTD.

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