Endocannabinoid-mediated long-term plasticity requires cAMP/PKA signaling and RIM1alpha.
paper
Cited
Public
Unavailable
- Authors
- Chevaleyre, Vivien; Heifets, Boris D; Kaeser, Pascal S; SΓΌdhof, Thomas C; Castillo, Pablo E
- Year
- 2007
- Journal
- Neuron
- PMID
- 17553427
- DOI
- 10.1016/j.neuron.2007.05.020
- PMCID
- PMC2001295
Endocannabinoids (eCBs) have emerged as key activity-dependent signals that, by activating presynaptic cannabinoid receptors (i.e., CB1) coupled to G(i/o) protein, can mediate short-term and long-term synaptic depression (LTD). While the presynaptic mechanisms underlying eCB-dependent short-term depression have been identified, the molecular events linking CB1 receptors to LTD are unknown. Here we show in the hippocampus that long-term, but not short-term, eCB-dependent depression of inhibitory transmission requires presynaptic cAMP/PKA signaling. We further identify the active zone protein RIM1alpha as a key mediator of both CB1 receptor effects on the release machinery and eCB-dependent LTD in the hippocampus. Moreover, we show that eCB-dependent LTD in the amygdala and hippocampus shares major mechanistic features. These findings reveal the signaling pathway by which CB1 receptors mediate long-term effects of eCBs in two crucial brain structures. Furthermore, our results highlight a conserved mechanism of presynaptic plasticity in the brain.
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