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Chunk #39 — 1.3 SYNAPTIC MODULATION BY eCBs IN THE AMYGDALA — 1.3.3 eCB modulation of synaptic signaling in the CeA

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Endocannabinoid signaling in the amygdala: anatomy, synaptic signaling, behavior, and adaptations to stress.
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The first study that examined CB1 receptor signaling in the CeA found no effect of Win 55212-2 on GABAergic transmission in this region (Katona et al., 2001). However a subsequent study by Roberto et al. examined eIPSPs from neurons within the CeAM, and found that Win 55212 caused a ~50% depression in eIPSP amplitude (Roberto et al., 2010). Interestingly, blockade of CB1 receptors with SR141716 caused a ~130% increase in eIPSP amplitude, suggesting a significant tonic eCB-mediated suppression GABA release at these synapses. The SR141716-induced increase in eIPSP amplitude was abolished by postsynaptic calcium chelation, supporting the notion of enhanced eCB tone, rather than effects due to the inverse-agonist properties of SR141716. In this study, Win 55212-2 was able to reverse the effects of ethanol to enhance eIPSP amplitude (Roberto et al., 2010).