In addition to CB1 agonist-induced synaptic suppression, DSI and DSE have both been demonstrated within the CeAM. Kamprath et al. recently demonstrated that GABAergic inputs from the CeAL to the CeAM were susceptible to DSI (Kamprath et al., 2011). In fact, depolarizations as short as 100 ms induced DSI in these neurons. Similarly, excitatory BLA inputs to CeAM were susceptible to DSE: however much longer depolarization times were required (up to 10 seconds). Moreover, both DSI and DSE were blocked by CB1 receptor antagonists and absent in CB1−/− mice and showed rapid adaptations to acute foot-shock stress as will be discussed below (Kamprath et al., 2011). Taken together, these data indicate a high level of eCB tone regulating GABAergic transmission in the CeAM, and excitatory synapses are less susceptible than GABAergic synapses to eCB-mediated retrograde signaling. Whether these differences are due to either reduced CB1 receptor function at glutamatergic synapses (relative to GABAergic synapses) or differences in eCB production at these different synapses remains to be determined.
