Fig. 1.

Simplified schematic of rodent CeA circuitry and hypothetical sites of ethanol and CRF action on GABAergic synapses. Most neurons in the CeA are GABAergic inhibitory projection or interneurons that contain CRF or other neuropeptides as cotransmitters. (Upper synapse) Ethanol may enhance the release of GABA (filled ellipsoids) from GABAergic afferents or interneurons either via the release from the same terminal as CRF (gray triangles), which then acts on CRF1 receptors on the terminal to elicit (black arrow) release of more GABA via a PKCε-mediated mechanism, or direct activation of CRF1 receptors to elicit the release of more GABA. Thus, CRF and ethanol both augment the inhibition of CeA projection interneurons (cocontaining CRF, opioids, or NPY), leading to excitation of downstream (e.g., BNST) neurons by disinhibition. Activation of presynaptic opioid, CB1, or NPY receptors (data not shown) may reduce GABA release onto CeA inhibitory projection neurons, increasing their excitability and release of GABA onto downstream targets such as the BNST. (Lower synapse) Glutamatergic afferents from basolateral amygdala (BLA) or prefrontal cortex (PFC) excite the CeA inhibitory neurons via release of glutamate (filled rectangles) and activation of glutamate receptors.