FIGURE 2.

Model of noradrenergic regulation of PVN CRH neuron activity. Noradrenergic inputs (NE) originate in the brainstem and regulate CRH neuronal activity by modulating glutamate and GABA release. Norepinephrine both suppresses and enhances GABAergic inhibition of CRH neuron activity, suppressing GABA release via α₂-adrenoceptor activation at presynaptic terminals and promoting GABA release by activating α₁-adrenoceptors on upstream GABAergic somata/dendrites. Noradrenergic facilitation of glutamate release onto CRH neurons is spike-dependent and is mediated by α₁-adrenoceptor activation. Preliminary evidence suggests that the facilitatory effect on glutamate release may be mediated by the release of a retrograde messenger that stimulates upstream local glutamatergic circuits (dashed arrow). 3V, thrid ventricle; OT, optic tract.