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. Author manuscript; available in PMC: 2014 Mar 18.
Published in final edited form as: Cell Mol Neurobiol. 2012 Feb 1:10.1007/s10571-012-9801-y. doi: 10.1007/s10571-012-9801-y

Figure 3.

Figure 3

Glucocorticoid negative feedback can generally be divided into three interacting domains. First, GCs provide rapid, nongenomic inhibition of excitatory inputs to the PVN. Additionally, GCs affect RNA stability in brain structures with direct, excitatory innervation of the PVN. Forebrain genomic GC signaling is also a key component of feedback regulation. Importantly, these structures have little or no direct interactions with the PVN and require intermediary synapses in PVN-projecting cell groups. Specifically, GCs act in the plPFC and the ventral subiculum to inhibit the PVN via GABAergic synaptic relays. BST: bed nucleus of stria terminalis, DMH: dorsomedial hypothalamus, EC: endocannabinoid, GLP-1: glucagon-like peptide-1, Glu: glutamate, NTS: nucleus of the solitary tract, PH: posterior hypothalamus, plPFC: prelimbic prefrontal cortex, VMH: ventromedial hypothalamus, vSub: ventral subiculum, + denotes excitation and − inhibition.