Figure 3.

Neural mechanisms of acute stress excitation. Data suggest corticotropin releasing hormone neurons in the medial dorsal paraventricular nucleus (mpPVN) can be driven by neurons communicating homeostatic challenge, including the nucleus of the solitary tract (NTS), among others. The PVN also has numerous connections with hypothalamic nuclei and subcortical telencephalic structures, including excitatory (posterior hypothalamus (PH), ventrolateral region of the bed nucleus of the stria terminalis (BST)) and inhibitory (medial preoptic nucleus (mPOA), dorsomedial nucleus (DMH), periPVN, and posterior BST) inputs. Inhibitory input to the PVN provides a substantial inhibitory tone, which can be disrupted by inhibition from upstream sites such as the medial and central amygdaloid nuclei (MeA, CeA), providing a mechanism for transsynaptic disinhibition from the limbic forebrain. There is also some evidence suggesting that some cortical regions, such as the infralimbic region (il) of the medial prefrontal cortex, may also provide transsynaptic excitation, perhaps via relays in the brainstem. There is less evidence for excitatory input from other forebrain stress circuits, such as the ventral subiculum (vSUB), prelimbic division of the mPFC or paraventricular thalamus. Input from limbic regions may also access the PVN by interaction with local interneurons in the PVN surround (periPVN). Open circles: inhibitory (e.g., GABAergic) neurons; closed circles: excitatory (e.g., glutamatergic) neurons; squares: inhibitory input; arrowheads: excitatory inputs. Adapted from (79), with permission.