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. Author manuscript; available in PMC: 2016 Jan 1.
Published in final edited form as: Neurobiol Stress. 2015 Jan 1;1:33–43. doi: 10.1016/j.ynstr.2014.09.007

Figure 1. Putative modulation of arousal behavior by NPY within stress-integrative circuitry.

Figure 1

Excitatory glutamatergic (Glu) projections from the basolateral amygdala (BLA) activate the central nucleus of the amygdala (CeA) in response to stress. Subsequent activation of afferents expressing corticotropin-releasing factor (CRF) leads to enhanced activity of norepinephrine (NE) neurons in the locus coeruleus (LC), which then project to and activate regions of the forebrain to regulate arousal behavior. Putative interactions of NPY with stress responsive regions are shown. Activation of Y1 receptors on Glu neurons in the BLA may decrease activation of the CeA in response to stress [25]. NPY may suppress noradrenergic activation in the LC via Y2R located on NE neurons [26, 114], or suppress Y2R–expressing GABAergic interneurons in the CeA leading to disinhibition of GABA output to the LC (not shown) [176]. Alternatively, we hypothesize that NPY axon terminals may directly interact with CRF neurons in the CeA to suppress the activity of the LC-NE system in response to stress.