Endocannabinoid signaling and HPA axis plasticity


Meeting Abstract

P3-48  Tuesday, Jan. 6 15:30  Endocannabinoid signaling and HPA axis plasticity DICKENS, MJ*; HILL, MN; BENTLEY , GE; UC Berkeley, Integ Biol; U Calgary, Cell Biol and Anatomy; UC Berkeley, Integ Biol m.dickens@berkeley.edu

When the brain responds to acute stress, pathways connecting the hippocampus, amygdala and hypothalamus use endocannabinoid (eCB) signaling to regulate the response of the hypothalamic pituitary adrenal (HPA) axis. Functioning predominantly through retrograde signaling, the eCBs (2-arachidonoylglycerol, 2-AG, and anandamide, AEA) bind cannabinoid 1 (CB1) receptors located on the pre-synaptic neuron to generally inhibit HPA activity. In our study, we used European starlings (Sturnus vulgaris) to investigate the role of eCB signaling in the transition between breeding season and molt when the most dynamic changes in HPA responsiveness occur. We measured eCB concentrations in dissected hypothalamus, amygdala and hippocampus at baseline and after acute stress (30min restraint). In the amygdala, stress-induced decreases in AEA and 2-AG content were robust during the breeding season but reduced or non-existent during molt. CB1 in the amygdala has been shown to “gate” the initiation of the HPA response by stress-induced metabolism of ligand releasing inhibition on hypothalamus. The observed difference suggests a potential role for amygdalar eCB signaling in HPA plasticity since the rapid change in content occurs when the response requires a dynamic range (breeding) but not when the response is restricted (molt). In contrast, there were no changes in tissue eCB content in response to stress in hypothalamus or hippocampus where the predominant role of eCB signaling is glucocorticoid negative feedback. These data provide new insight into neural mechanisms that may regulate the transition in HPA responsiveness between breeding season and molt and further demonstrate the comparative nature of neural stress signals.

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