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Chunk #22 — Results — Suppression of AEA/CB1 receptor signaling within the basolateral amygdala complex contributes to stress-induced activation of the HPA axis

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Suppression of amygdalar endocannabinoid signaling by stress contributes to activation of the hypothalamic-pituitary-adrenal axis.
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In the next set of studies, we examined the effects of intra-amygdalar infusion of a direct CB1 receptor agonist on basal and stress-induced serum corticosterone. There was a significant interaction between administration of the CB1 receptor agonist HU-210 into the BLA and stress on serum corticosterone [F (1, 15) = 12.72, p < 0.005; Fig. 6]. Post hoc analysis revealed that HU-210 administration into the BLA had no effect on serum corticosterone levels in non-stressed rats; however, administration of HU-210 into the BLA prior to stress resulted in a significant reduction of stress-induced corticosterone secretion compared to vehicle (p < 0.01). When HU-210 was co-administered with the CB1 receptor antagonist AM251 into the BLA (Fig. 6), corticosterone levels following stress were no different than those of animals receiving a vehicle infusion prior to stress (p > 0.05) and were significantly higher than those following HU-210 infusion alone (p < 0.05).