Chunk #19 — Results — Suppression of AEA/CB1 receptor signaling within the basolateral amygdala complex contributes to stress-induced activation of the HPA axis
To further explore the relationship between amygdalar FAAH activity, AEA content and serum corticosterone, we determined the effect of local inhibition of FAAH activity within the BLA, CeA and MeA on stress-induced corticosterone secretion. Administration of the FAAH inhibitor URB597 blocks AEA hydrolysis by FAAH and increases AEA content (Kathuria et al., 2003), providing an ideal tool to examine this relationship. Within the BLA there was a significant effect of infusion of the FAAH inhibitor, URB597, on stress-induced corticosterone secretion [F (4, 26) = 65.7, p < 0.001; Fig. 4], with post hoc analysis revealing that administration of 0.1 μg URB597 into the BLA significantly reduced stress-induced increases in corticosterone secretion (p < 0.05). The fact that 1 μg of URB597 into the BLA did not mimic the effects seen with the lower dose is consistent with previous work demonstrating that URB597 is optimally effective at a dose of 0.1 μg, presumably due to the fact that greater increases in AEA are believed to lose selectivity for the CB1 receptor and begin to saturate TRPV1 vanilloid receptors (Rubino et al.,
