Corticotropin-releasing factor-1 receptors in the basolateral amygdala mediate stress-induced anorexia.

Abstract

Corticotropin-releasing factor (CRF) receptor activation within the basolateral amygdala (BLA) has been relatively unexplored compared with the central nucleus of the amygdala (CeA), despite the fact that CRF receptors are more densely distributed in BLA than in CeA. The authors show that infusion of CRF into BLA, but not CeA, decreases feeding and increases grooming. These effects are mediated by CRF-sub-1 receptors, because they are blocked by intra-BLA treatment with NBI27914 (NBI), a CRF-sub-1 antagonist, but not Astressin 2B, a CRF-sub-2 antagonist. Exposure to a stressor results in behaviors identical to those seen after intra-BLA CRF infusion. These stress-induced changes are prevented by pre-stress treatment with NBI but not Astressin 2B. These data demonstrate that stimulation of intra-BLA CRF-sub-1 receptors is both necessary and sufficient for eliciting stress-induced anorexia and grooming.

Stimulation of Lateral Septum CRF2Receptors Promotes Anorexia and Stress-Like Behaviors: Functional Homology to CRF1Receptors in Basolateral Amygdala

“…Rats were then tested in behavioral observation cages as described above. Our previous work indicates that CRF infusions into the BLA cause dramatic reductions in feeding and increases in grooming behavior similar to those observed in the present studies with UCN into LS (Jochman et al, 2005). Based on this work, it was predicted that this dose of NBI would reverse the intra-BLA CRF-induced anorexia.…”

“…To verify that the doses of NBI used in the LS were sufficiently high to produce behavioral effects, experiment 8 tested the hypothesis that NBI would block the effects of CRF microinfusion into the BLA, which we previously showed to cause decreases in feeding and increases in grooming similar to those of UCN in the LS (Jochman et al, 2005). Figure 6 displays the results of this experiment.…”

“…Thus, in experiment 6, the effects of either a moderate (500 ng; n ϭ 8) or a high (1000 ng; n ϭ 8) dose of NBI were examined; in experiment 7, the effects of 500 ng (n ϭ 7) or 1000 ng (n ϭ 8) of Astressin2B were studied. Antagonist doses were chosen based on our previous work indicating that this dose range prevents the behavioral effects elicited by CRF agonist infusion into other brain regions (Jochman et al, 2005).…”

Food-intake regulation during stress by the hypothalamo-pituitary-adrenal axis

“…CRH-2 receptor mRNA has been demonstrated to be highly expressed here (Lovenberg et al, 1995). Basolateral amygdala mediates CRH-induced anorexia through CRH-1 receptors (Jochman et al, 2005), while lateral septum and BNST through the CRH-2 receptor (Ohata and Shibasaki, 2011;Smagin et al, 1998). However, pharmacological and neuromorphological studies have demonstrated that Ucn-3 rather than CRH is the most potent and specific endogenous ligand for CRH-2 receptor .…”

Cellular and molecular mechanisms of hippocampal activation by acute stress are age-dependent

“…2,25,41,43 Contribution of CRH to the effects of stress on neuronal function within the brain has also been delineated, and demonstrates age-dependent properties. For example, central administration of CRH activates neurons in the amygdala, contributing to anxiety-like behaviors 44,45 as well as to memory consolidation. 46 The peptide modulates neuronal activity in amygdala in a complex manner 47 and, in larger amounts, can lead to hyperexcitability, a kindling effect, and seizures.…”