CRF (human, rat)

Corticotropin-releasing factor human (Human CRF; Human corticotropin-releasing factor) stimulates the synthesis and secretion of adrenocorticotropin in the anterior pituitary.

CRF increases excitability of type II dlBNST neurons through activation of the AC-cAMP-PKA pathway, thereby causing pain-induced aversive responses[1].

The findings are consistent with a mechanism whereby the excess CRF that characterizes stress-related diseases initiates distinct cellular processes in male and female brains, as a result of sex-biased CRF1 signaling[2]. CRF injection on food intake (FI), CRF suppresses FI in 3-month male and female animals[3].

References:
[1]. Kaneko T et al. Activation of adenylate cyclase-cyclic AMP-protein kinase A signaling by corticotropin-releasing factorwithin the dorsolateral bed nucleus of the stria terminalis is involved in pain-induced aversion. Eur J Neurosci. 2016 Sep 30.
[2]. Bangasser DA et al. Corticotropin-releasing factor overexpression gives rise to sex differences in Alzheimer's disease-related signaling. Mol Psychiatry. 2016 Oct 18.
[3]. Tenk J et al. Acute central effects of corticotropin-releasing factor (CRF) on energy balance: Effects of age and gender. Peptides. 2016 Nov;85:63-72.