info:eu-repo/semantics/article
Ghrelin activates hypophysiotropic corticotropin-releasing factor neurons independently of the arcuate nucleus
Date
2016-05Registration in:
Cabral, Agustina Soledad; Portiansky, Enrique Leo; Sánchez Jaramillo, Edith; Zigman, Jeffrey M.; Perello, Mario; Ghrelin activates hypophysiotropic corticotropin-releasing factor neurons independently of the arcuate nucleus; Pergamon-Elsevier Science Ltd; Psychoneuroendocrinology; 67; 5-2016; 27-39
0306-4530
CONICET Digital
CONICET
Author
Cabral, Agustina Soledad
Portiansky, Enrique Leo
Sánchez Jaramillo, Edith
Zigman, Jeffrey M.
Perello, Mario
Abstract
Previous work has established that the hormone ghrelin engages the hypothalamic-pituitary-adrenal neuroendocrine axis via activation of corticotropin-releasing factor (CRF) neurons of the hypothalamic paraventricular nucleus (PVN). The neuronal circuitry that mediates this effect of ghrelin is currently unknown. Here, we show that ghrelin-induced activation of PVN CRF neurons involved inhibition of γ-aminobutyric acid (GABA) inputs, likely via ghrelin binding sites that were localized at GABAergic terminals within the PVN. While ghrelin activated PVN CRF neurons in the presence of neuropeptide Y (NPY) receptor antagonists or in arcuate nucleus (ARC)-ablated mice, it failed to do it so in mice with ghrelin receptor expression limited to ARC agouti gene related protein (AgRP)/NPY neurons. These data support the notion that ghrelin activates PVN CRF neurons via inhibition of local GABAergic tone, in an ARC-independent manner. Furthermore, these data suggest that the neuronal circuits mediating ghrelin's orexigenic action vs. its role as a stress signal are anatomically dissociated.