Abstract：
:Cannabinoid receptor type 1 (CB1)-dependent signaling in the brain is known to modulate food intake. Recent evidence has actually shown that CB1 can both inhibit and stimulate food intake in fasting/refeeding conditions, depending on the specific neuronal circuits involved. However, the exact brain sites where this bimodal control is exerted and the underlying neurobiological mechanisms are not fully understood yet. Using pharmacological and electrophysiological approaches, we show that local CB1 blockade in the paraventricular nucleus of the hypothalamus (PVN) increases fasting-induced hyperphagia in rats. Furthermore, local CB1 blockade in the PVN also increases the orexigenic effect of the gut hormone ghrelin in animals fed ad libitum. At the electrophysiological level, CB1 blockade in slices containing the PVN potentiates the decrease of the activity of PVN neurons induced by long-term application of ghrelin. Hence, the PVN is (one of) the site(s) where signals associated with the body's energy status determine the direction of the effects of endocannabinoid signaling on food intake.
journal_name
Neurosciencejournal_title
Neuroscienceauthors
Soria-Gómez E,Massa F,Bellocchio L,Rueda-Orozco PE,Ciofi P,Cota D,Oliet SH,Prospéro-García O,Marsicano Gdoi
10.1016/j.neuroscience.2014.01.005subject
Has Abstractpub_date
2014-03-28 00:00:00pages
46-53eissn
0306-4522issn
1873-7544pii
S0306-4522(14)00009-8journal_volume
263pub_type
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