Central structures necessary and sufficient for ingestive and glycemic responses to Urocortin I administration.

CNS delivery of Urocortin I (UcnI), a member of the corticotropin-releasing factor family, suppresses feeding behavior and increases plasma glucose. The sites of action necessary and sufficient for these responses remain unclear. The contribution of the caudal brainstem was explored using chronically maintained decerebrate (CD) and neurologically intact control rats given fourth-ventricle injections of UcnI. Ingestive and glycemic responses were evaluated, and Fos immunoreactivity was measured in the paraventricular nucleus of the hypothalamus (PVN), the parabrachical nucleus (PBN), the rostral ventrolateral medulla (RVLM), and the nucleus of the solitary tract (NTS). CD rats, like the neurologically intact controls, decreased intraoral food intake and had elevated plasma glucose in response to Unc1 injections, indicating that forebrain structures are not required for these behavioral and physiological actions of UcnI. Fos immunohistochemistry, however, revealed notable differences in the pattern of UcnI-induced activation between intact and CD rats. UcnI-related activation was observed in each of the four aforementioned brain areas of neurologically intact rats but only in the NTS of CD rats. The intact behavioral and physiological responses to UcnI in the absence of neural activation in the PVN, PBN, and RVLM help limit the list of structures necessary for the stimulation and mediation of these responses to UcnI and suggest that the NTS may serve as a primary site of UcnI action.