Morphological Analysis of the Hindbrain Glucose Sensor-Hypothalamic Neural Pathway Activated by Hindbrain Glucoprivation

Abstract Lowered glucose availability, sensed by the hindbrain, has been suggested to enhance gluconeogenesis and food intake as well suppress reproductive function. In fact, our previous histological in vitro studies suggest that hindbrain ependymal cells function a sensor. The present study aimed clarify sensor-hypothalamic neural pathway activated response glucoprivation mediate counterregulatory physiological responses. Administration of 2-deoxy-D-glucose (2DG), an inhibitor utilization, into fourth ventricle (4V) male rats for 0.5 hour induced messenger RNA (mRNA) expression c-fos, marker cellular activation, 4V, but not lateral ventricle, third or central canal without significant change blood testosterone levels. 2DG 4V 1 significantly increased levels, intake, decreased Simultaneously, c-Fos protein was detected cells; dopamine ?-hydroxylase-immunoreactive C1, C2, A6 regions; neuropeptide Y (NPY) mRNA-positive C2; corticotropin-releasing hormone (CRH) hypothalamic paraventricular nucleus (PVN); NPY arcuate (ARC). Taken together, these results lowered cells, activates catecholaminergic and/or neurons followed CRH PVN ARC, thereby leading responses, such enhancement gluconeogenesis, suppression sex steroid secretion.