Medullary c-Fos activation in rats after ingestion of a satiating meal

L Rinaman, EA Baker, GE Hoffman… - American Journal …, 1998 - journals.physiology.org
L Rinaman, EA Baker, GE Hoffman, EM Stricker, JG Verbalis
American Journal of Physiology-Regulatory, Integrative and …, 1998journals.physiology.org
The distribution and chemical phenotypes of hindbrain neurons that are activated in rats
after food ingestion were examined. Rats were anesthetized and perfused with fixative 30
min after the end of 1-h meals of an unrestricted or rationed amount of food, or after no meal.
Brain sections were processed for localization of the immediate-early gene product c-Fos, a
marker of stimulus-induced neural activation. Hindbrain c-Fos expression was low in rats
that ate a rationed meal or no meal. Conversely, c-Fos was prominent in the medial nucleus …
The distribution and chemical phenotypes of hindbrain neurons that are activated in rats after food ingestion were examined. Rats were anesthetized and perfused with fixative 30 min after the end of 1-h meals of an unrestricted or rationed amount of food, or after no meal. Brain sections were processed for localization of the immediate-early gene product c-Fos, a marker of stimulus-induced neural activation. Hindbrain c-Fos expression was low in rats that ate a rationed meal or no meal. Conversely, c-Fos was prominent in the medial nucleus of the solitary tract (NST) and area postrema in rats that ate to satiety. There was a significant positive correlation between postmortem weight of gastric contents and the proportion of NST catecholaminergic neurons expressing c-Fos. Cells in the ventrolateral medulla (VLM) were not activated in rats after food ingestion, in contrast with previous findings that stimulation of gastric vagal afferents with anorexigenic doses of cholecystokinin activates c-Fos expression in both NST and VLM catecholaminergic cells. These findings indicate that anatomically distinct subsets of hindbrain catecholaminergic neurons are activated in rats after food ingestion and that activation of these cells is quantitatively related to the magnitude of feeding-induced gastric distension.
American Physiological Society