Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activation of FOS proto-oncogene protein has been used as an anatomical marker of activated brain areas. Immunocytochemical detection of FOS can provide information about the sites of action of extracellular stimuli, in spite of the relative absence of specific receptors, at the level of single cell resolution. Following the intracerebroventricular (i.c.v.) injection of recombinant human interleukin-1 (alpha) the c-fos mRNA levels isolated from rat hypothalamus were activated rapidly. In association with c-fos mRNA activation, the i.c.v. injection of interleukin-1 (alpha and beta) markedly induced the FOS immunoreactivity in the hypothalamus including periventricular (PE), paraventricular (PVN), supraoptic (SON), arcuate (ARC), and supramammillary (SuM) nuclei. Within the magnocellular neurons of the SON and PVN, activation of FOS by IL-1 appeared to be greater in areas known to have a high proportion of oxytocin-containing cells than in those of vasopressin-containing cells. Parvocellular neurons were also activated in the PVN. These data suggest sites of action of interleukin-1 in the rat hypothalamic areas reported to have relative absence of interleukin-1 receptor expression.
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PMID:Interleukin-1 activation of FOS proto-oncogene protein in the rat hypothalamus. 837 34

Expression of the proto-oncogene protein c-Fos was evaluated immunocytochemically in individual brain cells as a marker of treatment-related neuronal activation following pharmacological and physiological treatments that are known to alter food intake and gastric motility in rats. c-Fos expression in response to each treatment was analyzed in the brainstem dorsal vagal complex, the limbic system, and the hypothalamus, representing the areas thought to be involved in coordinating the autonomic, behavioral, and neuroendocrine responses that occur during conditions of stimulated or inhibited food intake. Our results indicate that the patterns of brain c-Fos expression associated with treatments that inhibit food intake differ significantly from the patterns produced by treatments that potentiate food intake. Treatments that inhibited food intake (administration of the anorexigenic agents cholecystokinin, LiCl, and hypertonic saline, and food ingestion following fasting or insulin treatment) were associated with widespread stimulation of c-Fos expression in cells in the nucleus tractus solitarius (NTS), and to a more variable degree the area postrema (AP), but without significant activation of neurons in the dorsal motor nucleus of the vagus nerve (DMN). In contrast, treatments that potentiated food intake (food deprivation and insulin-induced hypoglycemia) were associated with marked stimulation of c-Fos expression in DMN neurons, but little or no activation in cells in the NTS or the AP. Pharmacological treatments that inhibited food intake and gastric motility also were associated with pronounced c-Fos expression in several forebrain areas, including the parvocellular and magnocellular subdivisions of the paraventricular nucleus of the hypothalamus (PVN), the central nucleus of the amygdala (CeA), and the bed nucleus of the stria terminalis (BNST). In contrast, more physiological inhibition of food intake resulting from spontaneous food ingestion did not cause significant activation of c-Fos expression in these forebrain regions, nor did treatments that stimulated food intake. Central administration of oxytocin, which also is known to inhibit food intake, was associated with a pattern of c-Fos activation analogous to that produced by spontaneous food ingestion after fasting (c-Fos expression in the NTS and AP, but without significant activation in the DMN or forebrain areas). Finally, acute gastric distension produced complex results, in that it was associated with activation of c-Fos expression in all areas of the brainstem (NTS, AP, and DMN), as well as in multiple forebrain areas (PVN, CeA, and BNST). Our results therefore demonstrate that specific patterns of brain c-Fos expression are associated with treatments that alter food intake in rats, and indicate that assessment of c-Fos immunoreactivity in different brain areas can identify common functional neuroanatomical networks that are activated by diverse treatments which nonetheless produce similar behavioral, autonomic, and neuroendocrine effects in animals.
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PMID:c-Fos Expression in Rat Brain and Brainstem Nuclei in Response to Treatments That Alter Food Intake and Gastric Motility. 1991 12