Title : Nicotine modulation of stress-related peptide neurons.

Pub. Date : 2006 Aug 1

PMID : 16739166






4 Functional Relationships(s)
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1 Film autoradiographic studies showed that nicotine significantly increased c-fos mRNA expression in both PVN and CEA. Nicotine Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus
2 Pretreatment with the centrally acting nicotinic antagonist, mecamylamine (1 mg/kg), blocked nicotine"s effects, whereas pretreatment with the peripherally acting antagonist, hexamethonium (5 mg/kg), did not, indicating that c-fos induction was mediated by a central nicotinic receptor. Nicotine Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus
3 Double labeling studies showed that nicotine induced c-fos expression within CRF cells in the PVN, as well as in a small population of ENK cells, but not in PVN DYN cells. Nicotine Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus
4 In contrast, there was no significant nicotine-induced increase in c-fos expression in CEA CRF or DYN cells, whereas nicotine treatment did increase c-fos expression within CEA ENK cells. Nicotine Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus