title: Osmotic stimulation differentially affects cellular levels of corticotropin-releasing hormone and neurotensin/neuromedin N mRNAs in the lateral hypothalamic area and central nucleus of the amygdala.
abstract: To investigate the effects of osmotic stimulation on neural circuits concerned with non-neuroendocrine aspects of homeostatic regulation, the levels of the mRNAs coding for corticotropin-releasing hormone (CRH) and neurotensin/neuromedin N (NT/NMN) in the lateral hypothalamic area (LHA) and central nucleus of the amygdala (CEA) of animals given 2.5% saline to drink overnight were measured semiquantitatively using in situ hybridization. Overnight osmotic stimulation leads to converse effects on the levels of these two mRNAs in different anatomical regions; increased levels of both mRNAs are seen in the LHA, but levels decrease in the CEA. While a number of previous studies have shown that ppCRH mRNA in the paraventricular (PVH) and supraoptic (SO) nuclei of the hypothalamus may contribute to the neuroendocrine response to osmotic stimulation, the present results show that in response to osmotic stimulation neurons located outside the PVH and SO may also modulate their synthetic potential, not just for CRH but also NT/NMN. These results suggest that a physiological stimulus may modulate the levels of two peptides previously identified in circuits projecting from the forebrain to nuclei in the brainstem, and as such, CRH and NT/NMN may participate in the regulation by the forebrain of the autonomic and/or behavioral responses of the animal to dehydration. Furthermore, these data show that a particular stimulus has opposite effects on the level of both peptide mRNAs when expressed in two different cell groups, suggesting first, that these peptides may have more than one role in the response, and second, the existence and influence of differential control mechanisms.
authors.affiliation: Department of Biological Sciences, University of Southern California, Los Angeles 90089-2520.
authors.forename: A G
authors.initials: AG
authors.lastname: Watts
mesh_terms: D000679:Amygdala / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D001345:Autoradiography; D003346:Corticotropin-Releasing Hormone / Q000235:genetics*; D007026:Hypothalamic Area, Lateral / Q000187:drug effects / Q000502:physiology*; D008297:Male; D009496:Neurotensin / Q000235:genetics*; D009928:Organ Specificity; D010446:Peptide Fragments / Q000235:genetics*; D011498:Protein Precursors / Q000235:genetics; D015347:RNA Probes; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D012965:Sodium Chloride / Q000494:pharmacology*; D013462:Sulfur Radioisotopes
chemical_list: D010446:Peptide Fragments; D011498:Protein Precursors; D015347:RNA Probes; D012333:RNA, Messenger; D013462:Sulfur Radioisotopes; C052457:neuromedin N precursor; C041645:pro-corticotropin releasing hormone; C042090:neuromedin N; D009496:Neurotensin; D012965:Sodium Chloride; D003346:Corticotropin-Releasing Hormone