Region-specific regulation of neuropeptide mRNAs in rat limbic forebrain neurones by aldosterone and corticosterone
1. We have determined in adrenalectomized male rats the effects of clamping plasma corticosterone and aldosterone at various concentrations on corticotropin-releasing hormone (CRH), neurotensin/neuromedin N (NT/N) and proenkephalin (pENK) mRNAs in the hypothalamus and amygdala using semi-quantitativ...
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| Veröffentlicht in: | The Journal of physiology 1995-05, Vol.484 (Pt 3), p.721-736 |
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| description | 1. We have determined in adrenalectomized male rats the effects of clamping plasma corticosterone and aldosterone at various
concentrations on corticotropin-releasing hormone (CRH), neurotensin/neuromedin N (NT/N) and proenkephalin (pENK) mRNAs in
the hypothalamus and amygdala using semi-quantitative in situ hybridization. 2. Corticosterone differentially regulated the
levels of CRH and NT/N but not pENK mRNA. These effects were cell specific. CRH mRNA was reduced in the hypothalamic paraventricular
nucleus (PVH), but increased in the central nucleus of the amygdala and bed nuclei of the stria terminalis. NT/N mRNA was
never seen in the PVH, whereas levels increased in the central nucleus of the amygdala, but were unaffected in the lateral
hypothalamic area. In those regions expressing pENK mRNA, levels were unaffected in all treatment groups. 3. CRH mRNA in both
the central nucleus of the amygdala and PVH, and NT/N mRNA in the central nucleus of the amygdala were most sensitive to plasma
corticosterone concentrations of less than 120 ng ml-1, i.e. those seen away from the peak of the diurnal rhythm. In adrenalectomized
animals CRH mRNA in both the central nucleus of the amygdala and PVH could be set at levels usually seen in intact animals
by the same plasma concentration of corticosterone. 4. The levels of CRH mRNA in the PVH and the central nucleus of the amygdala
were closely correlated, while CRH and NT/N mRNA levels were similarly correlated in the central nucleus of the amygdala suggesting
the existence of a common regulatory mechanism. The ED50 of their responses to corticosterone and correlations with thymus
weight suggested the operation of glucocorticoid (type II) receptor mechanisms. 5. In the absence of corticosterone, aldosterone
increased CRH and NT/N mRNA accumulation in the central nucleus of the amygdala, and increased CRH but not NT/N mRNA accumulation
in the PVH. Aldosterone also blunted the dose-response effects of corticosterone on CRH and NT/N mRNA levels in the central
nucleus of the amygdala, but not in the PVH. 6. These results suggest that, in intact animals, adrenal steroids play a major
role in maintaining the levels of neuropeptide mRNAs in the PVH, bed nuclei of the stria terminalis and central nucleus of
the amygdala. The results underscore the importance of cell-specific mechanisms operating to regulate the expression of neuropeptide
genes in different cell types in response to diverse physiological conditions. |
| doi_str_mv | 10.1113/jphysiol.1995.sp020698 |
| format | Article |
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concentrations on corticotropin-releasing hormone (CRH), neurotensin/neuromedin N (NT/N) and proenkephalin (pENK) mRNAs in
the hypothalamus and amygdala using semi-quantitative in situ hybridization. 2. Corticosterone differentially regulated the
levels of CRH and NT/N but not pENK mRNA. These effects were cell specific. CRH mRNA was reduced in the hypothalamic paraventricular
nucleus (PVH), but increased in the central nucleus of the amygdala and bed nuclei of the stria terminalis. NT/N mRNA was
never seen in the PVH, whereas levels increased in the central nucleus of the amygdala, but were unaffected in the lateral
hypothalamic area. In those regions expressing pENK mRNA, levels were unaffected in all treatment groups. 3. CRH mRNA in both
the central nucleus of the amygdala and PVH, and NT/N mRNA in the central nucleus of the amygdala were most sensitive to plasma
corticosterone concentrations of less than 120 ng ml-1, i.e. those seen away from the peak of the diurnal rhythm. In adrenalectomized
animals CRH mRNA in both the central nucleus of the amygdala and PVH could be set at levels usually seen in intact animals
by the same plasma concentration of corticosterone. 4. The levels of CRH mRNA in the PVH and the central nucleus of the amygdala
were closely correlated, while CRH and NT/N mRNA levels were similarly correlated in the central nucleus of the amygdala suggesting
the existence of a common regulatory mechanism. The ED50 of their responses to corticosterone and correlations with thymus
weight suggested the operation of glucocorticoid (type II) receptor mechanisms. 5. In the absence of corticosterone, aldosterone
increased CRH and NT/N mRNA accumulation in the central nucleus of the amygdala, and increased CRH but not NT/N mRNA accumulation
in the PVH. Aldosterone also blunted the dose-response effects of corticosterone on CRH and NT/N mRNA levels in the central
nucleus of the amygdala, but not in the PVH. 6. These results suggest that, in intact animals, adrenal steroids play a major
role in maintaining the levels of neuropeptide mRNAs in the PVH, bed nuclei of the stria terminalis and central nucleus of
the amygdala. The results underscore the importance of cell-specific mechanisms operating to regulate the expression of neuropeptide
genes in different cell types in response to diverse physiological conditions.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/jphysiol.1995.sp020698</identifier><identifier>PMID: 7623287</identifier><language>eng</language><publisher>England: The Physiological Society</publisher><subject>Adrenalectomy ; Aldosterone - blood ; Aldosterone - pharmacology ; Animals ; Appetite - drug effects ; Corticosterone - blood ; Corticosterone - pharmacology ; Drinking ; Limbic System - cytology ; Limbic System - metabolism ; Male ; Neurons - metabolism ; Neuropeptides - genetics ; Organ Size - drug effects ; Prosencephalon - cytology ; Prosencephalon - metabolism ; Rats ; Rats, Sprague-Dawley ; RNA, Messenger - metabolism ; Sodium ; Thymus Gland - anatomy & histology ; Tissue Distribution</subject><ispartof>The Journal of physiology, 1995-05, Vol.484 (Pt 3), p.721-736</ispartof><rights>1995 The Physiological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4511-20036bafc3613ebc3a6c78c9380905c0bd2ec66081cb69988ccb273d661bc1863</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1157955/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1157955/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,1417,27924,27925,45574,45575,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7623287$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Watts, A G</creatorcontrib><creatorcontrib>Sanchez-Watts, G</creatorcontrib><title>Region-specific regulation of neuropeptide mRNAs in rat limbic forebrain neurones by aldosterone and corticosterone</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>1. We have determined in adrenalectomized male rats the effects of clamping plasma corticosterone and aldosterone at various
concentrations on corticotropin-releasing hormone (CRH), neurotensin/neuromedin N (NT/N) and proenkephalin (pENK) mRNAs in
the hypothalamus and amygdala using semi-quantitative in situ hybridization. 2. Corticosterone differentially regulated the
levels of CRH and NT/N but not pENK mRNA. These effects were cell specific. CRH mRNA was reduced in the hypothalamic paraventricular
nucleus (PVH), but increased in the central nucleus of the amygdala and bed nuclei of the stria terminalis. NT/N mRNA was
never seen in the PVH, whereas levels increased in the central nucleus of the amygdala, but were unaffected in the lateral
hypothalamic area. In those regions expressing pENK mRNA, levels were unaffected in all treatment groups. 3. CRH mRNA in both
the central nucleus of the amygdala and PVH, and NT/N mRNA in the central nucleus of the amygdala were most sensitive to plasma
corticosterone concentrations of less than 120 ng ml-1, i.e. those seen away from the peak of the diurnal rhythm. In adrenalectomized
animals CRH mRNA in both the central nucleus of the amygdala and PVH could be set at levels usually seen in intact animals
by the same plasma concentration of corticosterone. 4. The levels of CRH mRNA in the PVH and the central nucleus of the amygdala
were closely correlated, while CRH and NT/N mRNA levels were similarly correlated in the central nucleus of the amygdala suggesting
the existence of a common regulatory mechanism. The ED50 of their responses to corticosterone and correlations with thymus
weight suggested the operation of glucocorticoid (type II) receptor mechanisms. 5. In the absence of corticosterone, aldosterone
increased CRH and NT/N mRNA accumulation in the central nucleus of the amygdala, and increased CRH but not NT/N mRNA accumulation
in the PVH. Aldosterone also blunted the dose-response effects of corticosterone on CRH and NT/N mRNA levels in the central
nucleus of the amygdala, but not in the PVH. 6. These results suggest that, in intact animals, adrenal steroids play a major
role in maintaining the levels of neuropeptide mRNAs in the PVH, bed nuclei of the stria terminalis and central nucleus of
the amygdala. The results underscore the importance of cell-specific mechanisms operating to regulate the expression of neuropeptide
genes in different cell types in response to diverse physiological conditions.</description><subject>Adrenalectomy</subject><subject>Aldosterone - blood</subject><subject>Aldosterone - pharmacology</subject><subject>Animals</subject><subject>Appetite - drug effects</subject><subject>Corticosterone - blood</subject><subject>Corticosterone - pharmacology</subject><subject>Drinking</subject><subject>Limbic System - cytology</subject><subject>Limbic System - metabolism</subject><subject>Male</subject><subject>Neurons - metabolism</subject><subject>Neuropeptides - genetics</subject><subject>Organ Size - drug effects</subject><subject>Prosencephalon - cytology</subject><subject>Prosencephalon - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>RNA, Messenger - metabolism</subject><subject>Sodium</subject><subject>Thymus Gland - anatomy & histology</subject><subject>Tissue Distribution</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkV2L1DAYhYMo6zj6E5RciQgd89EmzY2wLn6y6LKs1yFJ385kaZuatC7997Z2ZtEb8SrknOc95M1B6AUlO0opf3PbH6bkQ7OjShW71BNGhCofoA3NhcqkVPwh2hDCWMZlQR-jJyndEkI5UeoMnUnBOCvlBqVr2PvQZakH52vvcIT92Jhh1nCocQdjDD30g68At9dfzxP2HY5mwI1v7YzXIYKNZhZ_ox0kbCdsmiqkAZY7Nl2FXYiDdyfpKXpUmybBs-O5Rd8_vL-5-JRdfvv4-eL8MnN5QWnGCOHCmtpxQTlYx41wsnSKl0SRwhFbMXBCkJI6K5QqS-csk7wSglpHS8G36O2a24-2hcpBN0TT6D761sRJB-P1307nD3offmpKC6mKYg54eQyI4ccIadCtTw6axnQQxqSlzOcq5k_dolf_BKkseC5ZwdmMihV1MaQUob5_DyV6aVafmtVLs_rU7Dz4_M9t7seOVc7-u9W_8w1M_5mqb75cLUJe5lyyZZHXa8jB7w93PoJex1JwHoZJz5y-GjTXC_wLhR_Jkg</recordid><startdate>19950501</startdate><enddate>19950501</enddate><creator>Watts, A G</creator><creator>Sanchez-Watts, G</creator><general>The Physiological Society</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19950501</creationdate><title>Region-specific regulation of neuropeptide mRNAs in rat limbic forebrain neurones by aldosterone and corticosterone</title><author>Watts, A G ; Sanchez-Watts, G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4511-20036bafc3613ebc3a6c78c9380905c0bd2ec66081cb69988ccb273d661bc1863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Adrenalectomy</topic><topic>Aldosterone - blood</topic><topic>Aldosterone - pharmacology</topic><topic>Animals</topic><topic>Appetite - drug effects</topic><topic>Corticosterone - blood</topic><topic>Corticosterone - pharmacology</topic><topic>Drinking</topic><topic>Limbic System - cytology</topic><topic>Limbic System - metabolism</topic><topic>Male</topic><topic>Neurons - metabolism</topic><topic>Neuropeptides - genetics</topic><topic>Organ Size - drug effects</topic><topic>Prosencephalon - cytology</topic><topic>Prosencephalon - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>RNA, Messenger - metabolism</topic><topic>Sodium</topic><topic>Thymus Gland - anatomy & histology</topic><topic>Tissue Distribution</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Watts, A G</creatorcontrib><creatorcontrib>Sanchez-Watts, G</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Watts, A G</au><au>Sanchez-Watts, G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Region-specific regulation of neuropeptide mRNAs in rat limbic forebrain neurones by aldosterone and corticosterone</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>1995-05-01</date><risdate>1995</risdate><volume>484</volume><issue>Pt 3</issue><spage>721</spage><epage>736</epage><pages>721-736</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><abstract>1. We have determined in adrenalectomized male rats the effects of clamping plasma corticosterone and aldosterone at various
concentrations on corticotropin-releasing hormone (CRH), neurotensin/neuromedin N (NT/N) and proenkephalin (pENK) mRNAs in
the hypothalamus and amygdala using semi-quantitative in situ hybridization. 2. Corticosterone differentially regulated the
levels of CRH and NT/N but not pENK mRNA. These effects were cell specific. CRH mRNA was reduced in the hypothalamic paraventricular
nucleus (PVH), but increased in the central nucleus of the amygdala and bed nuclei of the stria terminalis. NT/N mRNA was
never seen in the PVH, whereas levels increased in the central nucleus of the amygdala, but were unaffected in the lateral
hypothalamic area. In those regions expressing pENK mRNA, levels were unaffected in all treatment groups. 3. CRH mRNA in both
the central nucleus of the amygdala and PVH, and NT/N mRNA in the central nucleus of the amygdala were most sensitive to plasma
corticosterone concentrations of less than 120 ng ml-1, i.e. those seen away from the peak of the diurnal rhythm. In adrenalectomized
animals CRH mRNA in both the central nucleus of the amygdala and PVH could be set at levels usually seen in intact animals
by the same plasma concentration of corticosterone. 4. The levels of CRH mRNA in the PVH and the central nucleus of the amygdala
were closely correlated, while CRH and NT/N mRNA levels were similarly correlated in the central nucleus of the amygdala suggesting
the existence of a common regulatory mechanism. The ED50 of their responses to corticosterone and correlations with thymus
weight suggested the operation of glucocorticoid (type II) receptor mechanisms. 5. In the absence of corticosterone, aldosterone
increased CRH and NT/N mRNA accumulation in the central nucleus of the amygdala, and increased CRH but not NT/N mRNA accumulation
in the PVH. Aldosterone also blunted the dose-response effects of corticosterone on CRH and NT/N mRNA levels in the central
nucleus of the amygdala, but not in the PVH. 6. These results suggest that, in intact animals, adrenal steroids play a major
role in maintaining the levels of neuropeptide mRNAs in the PVH, bed nuclei of the stria terminalis and central nucleus of
the amygdala. The results underscore the importance of cell-specific mechanisms operating to regulate the expression of neuropeptide
genes in different cell types in response to diverse physiological conditions.</abstract><cop>England</cop><pub>The Physiological Society</pub><pmid>7623287</pmid><doi>10.1113/jphysiol.1995.sp020698</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Access via Wiley Online Library; IngentaConnect Free/Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Adrenalectomy Aldosterone - blood Aldosterone - pharmacology Animals Appetite - drug effects Corticosterone - blood Corticosterone - pharmacology Drinking Limbic System - cytology Limbic System - metabolism Male Neurons - metabolism Neuropeptides - genetics Organ Size - drug effects Prosencephalon - cytology Prosencephalon - metabolism Rats Rats, Sprague-Dawley RNA, Messenger - metabolism Sodium Thymus Gland - anatomy & histology Tissue Distribution |
| title | Region-specific regulation of neuropeptide mRNAs in rat limbic forebrain neurones by aldosterone and corticosterone |
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