{"id":{"repo_id":"buffalo","oai_identifier":"oai:ubir.buffalo.edu:10477/78507"},"canonical_url":"https://search.dev.ndltd.org/etd/buffalo/oai:ubir.buffalo.edu:10477/78507","repository":{"repo_id":"buffalo","name":"Buffalo","base_url":"https://ubir.buffalo.edu/oai/request"},"display":{"title":"Amylin Receptor Expression in the Mesocorticolimbic System","abstract":"M.S.","abstract_html":"M.S.","abstract_has_math":false,"creators":["Nashawi, Houda"],"institution":"State University of New York at Buffalo","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["Mietlicki-Baase, Elizabeth","Neuroscience"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2018,"date_issued":"2018-10-26T02:54:32Z","date_published":"2018-10-26T02:54:32Z","updated_at":"2026-07-27T19:05:09Z","subjects":["neurosciences","nutrition","psychobiology"],"languages":["eng"],"rights":["Users of works found in University at Buffalo Institutional Repository (UBIR) are responsible for identifying and contacting the copyright owner for permission to reuse. University at Buffalo Libraries do not manage rights for copyright-protected works and cannot assist with permissions.","Copyright retained by author."],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/10477/78507","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Mietlicki-Baase, Elizabeth","Neuroscience"]},{"key":"dc:creator","label":"Author","values":["Nashawi, Houda"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2018-10-26T02:54:32Z","2018","2018-07-04 09:58:55"]},{"key":"dc:publisher","label":"Institution","values":["State University of New York at Buffalo"]},{"key":"dc:type","label":"Dc Type","values":["Text","Thesis"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["neurosciences","nutrition","psychobiology"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]},{"key":"dc:rights","label":"Dc Rights","values":["Users of works found in University at Buffalo Institutional Repository (UBIR) are responsible for identifying and contacting the copyright owner for permission to reuse. University at Buffalo Libraries do not manage rights for copyright-protected works and cannot assist with permissions.","Copyright retained by author."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/10477/78507"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["M.S.","Despite the fact that obesity is prevalent in modern society and is a risk factor for many life-threatening conditions, effective non-invasive treatments remain limited. Amylin is a pancreatic and brain-derived peptide that acts within the central nervous system (CNS) to reduce food intake and body weight, and is considered a promising candidate for obesity treatment. The nuclei at which amylin acts to exert its energy balance effects have not been comprehensively studied, and although amylin binds throughout the CNS, including several mesocorticolimbic areas known to control energy balance and food reward, the role for most of these nuclei in amylinergic control of energy balance is largely untested. Furthermore, it is unclear how diet may impact CNS amylin receptor expression. To begin to investigate this, the expression of amylin receptor components in key mesocorticolimbic nuclei was evaluated in chow-maintained rats given access to a fat emulsion or access to only tap water as a control, 1 hr/day for ~1 month (no more than 2 days at a time with no fat access). Specifically, mRNA expression of the components of the amylin receptor complex in the nucleus accumbens core (NAcC), nucleus accumbens shell (NAcSh), central nucleus of the amygdala (CeA), and medial prefrontal cortex (mPFC) was evaluated using qPCR. The results confirm previous findings that all amylin receptor components are expressed in the NAcC and NAcSh in chow-fed rats. Whereas fat exposure did not have any significant effects on their expression in the NAcC, RAMP-3 expression was significantly reduced in the NAcSh in fat-exposed rats (p<0.05). In addition, this project shows that all components of amylin receptors are expressed in mPFC and CeA and that fat access significantly reduced the expression of calcitonin receptor-A (CTR-A) in the CeA and receptor activity-modifying protein 2 (RAMP-2) in the mPFC (p<0.05). To begin to assess the function of amylin receptors in these sites, in a separate experiment, the effect of amylin-mediated signaling in the CeA on chow intake was evaluated using salmon calcitonin (sCT), a potent amylin receptor agonist. Intra-CeA sCT (0.4 μg) suppressed intake 6 hr post-injection and also reduced 24 hr body weight gain. Collectively, these results suggest that amylin signaling in the mesocorticolimbic system may have a role in mediating the effects of amylin on food intake and body weight, which encourages further attention and experimental probing to understand the mechanisms by which amylin may act at these sites to promote negative energy balance."]},{"key":"dc:format","label":"Dc Format","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["Amylin Receptor Expression in the Mesocorticolimbic System"]}]}],"canonical_facts":{"dc:contributor":["Mietlicki-Baase, Elizabeth","Neuroscience"],"dc:creator":["Nashawi, Houda"],"dc:date":["2018-10-26T02:54:32Z","2018","2018-07-04 09:58:55"],"dc:description":["M.S.","Despite the fact that obesity is prevalent in modern society and is a risk factor for many life-threatening conditions, effective non-invasive treatments remain limited. Amylin is a pancreatic and brain-derived peptide that acts within the central nervous system (CNS) to reduce food intake and body weight, and is considered a promising candidate for obesity treatment. The nuclei at which amylin acts to exert its energy balance effects have not been comprehensively studied, and although amylin binds throughout the CNS, including several mesocorticolimbic areas known to control energy balance and food reward, the role for most of these nuclei in amylinergic control of energy balance is largely untested. Furthermore, it is unclear how diet may impact CNS amylin receptor expression. To begin to investigate this, the expression of amylin receptor components in key mesocorticolimbic nuclei was evaluated in chow-maintained rats given access to a fat emulsion or access to only tap water as a control, 1 hr/day for ~1 month (no more than 2 days at a time with no fat access). Specifically, mRNA expression of the components of the amylin receptor complex in the nucleus accumbens core (NAcC), nucleus accumbens shell (NAcSh), central nucleus of the amygdala (CeA), and medial prefrontal cortex (mPFC) was evaluated using qPCR. The results confirm previous findings that all amylin receptor components are expressed in the NAcC and NAcSh in chow-fed rats. Whereas fat exposure did not have any significant effects on their expression in the NAcC, RAMP-3 expression was significantly reduced in the NAcSh in fat-exposed rats (p<0.05). In addition, this project shows that all components of amylin receptors are expressed in mPFC and CeA and that fat access significantly reduced the expression of calcitonin receptor-A (CTR-A) in the CeA and receptor activity-modifying protein 2 (RAMP-2) in the mPFC (p<0.05). To begin to assess the function of amylin receptors in these sites, in a separate experiment, the effect of amylin-mediated signaling in the CeA on chow intake was evaluated using salmon calcitonin (sCT), a potent amylin receptor agonist. Intra-CeA sCT (0.4 μg) suppressed intake 6 hr post-injection and also reduced 24 hr body weight gain. Collectively, these results suggest that amylin signaling in the mesocorticolimbic system may have a role in mediating the effects of amylin on food intake and body weight, which encourages further attention and experimental probing to understand the mechanisms by which amylin may act at these sites to promote negative energy balance."],"dc:format":["application/pdf"],"dc:identifier":["http://hdl.handle.net/10477/78507"],"dc:language":["eng"],"dc:publisher":["State University of New York at Buffalo"],"dc:rights":["Users of works found in University at Buffalo Institutional Repository (UBIR) are responsible for identifying and contacting the copyright owner for permission to reuse. University at Buffalo Libraries do not manage rights for copyright-protected works and cannot assist with permissions.","Copyright retained by author."],"dc:subject":["neurosciences","nutrition","psychobiology"],"dc:title":["Amylin Receptor Expression in the Mesocorticolimbic System"],"dc:type":["Text","Thesis"]},"updated_at":"2026-07-27T19:05:09Z"}