{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/82513"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/82513","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Amygdalar Modulation of the Medial Geniculate Nucleus and Cingulate Cortex in Discriminative Avoidance Training","abstract":"Neurons in A29 and the lateral nucleus of the amygdala (LA) characteristically develop maximal dTIA in late stages of DAL. Experiment II tested the hypothesis that LA nucleus is responsible for the late dTIA in A29. As hypothesized, LA nuclear excitotoxic lesions decreased dTIA in A29. Moreover, A29 theta-like neuronal activity was weaker in these subjects. Not in accord with the hypothesis, LA nuclear lesions impaired the early developing dTIA in A24. Thus, the LA nucleus may contribute to dTIA induction in A24, or the lesion may have damaged regions outside of the LA nucleus. Taken together these studies add significantly to understanding amygdalar modulation of neurons in extra-amygdalar regions of the neural circuitry for DAL.","abstract_html":"Neurons in A29 and the lateral nucleus of the amygdala (LA) characteristically develop maximal dTIA in late stages of DAL. Experiment II tested the hypothesis that LA nucleus is responsible for the late dTIA in A29. As hypothesized, LA nuclear excitotoxic lesions decreased dTIA in A29. Moreover, A29 theta-like neuronal activity was weaker in these subjects. Not in accord with the hypothesis, LA nuclear lesions impaired the early developing dTIA in A24. Thus, the LA nucleus may contribute to dTIA induction in A24, or the lesion may have damaged regions outside of the LA nucleus. Taken together these studies add significantly to understanding amygdalar modulation of neurons in extra-amygdalar regions of the neural circuitry for DAL.","abstract_has_math":false,"creators":["Kashef, Alireza"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Neuroscience","degree_department":null,"school":null,"contributors":["Gabriel, Michael"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2015,"date_issued":"2015-09-25T20:45:38Z","date_published":"2015-09-25T20:45:38Z","updated_at":"2026-07-22T22:26:18Z","subjects":["Psychology, Behavioral"],"languages":["eng"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["(MiAaPQ)AAI3269937"],"render_values":[{"text":"(MiAaPQ)AAI3269937","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/82513","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Gabriel, Michael"]},{"key":"dc:creator","label":"Author","values":["Kashef, Alireza"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2015-09-25T20:45:38Z","10000-01-01","2007"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Neuroscience"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Psychology, Behavioral"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/2142/82513","(MiAaPQ)AAI3269937"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Neurons in A29 and the lateral nucleus of the amygdala (LA) characteristically develop maximal dTIA in late stages of DAL. Experiment II tested the hypothesis that LA nucleus is responsible for the late dTIA in A29. As hypothesized, LA nuclear excitotoxic lesions decreased dTIA in A29. Moreover, A29 theta-like neuronal activity was weaker in these subjects. Not in accord with the hypothesis, LA nuclear lesions impaired the early developing dTIA in A24. Thus, the LA nucleus may contribute to dTIA induction in A24, or the lesion may have damaged regions outside of the LA nucleus. Taken together these studies add significantly to understanding amygdalar modulation of neurons in extra-amygdalar regions of the neural circuitry for DAL.","Made available in DSpace on 2015-09-25T20:45:38Z (GMT). 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Experiment II tested the hypothesis that LA nucleus is responsible for the late dTIA in A29. As hypothesized, LA nuclear excitotoxic lesions decreased dTIA in A29. Moreover, A29 theta-like neuronal activity was weaker in these subjects. Not in accord with the hypothesis, LA nuclear lesions impaired the early developing dTIA in A24. Thus, the LA nucleus may contribute to dTIA induction in A24, or the lesion may have damaged regions outside of the LA nucleus. Taken together these studies add significantly to understanding amygdalar modulation of neurons in extra-amygdalar regions of the neural circuitry for DAL.","Made available in DSpace on 2015-09-25T20:45:38Z (GMT). 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