{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/22701"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/22701","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Hypothalamic and medullary modulation of cardiorespiratory responses to hypoxia and hypercapnia","abstract":"The role of ventrolateral medullary and caudal hypothalamic neurons in the cardiorespiratory response to hypoxia and hypercapnia was examined. Initial experiments performed on anesthetized rats demonstrated that microinjection into the rostral ventrolateral medulla (VLM) of the excitatory amino acid receptor antagonist kynurenic acid resulted in increased respiratory activity and enhanced respiratory responses to hypoxic and hypercapnic stimuli. Microinjections just caudal, however, typically resulted in apnea. The results suggest that excitatory amino acid transmission in the rostral VLM exerts a tonic inhibitory effect on respiratory activity and responses to hypoxia and hypercapnia. In contrast, excitatory amino acid transmission further caudal in the VLM may be required for the maintenance of respiratory activity. Remaining experiments used in vivo and in vitro preparations to examine responses of caudal hypothalamic neurons to hypoxia and hypercapnia. Hypothalamic single unit activity, phrenic nerve activity, and cervical sympathetic nerve activity were recorded in anesthetized cats. Caudal hypothalamic neurons were likely to be stimulated by hypoxia or hypercapnia, but seldom both stimuli. Computer averaging techniques showed that neurons responsive to these stimuli were more likely than unresponsive neurons to have a discharge related to cardiovascular and/or respiratory activity. Similar results were found in barodenervated, peripherally-chemodenervated cats. The results suggest separate subpopulations of caudal hypothalamic neurons modulate cardiorespiratory responses to hypoxia and hypercapnia. A brain slice preparation was subsequently used in an attempt to determine if caudal hypothalamic neurons are inherently responsive to hypoxia and hypercapnia. In addition, experiments were performed to determine if these types of neurons possess distinct electrophysiological and morphological properties. Results demonstrated that a large percentage of caudal hypothalamic neurons are stimulated by hypoxia in a reduced preparation; the majority of these retain their responsiveness when synaptic transmission is blocked, indicating they are inherently chemoresponsive and may be central hypoxia-sensitive chemoreceptors. A second, distinct population of caudal hypothalamic neurons is inherently responsive to hypercapnia; these neurons may function as traditional central chemoreceptors. Finally, it was found that hypoxia-stimulated, hypercapnia-stimulated, and unstimulated neurons possess several distinct electrophysiological and morphological properties. These properties may relate to how these types of neurons respond to a hypoxic or hypercapnic challenge.","abstract_html":"The role of ventrolateral medullary and caudal hypothalamic neurons in the cardiorespiratory response to hypoxia and hypercapnia was examined. Initial experiments performed on anesthetized rats demonstrated that microinjection into the rostral ventrolateral medulla (VLM) of the excitatory amino acid receptor antagonist kynurenic acid resulted in increased respiratory activity and enhanced respiratory responses to hypoxic and hypercapnic stimuli. Microinjections just caudal, however, typically resulted in apnea. The results suggest that excitatory amino acid transmission in the rostral VLM exerts a tonic inhibitory effect on respiratory activity and responses to hypoxia and hypercapnia. In contrast, excitatory amino acid transmission further caudal in the VLM may be required for the maintenance of respiratory activity. Remaining experiments used in vivo and in vitro preparations to examine responses of caudal hypothalamic neurons to hypoxia and hypercapnia. Hypothalamic single unit activity, phrenic nerve activity, and cervical sympathetic nerve activity were recorded in anesthetized cats. Caudal hypothalamic neurons were likely to be stimulated by hypoxia or hypercapnia, but seldom both stimuli. Computer averaging techniques showed that neurons responsive to these stimuli were more likely than unresponsive neurons to have a discharge related to cardiovascular and/or respiratory activity. Similar results were found in barodenervated, peripherally-chemodenervated cats. The results suggest separate subpopulations of caudal hypothalamic neurons modulate cardiorespiratory responses to hypoxia and hypercapnia. A brain slice preparation was subsequently used in an attempt to determine if caudal hypothalamic neurons are inherently responsive to hypoxia and hypercapnia. In addition, experiments were performed to determine if these types of neurons possess distinct electrophysiological and morphological properties. Results demonstrated that a large percentage of caudal hypothalamic neurons are stimulated by hypoxia in a reduced preparation; the majority of these retain their responsiveness when synaptic transmission is blocked, indicating they are inherently chemoresponsive and may be central hypoxia-sensitive chemoreceptors. A second, distinct population of caudal hypothalamic neurons is inherently responsive to hypercapnia; these neurons may function as traditional central chemoreceptors. Finally, it was found that hypoxia-stimulated, hypercapnia-stimulated, and unstimulated neurons possess several distinct electrophysiological and morphological properties. These properties may relate to how these types of neurons respond to a hypoxic or hypercapnic challenge.","abstract_has_math":false,"creators":["Dillon, Glenn Haley"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Molecular and Integrative Physiology","degree_department":null,"school":null,"contributors":["Waldrop, Tony G."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2011,"date_issued":"2011-05-07T13:48:35Z","date_published":"2011-05-07T13:48:35Z","updated_at":"2026-07-22T22:25:20Z","subjects":["Biology, Neuroscience","Biology, Animal Physiology"],"languages":["eng"],"rights":["Copyright 1993 Dillon, Glenn Haley"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["AAI9329015","(UMI)AAI9329015"],"render_values":[{"text":"AAI9329015","href":null,"code":true},{"text":"(UMI)AAI9329015","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/22701","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Waldrop, Tony G."]},{"key":"dc:creator","label":"Author","values":["Dillon, Glenn Haley"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2011-05-07T13:48:35Z","10000-01-01","1993"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Molecular and Integrative Physiology"]},{"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":["Biology, Neuroscience","Biology, Animal Physiology"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]},{"key":"dc:rights","label":"Dc Rights","values":["Copyright 1993 Dillon, Glenn Haley"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["AAI9329015","(UMI)AAI9329015","http://hdl.handle.net/2142/22701"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["The role of ventrolateral medullary and caudal hypothalamic neurons in the cardiorespiratory response to hypoxia and hypercapnia was examined. Initial experiments performed on anesthetized rats demonstrated that microinjection into the rostral ventrolateral medulla (VLM) of the excitatory amino acid receptor antagonist kynurenic acid resulted in increased respiratory activity and enhanced respiratory responses to hypoxic and hypercapnic stimuli. Microinjections just caudal, however, typically resulted in apnea. The results suggest that excitatory amino acid transmission in the rostral VLM exerts a tonic inhibitory effect on respiratory activity and responses to hypoxia and hypercapnia. In contrast, excitatory amino acid transmission further caudal in the VLM may be required for the maintenance of respiratory activity. Remaining experiments used in vivo and in vitro preparations to examine responses of caudal hypothalamic neurons to hypoxia and hypercapnia. Hypothalamic single unit activity, phrenic nerve activity, and cervical sympathetic nerve activity were recorded in anesthetized cats. Caudal hypothalamic neurons were likely to be stimulated by hypoxia or hypercapnia, but seldom both stimuli. Computer averaging techniques showed that neurons responsive to these stimuli were more likely than unresponsive neurons to have a discharge related to cardiovascular and/or respiratory activity. Similar results were found in barodenervated, peripherally-chemodenervated cats. The results suggest separate subpopulations of caudal hypothalamic neurons modulate cardiorespiratory responses to hypoxia and hypercapnia. A brain slice preparation was subsequently used in an attempt to determine if caudal hypothalamic neurons are inherently responsive to hypoxia and hypercapnia. In addition, experiments were performed to determine if these types of neurons possess distinct electrophysiological and morphological properties. Results demonstrated that a large percentage of caudal hypothalamic neurons are stimulated by hypoxia in a reduced preparation; the majority of these retain their responsiveness when synaptic transmission is blocked, indicating they are inherently chemoresponsive and may be central hypoxia-sensitive chemoreceptors. A second, distinct population of caudal hypothalamic neurons is inherently responsive to hypercapnia; these neurons may function as traditional central chemoreceptors. Finally, it was found that hypoxia-stimulated, hypercapnia-stimulated, and unstimulated neurons possess several distinct electrophysiological and morphological properties. These properties may relate to how these types of neurons respond to a hypoxic or hypercapnic challenge.","Made available in DSpace on 2011-05-07T13:48:35Z (GMT). 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Initial experiments performed on anesthetized rats demonstrated that microinjection into the rostral ventrolateral medulla (VLM) of the excitatory amino acid receptor antagonist kynurenic acid resulted in increased respiratory activity and enhanced respiratory responses to hypoxic and hypercapnic stimuli. Microinjections just caudal, however, typically resulted in apnea. The results suggest that excitatory amino acid transmission in the rostral VLM exerts a tonic inhibitory effect on respiratory activity and responses to hypoxia and hypercapnia. In contrast, excitatory amino acid transmission further caudal in the VLM may be required for the maintenance of respiratory activity. Remaining experiments used in vivo and in vitro preparations to examine responses of caudal hypothalamic neurons to hypoxia and hypercapnia. Hypothalamic single unit activity, phrenic nerve activity, and cervical sympathetic nerve activity were recorded in anesthetized cats. Caudal hypothalamic neurons were likely to be stimulated by hypoxia or hypercapnia, but seldom both stimuli. Computer averaging techniques showed that neurons responsive to these stimuli were more likely than unresponsive neurons to have a discharge related to cardiovascular and/or respiratory activity. Similar results were found in barodenervated, peripherally-chemodenervated cats. The results suggest separate subpopulations of caudal hypothalamic neurons modulate cardiorespiratory responses to hypoxia and hypercapnia. A brain slice preparation was subsequently used in an attempt to determine if caudal hypothalamic neurons are inherently responsive to hypoxia and hypercapnia. In addition, experiments were performed to determine if these types of neurons possess distinct electrophysiological and morphological properties. Results demonstrated that a large percentage of caudal hypothalamic neurons are stimulated by hypoxia in a reduced preparation; the majority of these retain their responsiveness when synaptic transmission is blocked, indicating they are inherently chemoresponsive and may be central hypoxia-sensitive chemoreceptors. A second, distinct population of caudal hypothalamic neurons is inherently responsive to hypercapnia; these neurons may function as traditional central chemoreceptors. Finally, it was found that hypoxia-stimulated, hypercapnia-stimulated, and unstimulated neurons possess several distinct electrophysiological and morphological properties. These properties may relate to how these types of neurons respond to a hypoxic or hypercapnic challenge.","Made available in DSpace on 2011-05-07T13:48:35Z (GMT). No. of bitstreams: 2 license.txt: 4922 bytes, checksum: 910b249b4beec47e7ab768910c8f966f (MD5) 9329015.pdf: 7320409 bytes, checksum: 96d776c3e8beb7da0319c3cbbe2661ba (MD5) Previous issue date: 1993","Item marked as restricted to the 'UIUC Users [automated]' Group (id=2) by Howard Ding (hding2@illinois.edu) on 2011-05-07T14:59:24Z Item is restricted indefinitely.","Restriction data tranferred 2014-07-01T11:28:01-05:00 Original Data Group with Access UIUC Users [automated] Release Date: none Reason: ETDs are only available to UIUC Users without author permission","ETDs are only available to UIUC Users without author permission","U of I Only"],"dc:identifier":["AAI9329015","(UMI)AAI9329015","http://hdl.handle.net/2142/22701"],"dc:language":["eng"],"dc:rights":["Copyright 1993 Dillon, Glenn Haley"],"dc:subject":["Biology, Neuroscience","Biology, Animal Physiology"],"dc:title":["Hypothalamic and medullary modulation of cardiorespiratory responses to hypoxia and hypercapnia"],"dc:type":["text"],"thesis:degree_discipline":["Molecular and Integrative Physiology"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Ph.D."],"thesis:institution_name":["University of Illinois at Urbana-Champaign"]},"updated_at":"2026-07-22T22:25:20Z"}