The data from recent clinical trails have reported that intranasal administration of non-inhaled 100% medical grade CO2 is an effective and safe treatment for migraine and allergic rhinosinusitis, but the exact mechanism of action of CO2 in treating these diseases is not well understood. Activation of trigeminal nerves, release of CGRP, and neuron-glia interactions through gap junctions in trigeminal ganglion are implicated in the pathology of migraine and allergic rhinosinusitis. The goal of this study was to determine whether administration of 100% CO2 to the nasal mucosa of rats inhibits trigeminal ganglion neuron-glia signaling and neuronal cell secretion. Increased signaling via gap junctions between trigeminal neurons and satellite glial cells was seen 2 hrs after capsaicin injection into the whisker pad. This gap junction communication was greatly reduced in animals treated with CO2 prior to capsaicin stimulation. CO2 treatment also blocked the stimulatory effect of capsaicin on Cx 26, S100B and CGRP expression. In addition, CO2 caused a decrease in levels of SNAP-25, a protein involved in controlling CGRP release from trigeminal nerves. Results from this in vivo study provide the first evidence of a unique regulatory mechanism by which CO2 inhibits sensory nerve activation, neuron-glial cell signaling, and subsequent neuropeptide release.
","abstract_html":"<p>The data from recent clinical trails have reported that intranasal administration of non-inhaled 100% medical grade CO2 is an effective and safe treatment for migraine and allergic rhinosinusitis, but the exact mechanism of action of CO2 in treating these diseases is not well understood. Activation of trigeminal nerves, release of CGRP, and neuron-glia interactions through gap junctions in trigeminal ganglion are implicated in the pathology of migraine and allergic rhinosinusitis. The goal of this study was to determine whether administration of 100% CO2 to the nasal mucosa of rats inhibits trigeminal ganglion neuron-glia signaling and neuronal cell secretion. Increased signaling via gap junctions between trigeminal neurons and satellite glial cells was seen 2 hrs after capsaicin injection into the whisker pad. This gap junction communication was greatly reduced in animals treated with CO2 prior to capsaicin stimulation. CO2 treatment also blocked the stimulatory effect of capsaicin on Cx 26, S100B and CGRP expression. In addition, CO2 caused a decrease in levels of SNAP-25, a protein involved in controlling CGRP release from trigeminal nerves. Results from this in vivo study provide the first evidence of a unique regulatory mechanism by which CO2 inhibits sensory nerve activation, neuron-glial cell signaling, and subsequent neuropeptide release.</p>","abstract_has_math":false,"creators":["Kankipati, Stanka Madhu Kumar"],"institution":null,"degree_name":"Master of Science in Biology","degree_level":"Masters","degree_discipline":"Biology","degree_department":null,"school":null,"contributors":["Paul Durham"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2008,"date_issued":"2008-01-01T08:00:00Z","date_published":"2008-01-01T08:00:00Z","updated_at":"2026-07-24T03:16:17Z","subjects":["neuron-glia interactions","gap junctions","Cx 26","CGRP","SNAP-25","S100B","trigeminal","Biology"],"languages":[],"rights":["© Stanka Madhu Kumar Kankipati"],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://bearworks.missouristate.edu/theses/1256","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Paul Durham"]},{"key":"dc:creator","label":"Author","values":["Kankipati, Stanka Madhu Kumar"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"thesis:degree_discipline","label":"Discipline","values":["Biology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Masters"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science in Biology"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["neuron-glia interactions","gap junctions","Cx 26","CGRP","SNAP-25","S100B","trigeminal","Biology"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:rights","label":"Dc Rights","values":["© Stanka Madhu Kumar Kankipati"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://bearworks.missouristate.edu/theses/1256"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["The data from recent clinical trails have reported that intranasal administration of non-inhaled 100% medical grade CO2 is an effective and safe treatment for migraine and allergic rhinosinusitis, but the exact mechanism of action of CO2 in treating these diseases is not well understood. Activation of trigeminal nerves, release of CGRP, and neuron-glia interactions through gap junctions in trigeminal ganglion are implicated in the pathology of migraine and allergic rhinosinusitis. The goal of this study was to determine whether administration of 100% CO2 to the nasal mucosa of rats inhibits trigeminal ganglion neuron-glia signaling and neuronal cell secretion. Increased signaling via gap junctions between trigeminal neurons and satellite glial cells was seen 2 hrs after capsaicin injection into the whisker pad. This gap junction communication was greatly reduced in animals treated with CO2 prior to capsaicin stimulation. CO2 treatment also blocked the stimulatory effect of capsaicin on Cx 26, S100B and CGRP expression. In addition, CO2 caused a decrease in levels of SNAP-25, a protein involved in controlling CGRP release from trigeminal nerves. Results from this in vivo study provide the first evidence of a unique regulatory mechanism by which CO2 inhibits sensory nerve activation, neuron-glial cell signaling, and subsequent neuropeptide release.
"]},{"key":"dc:title","label":"Title","values":["Effect of Intranasal Delivery of Carbon Dioxide on Trigeminal Ganglion Neurons: Inhibition of Neuron-Glia Gap Junction Communication and Neuropeptide Secretion"]}]}],"canonical_facts":{"dc:contributor":["Paul Durham"],"dc:creator":["Kankipati, Stanka Madhu Kumar"],"dc:description.abstract":["The data from recent clinical trails have reported that intranasal administration of non-inhaled 100% medical grade CO2 is an effective and safe treatment for migraine and allergic rhinosinusitis, but the exact mechanism of action of CO2 in treating these diseases is not well understood. Activation of trigeminal nerves, release of CGRP, and neuron-glia interactions through gap junctions in trigeminal ganglion are implicated in the pathology of migraine and allergic rhinosinusitis. The goal of this study was to determine whether administration of 100% CO2 to the nasal mucosa of rats inhibits trigeminal ganglion neuron-glia signaling and neuronal cell secretion. Increased signaling via gap junctions between trigeminal neurons and satellite glial cells was seen 2 hrs after capsaicin injection into the whisker pad. This gap junction communication was greatly reduced in animals treated with CO2 prior to capsaicin stimulation. CO2 treatment also blocked the stimulatory effect of capsaicin on Cx 26, S100B and CGRP expression. In addition, CO2 caused a decrease in levels of SNAP-25, a protein involved in controlling CGRP release from trigeminal nerves. Results from this in vivo study provide the first evidence of a unique regulatory mechanism by which CO2 inhibits sensory nerve activation, neuron-glial cell signaling, and subsequent neuropeptide release.
"],"dc:identifier":["https://bearworks.missouristate.edu/theses/1256"],"dc:rights":["© Stanka Madhu Kumar Kankipati"],"dc:subject":["neuron-glia interactions","gap junctions","Cx 26","CGRP","SNAP-25","S100B","trigeminal","Biology"],"dc:title":["Effect of Intranasal Delivery of Carbon Dioxide on Trigeminal Ganglion Neurons: Inhibition of Neuron-Glia Gap Junction Communication and Neuropeptide Secretion"],"thesis:degree_discipline":["Biology"],"thesis:degree_level":["Masters"],"thesis:degree_name":["Master of Science in Biology"]},"updated_at":"2026-07-24T03:16:17Z"}