While the classical function of myelin is to facilitate saltatory conduction, this membrane and the myelin-making oligodendrocytes (OLGs) are now recognized as regulators of plasticity and remodeling in the central nervous system (CNS). Thus, OLG maturation and myelination are highly vulnerable processes along CNS development. We previously showed that rat brain myelination is altered by perinatal exposure to buprenorphine, an opioid analogue in clinical trials for the treatment of pregnant opioid addicts. We now found that the in vivo effects on myelination could result from direct alteration in the balance between μ-opioid receptor (MOR) and nociceptin/orphanin FQ receptor (NOPR) activities in the OLGs. Furthermore, we found that myelination could also be affected by the FDA-approved methadone. A delicate balance between MOR and NOPR signaling may play a crucial role timing OLG maturation and myelin formation and exogenous opioids may disrupt this interplay, altering the developmental pattern of brain myelination.
","abstract_html":"<p>While the classical function of myelin is to facilitate saltatory conduction, this membrane and the myelin-making oligodendrocytes (OLGs) are now recognized as regulators of plasticity and remodeling in the central nervous system (CNS). Thus, OLG maturation and myelination are highly vulnerable processes along CNS development. We previously showed that rat brain myelination is altered by perinatal exposure to buprenorphine, an opioid analogue in clinical trials for the treatment of pregnant opioid addicts. We now found that the in vivo effects on myelination could result from direct alteration in the balance between μ-opioid receptor (MOR) and nociceptin/orphanin FQ receptor (NOPR) activities in the OLGs. Furthermore, we found that myelination could also be affected by the FDA-approved methadone. A delicate balance between MOR and NOPR signaling may play a crucial role timing OLG maturation and myelin formation and exogenous opioids may disrupt this interplay, altering the developmental pattern of brain myelination.</p>","abstract_has_math":false,"creators":["Vestal-Laborde, Allison"],"institution":null,"degree_name":"Master of Science","degree_level":"Thesis","degree_discipline":"Biochemistry","degree_department":null,"school":null,"contributors":["Carmen Sato-Bigbee"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2012,"date_issued":"2012-01-01T08:00:00Z","date_published":"2012-01-01T08:00:00Z","updated_at":"2026-07-24T05:53:56Z","subjects":["endogenous opioid system","opioid receptor","myelination","oligodendrocyte","oligodendrocyte differentiation","central nervous system","Biochemistry, Biophysics, and Structural Biology","Life Sciences"],"languages":[],"rights":["© The Author"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["https://scholarscompass.vcu.edu/etd/424"],"render_values":[{"text":"https://scholarscompass.vcu.edu/etd/424","href":"https://scholarscompass.vcu.edu/etd/424","code":true}]}]},"links":{"outbound_url":"https://doi.org/10.25772/DDF6-5464","outbound_label":"DOI","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Carmen Sato-Bigbee"]},{"key":"dc:creator","label":"Author","values":["Vestal-Laborde, Allison"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2017-10-01T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biochemistry"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["endogenous opioid system","opioid receptor","myelination","oligodendrocyte","oligodendrocyte differentiation","central nervous system","Biochemistry, Biophysics, and Structural Biology","Life Sciences"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:rights","label":"Dc Rights","values":["© The Author"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://doi.org/10.25772/DDF6-5464","https://scholarscompass.vcu.edu/etd/424"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["While the classical function of myelin is to facilitate saltatory conduction, this membrane and the myelin-making oligodendrocytes (OLGs) are now recognized as regulators of plasticity and remodeling in the central nervous system (CNS). Thus, OLG maturation and myelination are highly vulnerable processes along CNS development. We previously showed that rat brain myelination is altered by perinatal exposure to buprenorphine, an opioid analogue in clinical trials for the treatment of pregnant opioid addicts. We now found that the in vivo effects on myelination could result from direct alteration in the balance between μ-opioid receptor (MOR) and nociceptin/orphanin FQ receptor (NOPR) activities in the OLGs. Furthermore, we found that myelination could also be affected by the FDA-approved methadone. A delicate balance between MOR and NOPR signaling may play a crucial role timing OLG maturation and myelin formation and exogenous opioids may disrupt this interplay, altering the developmental pattern of brain myelination.
"]},{"key":"dc:title","label":"Title","values":["OPPOSING ROLES OF THE μ-OPIOID AND NOCICEPTIN/ORPHANIN FQ RECEPTORS IN OLIGODENDROCYTE DEVELOPMENT AND MYELINATION"]}]}],"canonical_facts":{"dc:contributor":["Carmen Sato-Bigbee"],"dc:creator":["Vestal-Laborde, Allison"],"dc:date.available":["2017-10-01T07:00:00Z"],"dc:description.abstract":["While the classical function of myelin is to facilitate saltatory conduction, this membrane and the myelin-making oligodendrocytes (OLGs) are now recognized as regulators of plasticity and remodeling in the central nervous system (CNS). Thus, OLG maturation and myelination are highly vulnerable processes along CNS development. We previously showed that rat brain myelination is altered by perinatal exposure to buprenorphine, an opioid analogue in clinical trials for the treatment of pregnant opioid addicts. We now found that the in vivo effects on myelination could result from direct alteration in the balance between μ-opioid receptor (MOR) and nociceptin/orphanin FQ receptor (NOPR) activities in the OLGs. Furthermore, we found that myelination could also be affected by the FDA-approved methadone. A delicate balance between MOR and NOPR signaling may play a crucial role timing OLG maturation and myelin formation and exogenous opioids may disrupt this interplay, altering the developmental pattern of brain myelination.
"],"dc:identifier":["https://doi.org/10.25772/DDF6-5464","https://scholarscompass.vcu.edu/etd/424"],"dc:rights":["© The Author"],"dc:subject":["endogenous opioid system","opioid receptor","myelination","oligodendrocyte","oligodendrocyte differentiation","central nervous system","Biochemistry, Biophysics, and Structural Biology","Life Sciences"],"dc:title":["OPPOSING ROLES OF THE μ-OPIOID AND NOCICEPTIN/ORPHANIN FQ RECEPTORS IN OLIGODENDROCYTE DEVELOPMENT AND MYELINATION"],"thesis:degree_discipline":["Biochemistry"],"thesis:degree_level":["Thesis"],"thesis:degree_name":["Master of Science"]},"updated_at":"2026-07-24T05:53:56Z"}