Methadone is often used in the maintenance and detoxification of opioid-dependent pregnant women. This use of methadone during pregnancy is known to be associated with teratogenic effects observed in the progeny. The present study is an attempt to gain insight into possible pathophysiologic mechanism(s) responsible for these teratogenic effects: specifically, a relationship between maternal methadone administration and the content of the endogenous opioid peptide, beta-endorphin, in the brain and pituitary of the rat progeny.
In brief, nulliparous mature female Sprague-Dawley rats received daily injections (5 mg./kg.) of methadone hydrochloride (methadone-treated) or a similar volume of physiological saline (controls), treatment started prior to conception and continued through weaning of the progeny. Following parturition, young rats aged 5, 15, 25 and 75 days were sacrificed by cervical dislocation, and their brain and pituitary removed and dissected. Beta-endorphin immunoreactivity was then determined in the midline telencephalon, diencephalon, medulla-midbrain, and whole pituitary by radioimmunossay. Protein content was also measured. In addition, a number of maternal and progenial morphological parameters were monitored throughout the study.
The results indicate that methadone exposure during gestation and lactation has no significant effect on beta-endorphin content in the whole pituitary or brain regions studied. The results indicate, however, that methadone exposure does significantly reduce protein content in the day 25 diencephalon, and in the day 5 and 15 whole pituitary. The results also tend to support previous studies which have shown methadone exposure to have significant effects on maternal and progenial weight gain, as well as, maternal mortality and perinatal viability.
In conclusion, it appears that maternal methadone exposure has little or no significant effect on beta-endorphin content in the brain or pituitary of the rat progeny; protein content, however, is reduced in both progenial diencephalon and pituitary.
","abstract_html":"<p>Methadone is often used in the maintenance and detoxification of opioid-dependent pregnant women. This use of methadone during pregnancy is known to be associated with teratogenic effects observed in the progeny. The present study is an attempt to gain insight into possible pathophysiologic mechanism(s) responsible for these teratogenic effects: specifically, a relationship between maternal methadone administration and the content of the endogenous opioid peptide, beta-endorphin, in the brain and pituitary of the rat progeny.</p> <p>In brief, nulliparous mature female Sprague-Dawley rats received daily injections (5 mg./kg.) of methadone hydrochloride (methadone-treated) or a similar volume of physiological saline (controls), treatment started prior to conception and continued through weaning of the progeny. Following parturition, young rats aged 5, 15, 25 and 75 days were sacrificed by cervical dislocation, and their brain and pituitary removed and dissected. Beta-endorphin immunoreactivity was then determined in the midline telencephalon, diencephalon, medulla-midbrain, and whole pituitary by radioimmunossay. Protein content was also measured. In addition, a number of maternal and progenial morphological parameters were monitored throughout the study.</p> <p>The results indicate that methadone exposure during gestation and lactation has no significant effect on beta-endorphin content in the whole pituitary or brain regions studied. The results indicate, however, that methadone exposure does significantly reduce protein content in the day 25 diencephalon, and in the day 5 and 15 whole pituitary. The results also tend to support previous studies which have shown methadone exposure to have significant effects on maternal and progenial weight gain, as well as, maternal mortality and perinatal viability.</p> <p>In conclusion, it appears that maternal methadone exposure has little or no significant effect on beta-endorphin content in the brain or pituitary of the rat progeny; protein content, however, is reduced in both progenial diencephalon and pituitary.</p>","abstract_has_math":false,"creators":["Braun, Randall L."],"institution":null,"degree_name":"Master of Science (MS)","degree_level":"Thesis","degree_discipline":"Pharmacology","degree_department":null,"school":null,"contributors":["Marvin A. Peters","Cecilia Y. Cheung","David A. Hessinger"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":1984,"date_issued":"1984-06-01T07:00:00Z","date_published":"1984-06-01T07:00:00Z","updated_at":"2026-07-24T02:53:44Z","subjects":["Animal Experimentation and Research","Laboratory and Basic Science Research","Pharmacology","Substance Abuse and Addiction","Methadone -- adverse effects; Rats"],"languages":["English"],"rights":["This title appears here courtesy of the author, who has granted Loma Linda University a limited, non-exclusive right to make this publication available to the public. The author retains all other copyrights."],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://scholarsrepository.llu.edu/etd/1448","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Marvin A. Peters","Cecilia Y. Cheung","David A. Hessinger"]},{"key":"dc:creator","label":"Author","values":["Braun, Randall L."]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"thesis:degree_discipline","label":"Discipline","values":["Pharmacology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science (MS)"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Animal Experimentation and Research","Laboratory and Basic Science Research","Pharmacology","Substance Abuse and Addiction","Methadone -- adverse effects; Rats"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["English"]},{"key":"dc:rights","label":"Dc Rights","values":["This title appears here courtesy of the author, who has granted Loma Linda University a limited, non-exclusive right to make this publication available to the public. The author retains all other copyrights."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://scholarsrepository.llu.edu/etd/1448"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Methadone is often used in the maintenance and detoxification of opioid-dependent pregnant women. This use of methadone during pregnancy is known to be associated with teratogenic effects observed in the progeny. The present study is an attempt to gain insight into possible pathophysiologic mechanism(s) responsible for these teratogenic effects: specifically, a relationship between maternal methadone administration and the content of the endogenous opioid peptide, beta-endorphin, in the brain and pituitary of the rat progeny.
In brief, nulliparous mature female Sprague-Dawley rats received daily injections (5 mg./kg.) of methadone hydrochloride (methadone-treated) or a similar volume of physiological saline (controls), treatment started prior to conception and continued through weaning of the progeny. Following parturition, young rats aged 5, 15, 25 and 75 days were sacrificed by cervical dislocation, and their brain and pituitary removed and dissected. Beta-endorphin immunoreactivity was then determined in the midline telencephalon, diencephalon, medulla-midbrain, and whole pituitary by radioimmunossay. Protein content was also measured. In addition, a number of maternal and progenial morphological parameters were monitored throughout the study.
The results indicate that methadone exposure during gestation and lactation has no significant effect on beta-endorphin content in the whole pituitary or brain regions studied. The results indicate, however, that methadone exposure does significantly reduce protein content in the day 25 diencephalon, and in the day 5 and 15 whole pituitary. The results also tend to support previous studies which have shown methadone exposure to have significant effects on maternal and progenial weight gain, as well as, maternal mortality and perinatal viability.
In conclusion, it appears that maternal methadone exposure has little or no significant effect on beta-endorphin content in the brain or pituitary of the rat progeny; protein content, however, is reduced in both progenial diencephalon and pituitary.
"]},{"key":"dc:title","label":"Title","values":["The Effects of Maternal Administration of Methadone on Beta-endorphin Content in the Brain and Pituitary of the Rat Progeny"]}]}],"canonical_facts":{"dc:contributor":["Marvin A. Peters","Cecilia Y. Cheung","David A. Hessinger"],"dc:creator":["Braun, Randall L."],"dc:description.abstract":["Methadone is often used in the maintenance and detoxification of opioid-dependent pregnant women. This use of methadone during pregnancy is known to be associated with teratogenic effects observed in the progeny. The present study is an attempt to gain insight into possible pathophysiologic mechanism(s) responsible for these teratogenic effects: specifically, a relationship between maternal methadone administration and the content of the endogenous opioid peptide, beta-endorphin, in the brain and pituitary of the rat progeny.
In brief, nulliparous mature female Sprague-Dawley rats received daily injections (5 mg./kg.) of methadone hydrochloride (methadone-treated) or a similar volume of physiological saline (controls), treatment started prior to conception and continued through weaning of the progeny. Following parturition, young rats aged 5, 15, 25 and 75 days were sacrificed by cervical dislocation, and their brain and pituitary removed and dissected. Beta-endorphin immunoreactivity was then determined in the midline telencephalon, diencephalon, medulla-midbrain, and whole pituitary by radioimmunossay. Protein content was also measured. In addition, a number of maternal and progenial morphological parameters were monitored throughout the study.
The results indicate that methadone exposure during gestation and lactation has no significant effect on beta-endorphin content in the whole pituitary or brain regions studied. The results indicate, however, that methadone exposure does significantly reduce protein content in the day 25 diencephalon, and in the day 5 and 15 whole pituitary. The results also tend to support previous studies which have shown methadone exposure to have significant effects on maternal and progenial weight gain, as well as, maternal mortality and perinatal viability.
In conclusion, it appears that maternal methadone exposure has little or no significant effect on beta-endorphin content in the brain or pituitary of the rat progeny; protein content, however, is reduced in both progenial diencephalon and pituitary.
"],"dc:identifier":["https://scholarsrepository.llu.edu/etd/1448"],"dc:language":["English"],"dc:rights":["This title appears here courtesy of the author, who has granted Loma Linda University a limited, non-exclusive right to make this publication available to the public. The author retains all other copyrights."],"dc:subject":["Animal Experimentation and Research","Laboratory and Basic Science Research","Pharmacology","Substance Abuse and Addiction","Methadone -- adverse effects; Rats"],"dc:title":["The Effects of Maternal Administration of Methadone on Beta-endorphin Content in the Brain and Pituitary of the Rat Progeny"],"thesis:degree_discipline":["Pharmacology"],"thesis:degree_level":["Thesis"],"thesis:degree_name":["Master of Science (MS)"]},"updated_at":"2026-07-24T02:53:44Z"}