title: Effect of prenatal opioid exposure on cholinergic development.
abstract: Opioid drugs such as methadone or buprenorphine are often used in the management of pregnant addicts. These drugs are generally thought of as nonteratogenic and preferable to repeated cycles of withdrawal in utero. However, evidence exists that perinatal exposure to these opioids delays and disrupts cholinergic development, particularly in the striatum. Acetylcholine (ACh) content and the expression of choline acetyltransferase protein and mRNA are reduced in the early postnatal period by prenatal opioid exposure in the rat. Although these indicators of the cholinergic phenotype return to normal levels over time, the activity of the cholinergic neurons remains disrupted, with a large increase in ACh turnover rate. The mechanism of these effects is unknown, but may involve changes in the expression of nerve growth factor, which is reduced by opioid exposure.
authors.affiliation: Department of Pharmacology and Toxicology, Medical College of Virginia, Campus of Virginia Commonwealth University, Richmond, VA 23298-0613, USA. serobins@hsc.vcu.edu
authors.forename: S E
authors.initials: SE
authors.lastname: Robinson
mesh_terms: D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D002795:Choline O-Acetyltransferase / Q000187:drug effects* / Q000378:metabolism*; D005314:Embryonic and Fetal Development / Q000187:drug effects*; D005260:Female; D006801:Humans; D009294:Narcotics / Q000009:adverse effects*; D010275:Parasympathetic Nervous System / Q000196:embryology / Q000254:growth & development*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats
chemical_list: D009294:Narcotics; D002795:Choline O-Acetyltransferase; D000109:Acetylcholine