Maternal methadone administration: deficit in development of alpha-noradrenergic responses in developing rat brain as assessed by norepinephrine stimulation of 33Pi incorporation into phospholipids in vivo.

Journal Article (Journal Article)

The effects of perinatal methadone exposure on the development of noradrenergic responses in the brain were examined by assessing the ability of intracisternally administered norepinephrine to stimulate 33Pi incorporation into phospholipids in vivo; the effect of norepinephrine is mediated by alpha1-receptors juxtaposed to noradrenergic nerve terminals. Although there was no difference in basal (unstimulated) incorporation of 33Pi, a deficit in norepinephrine-induced stimulation of incorporation was found throughout the preweaning period in offspring of dams treated daily with methadone beginning in midgestation. This effect was not seen when methadone was given during the postnatal period. Since perinatal methadone exposure also delays development of presynaptic catecholaminergic nerve terminals in the brain, these results support the view that perinatal exposure to methadone depresses overall central noradrenergic synaptic function; however, the effects on presynaptic development and on receptor-mediated responses appear to be separable in that they display differences in the critical age periods of sensitivity to perturbation by the drug.

Full Text

Duke Authors

Cited Authors

  • Slotkin, TA; Weigel, SJ; Whitmore, WL; Seidler, FJ

Published Date

  • May 15, 1982

Published In

Volume / Issue

  • 31 / 10

Start / End Page

  • 1899 - 1902

PubMed ID

  • 6285928

Pubmed Central ID

  • 6285928

International Standard Serial Number (ISSN)

  • 0006-2952

Digital Object Identifier (DOI)

  • 10.1016/0006-2952(82)90494-4


  • eng

Conference Location

  • England