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Effects of Prenatal Phenobarbital on Benzodiazepine Receptor Development
Author(s) -
Garrett Ken M.,
Tabakoff Boris
Publication year - 1986
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1986.tb00734.x
Subject(s) - forebrain , cerebellum , endocrinology , phenobarbital , medicine , flunitrazepam , receptor , benzodiazepine , offspring , fetus , gabaa receptor , chemistry , biology , pregnancy , central nervous system , genetics
Phenobarbital (PB) was administered to pregnant mice during days 9–21 of gestation. Forebrain and cerebellar [ 3 H]flunitrazepam ([ 3 H]FLU) binding was assayed in the offspring at birth and at 21 days of age. Prenatal treatment produced a decrease in the number ( B max ) of [ 3 H]FLU receptors in both the forebrain and cerebellum at birth. A small decrease in the [ 3 H]FLU dissociation constant ( K D ) values in the forebrain was also detected at birth, but no changes were seen in the [ 3 H]FLU K D values in the cerebellum. No changes were observed in forebrain and cerebellar [ 3 H]FLU B max or K D values at 21 days of age, indicating that the effects of prenatal exposure to PB on [ 3 H]FLU binding are eliminated during the postnatal development of the forebrain and cerebellum. The receptor affinity for the triazolopyridazine CL 218,872, which distinguishes the type I and type II benzodiazepine (BDZ) receptors, was not altered by prenatal PB treatment. The coupling of the BDZ receptor to the γ‐aminobutyric acid and pentobarbital binding sites was unaffected by exposure to PB in utero.