Perinatal substance abuse.

This article reviews medical, obstetrical, and neonatal complications of perinatal substance abuse. The psychological and social issues commonly encountered in drug-abusing pregnant women are also discussed. Treatment considerations that take into account the complex biopsychosocial parameters are presented.

The effects of ethanol on the efflux and release of norepinephrine and 5-hydroxytryptamine from slices of rat hypothalamus.

Studies were done to determine the effects of ethanol on release of norepinephrine, dopamine and 5-hydroxytryptamine from nerve terminals in the central nervous system. Superfused slices of rat hypothalamus were used in these studies and endogenous amines in the superfusate were quantitated using HPLC with electrochemical detection. In these experiments 'release' of transmitters was studied in the presence of amitriptyline to block neuronal uptake of amines, whereas 'efflux' was measured in its absence. A highly intoxicating concentration of ethanol (69.6 mM, 320 mg%) increased the K+-evoked release of norepinephrine, dopamine and serotonin without affecting basal release. Since this concentration of ethanol increased the basal efflux but not the basal release of 5-hydroxytryptamine, it appeared that neuronal uptake of 5-hydroxytryptamine under basal conditions may also be inhibited by intoxicating levels of ethanol.

Effects of estradiol on the basal and evoked efflux of norepinephrine and 5-hydroxytryptamine from slices of rat hypothalamus.

17-beta-Estradiol, at a concentration (100 ng/ml) approaching plasma levels found in pregnant women, inhibited the K+-evoked efflux of endogenous norepinephrine from superfused slices of rat hypothalamus. The same concentration of estradiol increased slightly the basal efflux of serotonin. Since estradiol crosses the blood-brain barrier with ease it is suggested that the inhibition of norepinephrine release from central neurons may contribute to the depression and emotional lability sometimes associated with estradiol therapy.

Contractions of canine intrapulmonary airways and their dependence on choline uptake.

The importance of high-affinity choline uptake in sustaining the synthesis of acetylcholine in isolated canine intrapulmonary airways was examined by using tissue bath techniques. Prolonged electrical stimulation of control airways caused contractions that decayed during the first few minutes of stimulation but eventually reached plateaus. In contrast, contractions decayed rapidly in airways exposed to 10(-4) M hemicholinium-3. Exogenously administered choline (10(-4) M), neostigmine (2 X 10(-6) M) and physostigmine (2 X 10(-6) M) all caused contractions of resting airways, which we conclude were mediated by the spontaneous release of acetylcholine because these responses were abolished by atropine and hemicholinium-3. Thus, the store of acetylcholine involved in spontaneous release could be abolished rapidly by hemicholinium-3, but sufficient acetylcholine remained for normal responses to brief periods of nerve stimulation. This differential depletion indicates that the acetylcholine involved in spontaneous release may originate from a different intraneuronal site than the vesicular acetylcholine involved in the exocytotic process that occurs during nerve stimulation.