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Biomedical subjects

M J Druse

Publications and source records attributed to M J Druse.

54 records · Page 3Linked to original sources
PubMed1981

Effects of maternal ethanol consumption of neurotransmitters and lipids in offspring.

The effects of maternal alcohol consumption on the levels and metabolism of neurotransmitters in offspring are reviewed. In addition, studies of CNS myelination and hepatic lipids are discussed. In utero exposure to ethanol is reported to alter the steady-state levels, metabolism or release of catecholamines, octopamine, serotonin, glutamate, GABA, acetylcholine and histamine. However, with the exception of a deficit of hypothalamic norepinephrine and a deficit of whole brain serotonin, most of the neurotransmitter alterations appear to be either transient or were detected when ethanol was present in the fetus or neonatal animals. There are conflicting reports on the effect of pre- and early postnatal exposure to ethanol on CNS myelination in the rat. However, it appears that if ethanol and control rats were of comparable body weights, there were only minor differences in myelination. Nonetheless, if the rat mothers consumed ethanol for 1 1/2--2 months prior to conception and during gestation, the offspring had increased myelin early in development. An examination of hepatic lipids in the fetal and neonatal rats that were exposed to ethanol in utero and at the time of sacrifice demonstrated an increased concentration of hepatic lipids and decreased fatty acid oxidation. The discussion of the neurotransmitter, myelin and hepatic lipid studies include an assessment of the nutritional status of the animals and the permanence of any observed abnormalities.

Alcohol Drinking↗
PubMed1978

Central nervous system myelination in rats exposed to ethanol in utero.

Pregnant rats were pair-fed using isocaloric control or 6.6% (v/v) ethanol liquid diets. At 18, 25, and 53 days, the in vivo incorporation of [3H] leucine and [14C] glucose into proteins and lipids of three central nervous system (CNS) myelin subfractions was examined in the offspring (control and ethanol pups) of control and ethanol-treated females. With few exceptions, the pattern of CNS myelination appeared near-normal in the ethanol pups. The ethanol pups had brain weights and total myelin protein content within the normal range. In addition, the amount of protein in light, medium, and heavy myelin was normal at 18 and 25 days. However, the ethanol pups had an excess of the chemically and morphologically immature heavy fraction at 53 days. The incorporation of [3H] leucine and [14C] glucose into myelin subfractions and separated proteins and lipids was similar in control and ethanol pups. The findings of near-normal CNS myelination in the offspring of female rats fed an ethanol liquid diet during gestation differ from our previous findings of a premature onset and slowdown of active CNS myelination in the offspring of female rats that consumed an ethanol liquid diet for one month prior to conception as well as during gestation.

Age Factors↗
PubMedDate not supplied

The influence of cholesterol on synaptic fluidity, dopamine D1 binding and dopamine-stimulated adenylate cyclase.

The present study examined the influence of the synaptic cholesterol/phospholipid ratio on fluorescence polarization, the binding of SCH23390 to dopaminergic D1 binding sites and dopamine-stimulated adenylate cyclase activity. The cholesterol/phospholipid ratio of synaptic membranes from bovine caudate was modified by incubating the membranes with a lipid transfer protein and liposomes which were either loaded with or lacking cholesterol. The results of this study demonstrated that the number of binding sites (Bmax) for SCH23390 was insensitive to alterations in the synaptic cholesterol/phospholipid ratio and membrane order. However, when the cholesterol/phospholipid ratio was decreased by 30%, membrane order and binding affinity (Kd) were decreased. Despite the lack of change in the number of D1 binding sites, the activity of dopamine-stimulated adenylate cyclase was markedly inhibited by an elevated cholesterol/phospholipid ratio. The results of these studies are discussed in terms of their potential relevance to aging.

Adenylyl Cyclases↗
PubMedDate not supplied

Maternal ethanol consumption: effect on (Na+-K+)-ATPase in rat offspring.

The activity of Mg2+-activated, ouabain-sensitive adenosine triphosphatase, (Na+-K+)-ATPase, was determined in homogenates of hypothalamus, cortex, cerebellum, and brain stem from the 19-day-old offspring of rats that were pair-fed control or (6.6%, v/v) ethanol liquid diets on a chronic basis prior to parturition. In the offspring of both control and ethanol-fed rats the specific activity of (Na+-K+)-ATPase was significantly (p less than 0.01) greater in the cortex than it was in the hypothalamus, brain stem or cerebellum (hypothalamus approximately brain stem approximately cerebellum). When the offspring of ethanol-fed and control rats were compared we observed no significant (p greater than 0.05) differences in the activity of (Na+-K+)-ATPase in any of the four brain regions examined. In addition, the results of kinetic analyses of cortical (Na+-K+)-ATPase were similar in the 19-day-old offspring of ethanol-fed rats and those whose mothers consumed either the control liquid diet or standard laboratory chow. The results of these studies suggest that the activity of the plasma membrane enzyme, (Na+-K+)-ATPase, was not affected in the 19-day-old offspring of ethanol-fed rats.

Adenosine Triphosphate↗
PubMedDate not supplied

Effects of in utero ethanol exposure on serotonin uptake in cortical regions.

Previously, this laboratory found that the 19- and 35- to 37-day-old offspring of rats that consumed ethanol on a chronic basis prior to parturition had a decreased cortical content of serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) as well as a decreased number of cortical 5-HT1 binding sites. These results emphasized the sensitivity of the developing cortical serotonergic nerves to the effects of in utero ethanol exposure. In the present study, we examined the effects of in utero ethanol exposure on an additional component of the developing cortical serotonergic systems. Specifically, we examined the uptake of [3H]-5-HT by synaptosomes which were isolated from the motor or somatosensory regions of the cerebral cortex. The results demonstrated that the Vmax for serotonin uptake was significantly decreased (p less than 0.025) by approximately 15-20% in the motor cortices of the 19- and 35-day-old offspring of rats that consumed ethanol on a chronic basis prior to parturition. In addition, there was a significantly (p less than 0.025) approximately 30% decrease in the Km for serotonin uptake in the motor cortex of 35-day-old offspring of ethanol-fed rats. In contrast, neither the (Km) nor the Vmax for serotonin uptake were significantly altered (p greater than 0.05) in the somatosensory cortices in 19- or 35-day-old offspring of ethanol-fed rats. These results emphasize the selective sensitivity of developing cortical projections of the serotonergic system.

Aging↗
PubMedDate not supplied

Effects of in utero ethanol exposure on cortical 5-HT2 binding sites.

Previous studies by this laboratory found that in utero ethanol exposure results in a decrease of several presynaptic components of serotonin (5-HT) containing neurons in the cerebral cortex and cortical regions. The present study examined whether in utero ethanol exposure similarly affects the development of the cortical targets of serotonergic projections. Specifically, we examined the influence of in utero ethanol exposure on 5-HT2 binding sites in the motor and somatosensory cortices of the offspring of rats that consumed a control or 6.6% (v/v) ethanol liquid diet on a chronic basis prior to parturition. These studies demonstrated that neither the Kd nor Bmax for the binding of [3H]-ketanserin to membranes from the motor and somatosensory cortices of 19- and 35-day-old rats were significantly altered by in utero ethanol exposure. These results suggest that the development of the postsynaptic target areas of cortical serotonergic projections are more resistant to the effects of in utero ethanol exposure than the presynaptic components of these projections.

Aging↗
PubMedDate not supplied

Chronic maternal ethanol consumption results in decreased serotonergic 5-HT1 sites in cerebral cortical regions from offspring.

This laboratory previously demonstrated that chronic maternal ethanol consumption results in a marked deficiency of cortical serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) and of 5-HT uptake sites in the 19- and 35-day-old offspring. In order to determine whether in utero exposure to ethanol similarly affects other components of the serotonergic system we examined the influence of chronic maternal ethanol consumption on cortical, serotonergic 5-HT1 binding sites in developing offspring. Female Sprague-Dawley rats were pair-fed, using control or 6.6% (v/v) ethanol liquid diets on a chronic basis prior to parturition. Serotonergic 5-HT1 sites were measured in synaptosomal membranes from whole cortex and cortical regions from developing offspring. Serotonergic 5-HT1 sites were assessed by measuring the binding of [3H]-5-HT to synaptosomal membranes in the presence and absence of nonradioactive 5-HT. Serotonergic 5-HT2 sites were blocked by including 100 nM spiperone in the assay buffer. The results demonstrated that the 19- and 37-day-old offspring of ethanol-fed rats had a significant (approximately 10-40%) reduction in the Bmax for serotonergic 5-HT1 binding sites on synaptosomal membranes from whole cortex (p less than 0.025), motor cortex (p less than 0.01), and somatosensory cortex (p less than 0.025). However, the binding affinity (Kd) for serotonin was not significantly altered (p greater than 0.05). These results emphasize the sensitivity of the developing cortical serotonergic system to prenatal ethanol exposure.

Aging↗