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Biomedical subjects

D A Peters

Publications and source records attributed to D A Peters.

At least 55 records · Page 3Linked to original sources
PubMed1984

Prenatal nicotine exposure increases adrenergic receptor binding in the rat cerebral cortex.

Adult female rats were given nicotine in drinking water for a minimum of 6 weeks prior to mating. The nicotine intake was then maintained at a level of 6.0 +/- 0.2 mg/kg/day throughout pregnancy. At birth the offspring were fostered to control females. Brain noradrenaline levels were elevated in cortex and hypothalamus in infancy but were within the control ranges in adult offspring. However, adrenergic receptor binding was significantly increased in cerebral cortex of adult offspring consistent with the view that prenatal nicotine exposure produces permanent changes in the functioning of central noradrenergic neurons. As in previous studies, the changes were found only in male offspring.

Animals↗
PubMed1982

Prenatal stress: effects on brain biogenic amine and plasma corticosterone levels.

Pregnant rats were subjected to once daily stress treatments consisting of handling and a saline injection. The offspring showed region-specific changes in brain 5-hydroxytryptamine (5-HT), 5-hydroxyindoleacetic acid (5-HIAA) and norepinephrine (NE) levels in infancy but only the hypothalamus still showed significant changes at 60 days of age. In a reaction-to-stress test 23-day-old offspring in the prenatal stress group showed a greater elevation in plasma corticosterone level but smaller changes in hypothalamic NE and 5-HIAA levels than control offspring suggesting that prenatal stress may have altered the functioning of the hypothalamic-pituitary-adrenal axis. It is suggested that changes in the development of specific monoamine-containing neurons may be associated with the reported behavioral deficits in offspring of female rats stressed during pregnancy.

Animals↗
PubMed1982

Sex-dependent biological changes following prenatal nicotine exposure in the rat.

Nicotine was administered to adult female rats in drinking water starting 6 weeks before mating and continuing throughout pregnancy. The litters were cross-fostered to control dams at birth. Prenatal nicotine treatment reduced both the number of male rats born and the male birth weight. Female offspring were not significantly affected. Rearing activity was reduced in male but not female offspring either when tested over a 24 hour period in a home cage environment or during a 10 minute exposure in an open field. Horizontal locomotor activity was reduced only during the first 5 minutes in the open field and again the effect was found only in the males. Baseline plasma corticosterone levels were reduced in both male and female offspring but there was no effect on stress-elevated corticosterone levels.

Animals↗
PubMed1981

Plasma free and total tryptophan, blood serotonin, and the hyperactivity syndrome: no evidence for the serotonin deficiency hypothesis.

Total and free plasma tryptophan and plasma cortisol levels were determined for children diagnosed as hyperactive or learning disabled and in normal siblings of these subjects. No differences were observed among the groups on any of the dependent variables related to a number of parameters measured for the hyperactive children such as degree of hyperactivity, presence of food allergies, favorable response to methylphenidate, and brain dysfunction. Moreover, in further comparisons no differences were found between hyperactive and age-matched controls on these variables as well as blood serotonin, nor were any differences found for a group of hyperactive children between placebo and methylphenidate trials. These data do not support earlier suggestions of a serotonin deficiency in hyperactive children.

Attention Deficit Disorder with Hyperactivity↗
PubMed1979

Postnatal effects of maternal nicotine exposure.

Rats were given dilute nicotine solutions as their only source of drinking water while control rats received distilled water. Two months after the start of treatment the rats were mated. At birth litters born to nicotine treated rats were either left with the dams until weaning (nicotine group) or cross-fostered to control dams (cross-fostered nicotine group). Both parents and offspring were tested when the pups were 60 to 80 days of age. The drug-treated adult rats showed a marked reduction in body weight gain during the period of drug treatment. The dams were more active during the day and exhibited a reduced plasma corticosterone response to stress. Male but not female offspring of nicotine treated rats were significantly lighter at birth than control males. Offspring in the nicotine group showed an increased spontaneous motor activity in the light which was not prevented by cross-fostering to control dams at birth. The results support the hypothesis that pre-natal exposure to nicotine causes significant changes in behavior in later life.

Adrenal Glands↗
PubMed1978

Tyrosine hydroxylase activity in brain regions after intraventricular 6-hydroxydopamine in the neonatal rat.

Intraventricular 6-OHDA treatment to newborn rats produced a marked reduction in tyrosine hydroxylase activity in most brain regions at maturity which correlated moderately well with the catecholamine levels. However, those regions in which NE levels were increased did not show a corresponding increase in total tyrosine hydroxylase activity. There was a much better correlation between NE levels and the particulate form of tyrosine hydroxylase which has been suggested to be the more functionally active form of the enzyme.

Animals↗
PubMed1976

Effects of chronic exposure to cadmium, lead and mercury of brain biogenic amines in the rat.

Effects of chronic (45 days) treatment with different doses of cadmium chloride (0.25 and 1.0 mg/kg/day), methylmercury chloride (0.4 and 4.0 mg/kg/day) and lead acetate (0.2 and 1.0 mg/kg/day) and of 28-day withdrawal of treatment on the levels of acetylcholine (ACh) and activity of acetylcholinesterase (AChE) in cerebral cortex, and concentration of norepinephrine (NE) and 5-hydroxytryptamine (5-HT) in brain-stem were examined in rats. Exposure to both cadmium and methylmercury produced significant decreases in cortical ACh and brain-stem 5-HT levels. In addition, brain-stem NE concentration was increased in methylmercury-treated rats. In contrast, chronic treatment with lead resulted in enhanced cerebrocortical ACh levels but a decreased brain-stem NE concentration. Treatment with cadmium also produced a transient enhancement of striatal dopamine levels. Cadmium-induced decrease in brain-stem 5-HT and lead-induced accumulation of cortical ACh persisted even after 28 day withdrawal of treatment. The data indicate that chronic exposure to low doses of heavy metals produces differential changes in regional levels of various brain biogenic amines. These changes may represent the early signs of adverse effects on CNS function since they occur before any overt symptoms of neurotoxic effects of heavy metals become apparent.

Acetylcholine↗
PubMed1975

Tyrosine hydroxylase activity in rat brain regions after chronic treatment with +/--propranolol.

Rats were injected twice daily with +/--propranolol (6 mg kg-1 day-1) for 14 days and killed 16 h after the final injection. Tyrosine hydroxylase activity was measured in both soluble and particle-bound forms in various brain regions. The activity of the soluble enzyme was not significantly altered by propranolol treatment in any of the brain regions studied. The tyrosine hydroxylase activity in the particulate fraction was significantly increased in corpus striatum and unchanged in other brain regions. The propranolol concentrations in the various brain regions in this chronic study were far lower than necessary to produce a significant change in tyrosine hydroxylase activity in acute experiments. It was concluded that chronic propranolol treatment produces a persistent increase in bound tyrosine hydroxylase activity in rat corpus striatum.

Animals↗