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At least 1,099 records · Page 61Linked to original sources
PubMed1978

Interaction of CDP-choline with synaptosomal transport of biogenic amines and their precursors in vitro and in vivo in the rat corpus striatum.

Added to a striatal synaptosomal homogenate of rat brain, CDP-choline 10(-4) M inhibits the uptake of norepinephrine (NE), dopamine (DA) and serotonin (5 HT) in a competitive fashion and enhances the uptake of tyrosine and tryptophan; administered to animals, CDP-choline (50 mg/kg/l h/i.v.) inhibits only the in vitro uptake of DA but enhances the uptake of precursors.

Animals↗
PubMed1977

Effects of 1-alkyl-1,2,3,4-tetrahydrocarbazole-1-ethanamines and related compounds, potential antidepressants, on biogenic amine uptake mechanisms.

A new series of compounds structurally related to the potential antidepressant tandamine, i.e., the 1-alkyl-1,2,3,4-tetrahydrocarbazole-1-ethanamines, inhibit the noradrenaline uptake mechanism and are relatively ineffective in inhibiting the serotonin uptake mechanism in vivo. The potency of the most effective compound (9-ethyl-N,N,1-trimethyl-1,2,3,4-tetrahydrocarbazole) is similar to that of desimipramine and is of potential use in the treatment of endogenously depressed patients.

5-Hydroxytryptophan↗
PubMed1990

Regional alterations of brain biogenic amines and GABA/glutamate levels in rats following chronic lead exposure during neonatal development.

Wistar rat pups were administered either a high dose of lead acetate (400 micrograms lead/g body weight/day) or a low dose (100 micrograms lead/g body weight/day) by gastric intubation, from 2 days through 60 days of age. The rats on both these doses exhibited statistically significant decreases in body and brain weights throughout the lead treatment period. A group of rats on high dose was also rehabilitated by discontinuing the lead from 60 days of age. In these rats, at 160 days of age, the body weight but not the brain weight recovered to normal levels. During the lead intake, the rats on high dose revealed significant elevations in the levels of noradrenaline (NA) in the hippocampus (HI), cerebellum (CE), hypothalamus (HY), brainstem (BS), and accumbens-striatum (SA). The elevated levels in all the above regions except in the HY persisted even after rehabilitation. The dopamine (DA) levels changed significantly in opposite directions in HY (elevation) and BS (reduction) during the lead treatment, and the HY recovered after rehabilitation. Under lead, the serotonin (5HT) levels were elevated significantly in the HI, BS and MC (motor cortex), while after rehabilitation the abnormality persisted only in the MC. Low dose lead treatment was also effective on the same areas of brain. In the low dose group, estimation of the levels of GABA and glutamate were also done, and a significant decrease of GABA in CE and glutamate in MC was observed. The differences observed in the neurotoxic effects (none or significant) of lead in the different regions for each of the transmitters (NA, DA, 5HT) supports the interesting conclusion that the vulnerability of the axon terminals of any given type is dependent on some regional factors, although the projections of the different regions originate from an apparently similar category of neurons in the brain stem.

Animals↗
PubMed1987

Reduced concentrations and increased metabolism of biogenic amines in a single case of Rett-syndrome: a postmortem brain study.

Preliminary data of a postmortem brain study in a single case with Rett-syndrome compared to a single control case show a severe reduction of dopamine (DA), noradrenaline (NA), and serotonin (5-HT) in most regions studied and in two regions of adrenaline (A). A marked increase in the 3,4-dihydroxyphenyl acetic acid (DOPAC)/DA, homovanillic acid (HVA)/DA, and the 5-hydroxyindole acetic acid (5-HIAA)/5-HT ratios indicates increased metabolism of DA and 5-HT. Also a marked reduction of 3H-spiroperidol-binding in putamen was found. This agrees with the assumption that a defect in maturation processes of central monoaminergic systems could be an underlying cause of Rett-syndrome.

Biogenic Amines↗
PubMed1996

A microdialysis study of the effects of the nicotinic agonist RJR-2403 on cortical release of acetylcholine and biogenic amines.

Transcortical dialysis was employed to investigate the effects of subcutaneous (s.c.) injections of RJR-2403 (1.2-7.2 mumol/kg) on extracellular levels of acetylcholine (ACh), norepinephrine (NE), dopamine (DA), and serotonin (5-HT) in rat. Systemic administration of RJR-2403 produced a 90% increase of cortical extracellular ACh levels that persisted for up to 90 minutes after injection. Norepinephrine and DA release were increased 124% and 131% above basal values, respectively. Serotonin (5-HT) levels in the dialysate were also significantly elevated by RJR-2403 (3.6 mumol/kg, s.c.) 70% above baseline at 90 minutes post-injection. Comparison of these responses to those of (-)nicotine from a previous study reveals little difference between the two compounds in their ability to influence cortical neurotransmitter release following systemic administration.

Acetylcholine↗
PubMed1983

Studies of the mechanisms of gastric bleeding under obstructive jaundice. Role of biogenic amines.

Mechanisms of gastric bleeding under obstructive jaundice were studied in adult male Wistar rats. Following ligation of the common bile duct, mucosal noradrenaline significantly decreased in both the pyloric and fundic gland areas of the gastric mucosa by 20 days after the operation. Serotonin increased only in the pyloric gland area, and histamine increased in the fundic gland area. Urinary excretion of free noradrenaline significantly increased after the ligation. Three weeks after the ligation, restraint and water immersion experiments were conducted. Under water immersion, gastric blood flow significantly reduced in rats with obstructive jaundice compared to controls. Acid output decreased in both groups. Gastric bleeding was noted in the fundic gland area significantly earlier in the ligated rats than in the non-ligated rats. Administration of noradrenaline s.c. 30 minutes before immersion significantly blocked the reduction in gastric blood flow and protected the gastric mucosa against acute bleeding under immersion. These results suggested that prolonged obstructive jaundice may deplete noradrenaline in the gastric mucosa, and that gastric mucosal ischemia caused by this sympathetic dysfunction plays an important role in the formation of acute gastric bleeding under obstructive jaundice.

Animals↗
PubMed1998

Influence of interleukin-1beta on exploratory behaviors, plasma ACTH, corticosterone, and central biogenic amines in mice.

Systemic administration of interleukin-1beta (IL-1beta) promoted behavioral changes in an open-field exploratory test. In particular, while the cytokine suppressed locomotor activities, these behaviors were not particularly sensitive to dosage differences. In contrast, dose-dependent biphasic variations that varied over time were evident with respect to the exploration of a novel container. Within this paradigm, the behavioral changes did not appear to be related to neophobia. In addition, despite the marked effects of IL-1beta on exploratory and locomotor behaviors, habituation/exploration in a free-running spontaneous alternation task was unaffected by the cytokine. In addition to the behavioral variations, IL-1beta dose-dependently increased plasma ACTH and corticosterone concentrations, and also induced several central monoamine alterations. In particular, IL-1beta increased the utilization of norepinephrine (NE) within the paraventricular nucleus, arcuate nucleus/median eminence, locus coeruleus, and prefrontal cortex, while the turnover of dopamine (DA) was evident in the arcuate nucleus/median eminence. It is suggested that although systemic IL-1beta treatment induces some stress-like effects, the profile of central neurochemical changes induced by the cytokine can be distinguished from psychological or processive types of stressors.

Adrenocorticotropic Hormone↗