Brain catecholamines

Besides behavior and blood pressure, catecholamine neurons also have important roles in other brain functions. Regulation of neuroendocrine function is a well-known action of catecholamines for example, DA agonists reduce semm prolactin concentration, especially in conditions of hypersecretion. Ingestive behavior can be modulated by brain catecholamines, and some appetite-suppressing dmgs are beheved to act via catecholaminergic influences. Catecholamines also participate in regulation of body temperature. 

Seiden, L.S. Fischman, M.W. and Schuster, C.R. Long-term methamphetamine induced changes in brain catecholamine in tolerant rhesus monkeys. Drug Alcohol Depend 1 215-219, 1975-76. 

Hornykiewicz, 0. Brain catecholamines in schizophrenia--a good case for noradrenaline. Nature 299 484-486, 1982. 

Inhibition of monoamine oxidase has been proposed as a possible mechanism underlying the hydrogen sulfide-mediated disruption of neurotransmission in brain stem nuclei controlling respiration (Warenycia et al. 1989a). Administration of sodium hydrosulfide, an alkali salt of hydrogen sulfide, has been shown to increase brain catecholamine and serotonin levels in rats. It has also been suggested that persulfide formation resulting from sulfide interaction with tissue cystine and cystinyl peptides may underlie some... 

Warenycia MW, Smith KA, Blashko CS, et al. 1989c. Monoamine oxidase inhibition as a sequel of hydrogen sulfide intoxication Increases in brain catecholamine and 5-hydroxytryptamine levels. Arch Toxicol 63 131-136. 

Prioux-Guyonneau M, Mocaer-Cretet E, Cohen Y, Jacquot C. (1984). Evidence for an activating effect of tabernanthine on rat brain catecholamine synthesis and elimination. Experientia. 40(12) 1388-89. Prohovnik I, Arnold SE, Smith G, Lucas LR. (1997). Physostigmine reversal of scopolamine-induced hypofrontality. Cereb Blood Flow Metab. 17(2) 220-28. 

The most commonly encountered side effects of a-methyldopa are sedation and drowsiness. These CNS effects are probably the result of reductions in brain catecholamine levels. Other side effects, also typical of sympathetic depression, are dry mouth, nasal congestion, orthostatic hypertension, and impotence. 

A.G. Nasello and O.A. Ramirez, Brain catecholamines metabolism in offspring of amphetamine treated rats, Pharmacol. Biochem. Behav., 9(1) (1978) 17-20. 

M. Goiter and I.A. Michaelson, Growth, behavior, and brain catecholamines in lead-exposed neonatal rats A reappraisal, Science, 187 (1975) 359-361. 

Adolfsson R, Gottfries CG, Roos BE, Winblad B (1979) Changes in the brain catecholamines in patients with dementia of Alzheimer type. Br. J. Psychiatry 135 216-223. 

Walters, D. E., and Carr, L. A. (1986). Changes in brain catecholamine mechanisms following perinatal exposure to marihuana. Pharmacol. Biochem. Behav. 25, 763-768. 

Hallman H, Olson L, Jonsson G (1984) Neurotoxicity of the meperidine analogue N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine on brain catecholamine neurons in the mouse. Eur J Pharmacol 97 133-136. 

Wagner GC, Seiden LS, Schuster CR (1979) Methamphetamine-induced changes in brain catecholamines in rats and guinea pigs. Drug Alcohol Depend Y 435—438. 

In its acute stages, benzene toxicity appears to be due primarily to the direct effects of benzene on the central nervous system, whereas the peripheral nervous system appears to be the target following chronic low-level exposures. In addition, because benzene may induce an increase in brain catecholamines, it may also have a secondary effect on the immune system via the hypothalamus-pituitary-adrenal axis (Hsieh et al. 1988b). Increased metabolism of catecholamines can result in increased adrenal corticosteroid levels, which are immunosuppressive (Hsieh et al. 1988b). 

Wliile the cyclics block the uptake of amines, MAOls prc cnt the breakdown of the neurotransmitters (Cohen, 1997 Cooperrider, 1988 Meyer Quenzer, 2005). The enzyme monoamine oxidase metabolizes a variety of neurotransmitters, including norepinephrine and serotonin. MAOls inhibit this degradation process and thus enhance the availability of the transmitter within the neuron. Thii.s, the actions of the cyclics and MAOls each arc consistent u ith the hypothesis that decreased brain catecholamine activity causes depression and that these antidepressants (using different mechanisms) reverse this process by increasing catecholamine activity in the brain. 

Greenshow AJ (1989) Functional interactions of 2-phenylethylamine and of tryptamine with brain catecholamines implications for psychotherapeutic drug action. Prog Neuro-Psychopharmacol Biol Psychiatry 13 431-443... 

Dasgupta PS, Lahiri T. 1992. Alteration of brain catecholamines during growth of benzo[a]pyrene induced murine fibrosarcoma. Neoplasma 39(3) 163-165. 

Magos L, Green A, Jarvis JA. 1974. Half life of CS2 in rats in relation to its effect on brain catecholamines. Internationales Archiv fuer Arbeitsmedizin 32 289-296. 

Because the best reliability is assured by in vivo monitoring, differential pulse voltammetry (DPV) has been applied for in vivo assay of brain catecholamines.168 The method was not very selective since ascorbic acid was the main interfering species. Furthermore, the implantation of an electrode... 

In a search for a possible biochemical means of investigating the mode of action of LSD it was noted that the administration of this drug to animals resulted in an elevation of brain 5-HT levels and a depression of brain catecholamine levels (Barchas and Freedman, 1963 Koenig-Bersin et al., 1970). It therefore seemed of interest to study the effects of LSD on an enzyme which could utilize both NA and 5-HT as substrates since it was considered that such an enzyme could be used as a model for those central receptors with which LSD must interact in order to produce its characteristic central effects. The enzyme which was eventually selected for study in this way was the copper-containing oxidase caeruloplasmin which utilizes both NA and... 

Coudray-Lucas, C., Prioux-Guyonneau, M., Sentenac, H., Cohen, Y., and Wepierre, J., Brain catecholamine metabolism changes and hypothermia in intoxication by anticholinesterase agents, Acta Pharmacol Toxicol, 52, 224, 1983. 

Reserpine exerts its antihypertensive action by virtue of its adrenergic neutronal blockade consequent to depletion of the catecholamines-containing granudles of the postganglionic sympathetic neuron. It, however, depletes both brain catecholamines and seritonins. 

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