Monoamines in brain

Ho AKS, Loh HH, Craves F, et al The effect of prolonged lithium treatment on the synthesis rate and turnover of monoamines in brain regions of rats. Fur J Pharmacol 10 72-78, 1970... 

The H3 receptor was initially detected as an autoreceptor controlling histamine synthesis and release in brain [22]. Thereafter it was shown to inhibit presynaptically the release of other monoamines in brain and peripheral tissues as well as of neuropeptides from unmyelinated C-fibers [23],... 

Wiser, P.G. and P. Bersin 1970, Turnover of monoamines in brain under the influence of muscimol and ibotenic acid, two psychoactiveprindpies cAAmanita muscaria In Efron, D.H. (Ed.) Psychotomimetic [sic] Dn. Raven, nv, pp. 155—162. 

Isoproterenol is given sublingually or by iv. It is metabolized by monoamine oxidase and catechol-0-methyltransferase in brain, Hver, and other adrenergically innervated organs. The pharmacological effects of isoproterenol are transient because of rapid inactivation and elimination. About 60% is excreted unchanged. Adverse effects using isoproterenol therapy include nervousness, hypotension, weakness, dizziness, headache, and tachycardia (86). 

It is generally felt that a substance is more likely to be a NT if it is unevenly distributed in the CNS although if it is widely used it will be widely distributed. Certainly the high concentration (5-10 pmol/g) of dopamine, compared with that of any other monoamine in the striatum or with dopamine in other brain areas, was indicative of its subsequently established role as a NT in that part of the CNS. This does not mean it cannot have an important function in other areas such as the mesolimbic system and parts of the cerebral cortex where it is present in much lower concentrations. In fact the concentration of the monoamines outside the striatum is very much lower than that of the amino acids but since the amino acids may have important biochemical functions that necessitate their widespread distribution, the NT component of any given level of amino acid is difficult to establish. 

This can be carried out in vitro (in brain slices, cultured cell preparations) or in vivo and involves penetrating the experimental tissue with a carbon-fibre electrode of 5-30 pm in diameter (Fig. 4.9). This serves as an oxidising electrode and the Faradaic current generated by the oxidation of solutes on the surface of the electrode is proportional to their concentration. Obviously, only neurotransmitters which can be oxidised can be measured in this way so the technique is mainly limited to the study of monoamines and their metabolites. The amplitude of each peak on the ensuing voltammogram is a measure of solute concentration and individual peaks can be identified because different... 

Monoamine concentrations or receptor binding in brain tissue post-mortem. 

The actions of amphetamine are widespread throughout the brain. Amphetamine s immediate effect is to alter the release of monoamines in a dose-dependent manner that is specific for each monoamine transmitter neuronal system. The net effect of amphetamine on monoamine release is complex, with some mechanisms tending to increase monoamine release (e.g., blockade of reuptake and nonimpulsedependent release), and several mechanisms tending to diminish release (e.g., activation of somatodendritic and terminal autoreceptors). 

Typically, neurotoxic effects of drugs on monoamine neurons have been assessed from reductions in brain levels of monoamines and their metabolites, decreases in the maximal activity of synthetic enzymes activity, and decreases in the active uptake carrier. In the present study, the traditional markers described above have been used, including the measurement of the content of monoamines and their metabolites in brain at several different timepoints following drug administration. Since reports in the literature have documented that MDMA and MDA can inhibit the activity of tryptophan hydroxylase (TPH), the rate-limiting enzyme in serotonin synthesis (Stone et al. 1986 Stone et al. 1987). it is unclear whether MDMA-induced reductions in the content of serotonin and its metabolite 5-hydroxyin-doleacetic acid (5-HlAA) may be due to suppressed neurotransmission in otherwise structurally intact serotonin neurons or may represent the eonsequenee of the destruction of serotonin neurons and terminals. 

Bogdanski, D.F. Weissbach, H. and Udenfriend, S. The distribution of serotonin, 5-hydroxytryptophan decarboxylase, and monoamine oxidase in brain. J Neurochem 1 272-278, 1957. 

Dahlstrom, A., and Fuxe, K. Evidence for the existence of monoamine containing neurons in the central nervous system. 1. Demonstration of monoamines in cell bodies of brain neurons. Acta Physiol Scand (Suppl 232) 62 1-55, 1964. 

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. 

Dahlstrom, A. Fuxe, K. (1964). Localization of monoamines in the lower brain stem. Experientia 20, 398-9. 

Buckholtz, N., Boggan, W. Monoamine oxidase inhibition in brain and liver produced by b-carbohnes structure activity relationships and substrate specihcity. Biochem. Pharmacol. 26 1991, 1977. 

FIGURE 14-3 Synthesis and metabolism of histamine. Solid lines indicate the pathways for histamine formation and catabolism in brain. Dashed lines show additional pathways that can occur outside the nervous system. HDC, histidine decarboxylase HMT, histamine methyltransferase DAO, diamine oxidase MAO, monoamine oxidase. Aldehyde intermediates, shown in brackets, have been hypothesized but not isolated. 

Mercuric chloride gives a decrease in monoamine [85, 92] and choline [92] uptake in brain synaptosomes which may be related to an inhibition of Na+/K +-ATPase [85, 92-94]. 

Honma T, Sudo A, Miyagawa M, et al. 1982. Significant changes in monoamines in rat brain induced by exposure to methyl bromide. Neurobehav Toxicol Teratol 4 521-524. 

Also, harmala alkaloids create effects on monoamine turnover. Postnatal rats administered harmaline (shortly before birth) have elevations in brain levels of the norepinephrine metabolite 3-methoxy-4-hydroxy-phenylglycol (MHPG), but decreases in the dopamine and serotonin metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and 5-hydroxyindole acetic acid (5-HIAA) (Okonmah et al. 

Tani Y, Saito K, Tsuneyoshi A, Imoto M, Ohno T. (1997). Nicotinic acetylcholine receptor (nACh-R) agonist-induced changes in brain monoamine turnover in mice. Psychopharmacology (Berlin). 129(3) 225-32. 

Wang A, Cao Y, Wang Y, Zhao R, Liu C. (1995). [Effects of Chinese ginseng root and stem-leaf saponins on learning, memory, and biogenic monoamines of brain in rats]. Chung Kuo Chung Yao Tsa Chih. 20(8) 493-95. 

Fucile S (2004) Ca + permeability of nicotinic acetylcholine receptors. Cell Calcium 35 1-8 Gaddnas H, Pietila K, Ahtee L (2000) Effects of chronic oral nicotine treatment and its withdrawal on locomotor activity and brain monoamines in mice. Behav Brain Res 113 65-72 Geisler S, Derst C, Veh RW, Zahm DS (2007) Glutamatergic afferents of the ventral tegmental area in the rat. J Neurosci 27 5730-5743... 

J.P. Johnston, Some observations upon a new inhibitor of monoamine oxidase in brain tissue, Biochem. Pharmacol. 17 (1968) 1285-1297. 

M.G. Palfreyman, I.A. McDonald, J.R. Fozard, Y. Mely, A.J. Sleight, M. Zreika, J. Wagner, P. Bey, P.J. Lewis, Inhibition of monoamine oxidase selectively in brain monoamine nerves using the bioprecursor (MDL 72394), a substrate for aromatic L-amino acid decarboxylase, J. Neurochem. 45 (1985) 1850-1860. 

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