Neurochemical changes

As a result of the neurochemical changes caused by MDMA, there is significant, observable functional impairment as well. These impairments occur in areas of the brain that have high concentrations of serotonergic neurons. Most notably affected are cognition and memory. Studies have shown decreases... 

Khan NA, Hasan M. 1988. Dose-related neurochemical changes in the levels of gangliosides and glycogen in various regions of the rat brain and spinal cord following methyl parathion administration. Exp Pathol 35 61-65. 

Procedures that have been suggested as models of depression and used to look for neurochemical changes that parallel the onset of the behavioural change, as well as to test how antidepressants affect the behaviour, are listed in Table 20.3. Those that have been used most, either as a drug screen or in research into the neurobiology of depression, are as follows. 

The first indication that some neurochemical changes developed only after prolonged treatment with antidepressants came from landmark experiments carried out by Vetulani... 

Obviously one limitation of all this work is that the drug effects have been tested in normal animals. So far, the neurochemical changes induced by long-term drug treatment have not been tested in combination with procedures such as learned helplessness, but it cannot be assumed that they will be the same as those in normal (non-depressed) subjects. 

Table 20.7 Neurochemical changes generally found after chronic administration of antidepressant drugs or repeated electroconvulsive shock...

Effects In Humans. Neither postmortem nor functional cerebrospinal fluid (CSF) studies in humans provide firm evidence for similar, long-term damages or alterations to monoaminergic neurons in chronic stimulant abusers. In part, the lack of demonstrable neurochemical changes may well be due to the obvious preclusion of well-controlled prospective experimentation in humans, as well as to variability in critical variables (e.g., individual sensitivity or pattern of abuse) encountered in clinical research. Possible relationship of the various complications of stimulant abuse including hyperpyrexia, seizure, anoxia, and metabolic exhaustion to neuronal chromatolysis, terminal destruction, and monoamine and enzymatic depletion have not been systematically explored in human autopsy eases. It should be also noted that, under nonperturbed conditions, overt behavioral deficits are rare in... 

Results from inhalation studies in animals suggest that hydrogen sulfide may be a developmental neurotoxicant. Neurochemical changes (in particular levels of the neurotransmitters gamma-aminobutyric acid, norepinephrine, and serotonin) and levels of the amino acids aspartate, glutamate, and taurine have been observed in various regions of the brain (Hannah et al. 1989, 1990 Skrajny et al. 

Haider SS, Hasan M. 1984. Neurochemical changes by inhalation of environmental pollutants sulfur dioxide and hydrogen sulfide Degradation of total lipids, elevation of lipid peroxidation and enzyme activity in discrete regions of the guinea pig brain and spinal cord. Ind Health 22 23-31. 

Chandra SV, Ali MM, Saxena DK, et al. 1981. Behavioral and neurochemical changes in rats simultaneously exposed to manganese and lead. Arch Toxicol 49 49-56. 

Peris J., Boyson S., Cass W. et al. Persistence of neurochemical changes in dopamine systems after repeated cocaine administration. J. Pharmacol. Exp. Ther. 253 35, 1990. 

Claye L., Akunne H., Davis M., DeMattos S., Soliman K. Behavioral and neurochemical changes in the dopaminergic system after repeated cocaine administration. Mol. Neurobiol. 11 55, 1995. 

Liu, J. and C.N. Pope. 1998. Comparative presynaptic neurochemical changes in rat striatum following exposure to chlorpyrifos or parathion. Jour. Toxicol. Environ. Health 53A 531-544. 

McGrath C, Norman TR. (1998). The effect of venlafaxine treatment on the behavioural and neurochemical changes in the olfactory bulbectomised rat. Psychopharmacology (Berlin). 136(4) 394-401. 

Thus there is evidence, albeit circumstantial, of a disturbance of glutamate systems in the disease. In addition there is evidence of GABAergic deficits. Adding to the relevance of these hypotheses of amino acid transmitter dysfunction is the opportunity to relate neurochemical changes directly to a neuronal pathology and, with some further extrapolation, to the aetiology of schizophrenia. 

Goodnick PJ, Gershon ES Lithium, in Handbook of Neurochemistry. Edited by Lajtha A. New York, Plenum, 1985, pp 103-149 Goodnick PJ, Meltzer HY Neurochemical changes during discontinuation of lithium prophylaxis, 1 increases in clonidine-induced hypotension. Biol Psychiatry 19 883-889, 1984... 

Sheehan M, de Belleroche J Facilitation of GABA release by cholecystokinin and caerulein in rat cerebral cortex. Neuropeptides 3 429-434, 1983 Sherman AD, Petty F Additivity of neurochemical changes in learned helplessness and imipramine. Behav Neural Biol 35 344-353, 1982 Sherman WR Lithium and the phosphoinositide signaling system, in Lithium and the Cell. Edited by Birch NJ. London, Academic Press, 1991, pp 121-157 Sherman WR, Munsell LY, Gish BG, et al Effects of systemically administered lithium on phosphoinositide metabolism in rat brain, kidney, and testis. J Neurochem 44 798-807, 1985... 

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