Brain neurotransmitter

Other studies indicate that sucrose does not cause hyperactivity. Carbohydrate ingestion increases levels of serotonin (5-hydroxytryptamine), a brain neurotransmitter that promotes relaxation and sleep. Dietary sucrose should theoretically have a calming effect and reduce activity, manifestations which have been observed in case studies (63). To date, clinical investigations have failed to show a significant connection between sucrose consumption and aggressive or dismptive behavior (66). 

Smith, J.E. Co, C. Freeman, M.E. and Lane, J.D. Brain neurotransmitter turnover correlated with morphine-seeking behavior of rats. Pharmacol Biochem Behav 16 509-519, 1982. 

Unlike many chemicals in the brain, neurotransmitters are not homogeneously distributed, but concentrated in certain regions. For example, almost two-thirds of the dopamine in the brain is found in the bilateral nigrostriatal (mesostriatal) tract (pathway), where the neuronal cell bodies are located in the substantia nigra and the axons terminate in the corpus striatum. When over 85% of these dopaminergic neurons are lost, the characteristic motor dysfunction of Parkinson s disease is seen. 

Spieler, R.E., A.C. Russo, and D.N. Weber. 1995. Waterborne lead affects circadian variations of brain neurotransmitters in fathead minnows. Bull. Environ. Contam. Toxicol. 55 412-418. 

On the basis of their own research as well as that of others, most authors in this volume have concluded that of all the brain neurotransmitters studied to date, none plays as crucial a role in drug-induced hallucinogenesis as serotonin. 

Malaviya M, Husain R, Seth PK et al (1993) Perinatal effects of two pyrethroids insecticides on brain neurotransmitter function in the neonatal rat. Vet Hum Toxicol 35 119-122... 

Hong JS, Tilson HA, Uphouse LL, et al. 1984. Effects of chlordecone exposure on brain neurotransmitters Possible involvement of the serotonin system in chlordecone-elicited tremor. Toxicol Appl Pharmacol 73 336-344. 

There are a number of studies that provide good quantitative dose- response data by the inhalation route, and inhalation MRLs have been derived for acute, intermediate and chronic inhalation exposure. The acute value is based on a study in rats in which exposure to 31 ppm for 8 hours caused altered levels of brain neurotransmitters, while 16 ppm had no effect (Honma 1987). The MRL of 0.05 ppm was obtained by adjusting the NOAEL (16 ppm) for less than continuous exposure (8 hour/day) and dividing by an uncertainty factor of 100 (10 for extrapolation from animals to humans, and 10 for human variability). The intermediate-duration inhalation MRL is based on a 3-week study in rats in which exposure to 10 ppm resulted in decreased brain neurotransmitters, while 5 ppm did not (Honma et al. 1982). The intermediate MRL of 0.05 ppm was derived from the NOAEL (5 ppm) by dividing by an uncertainty factor of 100, as described above. The chronic... 

Substances with a neuromodulatory effect on brain neurotransmitters by direct actions of specific receptors that modify the actions of the transmitters listed include prostaglandins, adenosine, enkephalins, substance P, cholecystokinin, endorphins, endogenous benzodiazepine receptor ligands, and possibly histamine. CNS, central nervous system. NMDA, N-methyl-D-aspartate. Strych, strychnine. 

The neurochemistry of schizophrenia has been considered in a variety of ways by numerous investigators and most have, as here, focussed on the role of abnormalities and/or dysfunction of brain neurotransmitter systems in the disease. Implicit in a book on the neurochemistry of consciousness is the assumption that this chapter will address the neurochemical basis of the disturbance (s) of consciousness that occurs in schizophrenia. Consciousness in its particular and generally-understood meaning is not obviously distorted in schizophrenia, although schizophrenic patients clearly have a different, or abnormal experience of the external world—their conscious awareness is disturbed. 

None of the TCAs seem to have an effect on dopaminergic neurotransmission in the central nervous system (CNS). This has been supported by the lack of alterations in dopamine receptor sensitivity in chronically treated patients who have shown response to treatment (Sugrue, 1983). More recent investigations have also shown that administration of DMI to depressed subjects had no effect on levels of homovanillic acid, the principal metabolite of dopamine, in a measure of brain neurotransmitter production. In this investigation, DMI administration did increase norepinephrine production and overall cerebral metabolism (Lambert, 2000). 

Kish, S.J., Kleinert, R., Minauf, M., Gilbert, J., Walter, G.F., Slimov-itch, C., Maurer, E., Rezvani, Y., Myers, R., and Hornykiewicz, O. (1990) Brain neurotransmitter changes in three patients who had a fatal hyperthermia syndrome. Am Psychiatry 147 1358-1363. 

Tricyclic antidepressants (TCAs) modulate various brain neurotransmitters, especially norepinephrine and serotonin, by blocking reuptake presynaptically. The secondary amines (desipramine, nortriptyline) are more selective for noradrenergic function and have less side effects in sensitive populations. Advantages of this class of drugs include their relative long half life (approximately 12 hours), absence of abuse potential, and putative positive effects on mood and anxiety, sleep, and tics. 

I nositol is a simple substance present normally in the diet at about 1 g/day and is an isomer of glucose. The phosphatidylinositol (PI) cycle is an important second messenger system for several brain neurotransmitters (Figure 9-1). Receptor (R) stimulation by an activator (A) leads to breakdown of membrane phosphatidylinositol 4,5-biphosphate (PIP2) to... 

Maggi A, Enna SJ Regional alterations in rat brain neurotransmitter systems following chronic lithium treatment. J Neurochem 34 888-892, 1980 Maggi A, Perez J Minireview role of female gonadal hormones in the CNS clinical and experimental aspects, life Sci 37 893-906, 1985 Maitre L, Baltzer V, Mondadori C Psychopharmacological and behavioural effects of anti-epileptic drugs in animals, in Anticonvulsants in Affective Disorders. Edited by Emrich HM, Okuma T, Muller AA. Amsterdam, Excerpta Medica, 1984, pp 3-13... 

Stimulants have chemical structures that are similar to key brain neurotransmitters called monoamines, including dopamine and norepinephrine. Their therapeutic effect is achieved by slow and steady increases of dopamine that are similar to the natural production of this chemical by the brain. The doses prescribed by physicians start low and increase gradually until a therapeutic effect is reached. However, when taken in doses and routes other than those prescribed, stimulants can increase the brain s dopamine levels in a rapid and highly amplified manner—as do most other drugs... 

The interaction of glutamate and its NMDA receptor with other brain neurotransmitters, including the aminergic dopamine and serotonin neuromodulators which are the main focus of this book, is very complex and only a few, simplified accounts of how NMDA receptor hypofunction... 

Depression has been noted in 10 to 15% of all patients who take reserpine for the treatment of hypertension. When used for the treatment of tuberculosis, isoniazid brings about mood elevation. Reserpine was found to diminish the levels of brain neurotransmitters such as dopamine, serotonin, and norepinephrine, whereas isoniazid, through its monoamine oxidase inhibitory actions, augments the levels of these substances. It was thus theorized that too much of one or more of these neurotransmitters might be associated with states of hypomania or mania, whereas too little would correlate with depression. 

Manipulating Brain Neurotransmitter Systems to Treat Alcoholism... 

M. Mirmiran and D.F. Svaab, Influence of drugs on brain neurotransmitters and behavioral states during development, Develop. Pharmacol. Therapeutics, (1987), (in press.). 

Muller, P. Seeman, P. 1977, Brain neurotransmitter receptors after long-term haloperidol dopamine, acetylcholine, serotonin, alpha-noradrenergic and naloxone receptors, Life Sci., vol. 21, no. 12, pp. 1751-1758. 

Lloyd KG, Hornykiewicz O, Davidson L, Shannak K, Farley L, Goldstein M, Shibuya M, Kelley WN, Fox IH (1981) Biochemical evidence of dysfunction of brain neurotransmitters in the Lesch-Nyhan syndrome. New Engl J Med 305 1106-1111. 

CO) compounds brain neurotransmitter [extremely toxic blocks... 

---