Taurine physiological activity

As NJ eurotransmitters. Several amino acids serve as specialized neurotransmitters in both vertebrate and invertebrate nervous systems. These amino acids can be classified as inhibitory transmitters, such as y-aminobutyric acid [56-12-2] (GABA) and glycine, and excitatory amino acids, examples of which are L-glutamic acid and L-aspartic acid. A number of other amino acids and theic related substances occur in the brain and have some physiological activity. These include taurine [107-35-7], serine, profine, pipecofic acid [535-75-1], N-acetyl-aspartic acid [997-55-7], a- and p-alanines, and L-cysteine sulfinic acid [2381-08-0]. Eor more details about neurotransmitter amino acids, see reference 112. 

Taurine (2-aminoethanesulfonic acid 4.235) is an inhibitory neurochemical that probably acts primarily as a neuromodulator rather than a neurotransmitter. It is formed from cysteine, and its accumulation can be prevented by the cardiac glycoside ouabain. Although receptor sites and specific actions cannot be elucidated without an antagonist, taurine has been implicated in epilepsy and, potentially, in heart disease. There are a large number of physiological effects attributed to taurine, among them cardiovascular (antiarrythmic), central (anticonvulsant, excitability modulation), muscle (membrane stabilizer), and reproductive (sperm motility factor) activity. Analogs of taurine, phthalimino-taurinamide (4.236) and its iV-alkyl derivatives, are less polar than taurine and are potent anticonvulsant molecules. 

The regulatory amino acid taurine in the retina requires an efficient uptake system to maintain the high physiological concentration of taurine in the retina. Stimulation and inhibition of PKC activity with TP A and with staurosporine, respectively, produced no significant effect on taurine uptake. On the other hand, chelerythrine significantly inhibited the taurine uptake systems, presumably through a PKC-independent mechanism [104]. 

In addition to changing the physical properties of bile acids, conjugation also alters their physiological properties. On the basis of extremely limited evidence, it seems likely that the bile acid pool of animals with exclusively taurine conjugates is maintained chiefly by active absorption from the ileum. 

We have, therefore, found a very unusual modulation of the influx of an amino acid. Stimulated uptake of taurine in the presence of adrenergic activation is probably the reason for the high levels found in congestive heart failure. Such a state is produced as the end result of prolonged stress on the heart, in which there has probably also been a prolonged or continuous activation of the 6-adrenergic system. A possible physiological function for this modulation is discussed below. 

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