Physiological actions of taurine

I. Introduction II. The EAA System: Overview, Description, and Localization in Neuroendocrine Tissues A. Endogenous EAAs and their localization in the hypothalamus B. Types of EAA receptors and their localization in the CNS and hypothalamus C. EAA transporters III. EAAs and Reproduction A. Effect of EAA agonists on LH secretion B. Effect of blockade of EAA neurotransmission on the steroid-induced and preovulatory LH surge and pulsatile LH secretion C. Site of action of EAAs in the control of LH secretion D. Mechanism of action of EAAs in the control of LH secretion E. The opioid-glutamate-nitric oxide-guanylate cyclase pathway in the control of GnRH secretion: a proposed model IV. Role of EAAs in Puberty and Reproductive Behavior A. Role of EAAs in puberty B. EAAs and reproductive behavior V. Role of EAAs in the Secretion of Other Anterior Pituitary Hormones A. ACTH B. GH C. PRL VI. Conclusions

Excitatory amino acids: evidence for a role in the control of reproduction and anterior pituitary hormone secretion.

In this study, using an enzymatic HPLC method in combination with D-aspartate oxidase, we show that N-methyl-D-aspartate (NMDA) is present at nanomolar levels in rat nervous system and endocrine glands as a natural compound, and it is biosynthesized in vivo and in vitro. D-aspartate (D-Asp) is its natural precursor and also occurs as an endogenous compound. Among the endocrine glands, the highest quantities of D-Asp (78 +/- 12 nmol/g) and NMDA (8.4 +/- 1.2 nmol/g) occur in the adenohypophysis, whereas the hypothalamus represents the area of the nervous system where these amino acids are most abundant (55 +/- 9 and 5.6 +/- 1.1 nmol/g for D-Asp and NMDA, respectively). When D-Asp is administered to rats by ip injection, there is a significant uptake of D-Asp into the adenohypophysis and a significant increase in the concentration of NMDA in the adenohypophysis, hypothalamus and hippocampus, suggesting that D-Asp is an endogenous precursor for NMDA biosynthesis. Experiments conducted on tissue homogenates confirm that D-Asp is the precursor of the NMDA and that the enzyme catalyzing this reaction is a methyltransferase. S-adenosyl-L-methionine (SAM) is the methyl group donor. In vivo experiments consisting of ip injections of sodium D-aspartate show that this amino acid induced a significant serum PRL elevation and this effect is dose and time dependent. In vitro experiments conducted on isolated adenohypophysis or adenohypophysis coincubated with the hypothalamus, showed that the release of PRL is caused by a direct action of D-Asp on the pituitary gland and also mediated by the indirect action of NMDA on the hypothalamus. Then, the latter induces the release of a putative factor that in turn stimulates the adenohypophysis reinforcing the PRL release. In conclusion, our data suggest that D-Asp and NMDA are present endogenously in the rat and are involved in the modulation of PRL release.

/pdf/the-role-of-d-aspartic-acid-and-n-methyl-d-aspartic-acid-in-1i7mem50th.pdf

The Role of d-Aspartic Acid and N-Methyl-d-Aspartic Acid in the Regulation of Prolactin Release

Previous studies have demonstrated the GABAergic system in the hippocampus to be a major controlling factor in the reversal of learned helplessness by antidepressants. In the present work, animals in which learned helplessness (LeH) was induced by exposure to uncontrollable electric shock demonstrated a decreased depolarization-induced release of GABA relative to controls, and an increased release of hippocampal glutamate. Injection of bicuculline but not glutamate into the hippocampus produced a behavioral state identical to that induced by uncontrallable shock, but had no influence on pain sensitivity. When flux through the “small” hippocampal pool of GABA was determined, chronic treatment with imipramine or iprindole, but not lorazepam or chlorpromazine elevated this measure. These three findings, along with those of prior experiments, suggest a controlling role for GABA in the learned helplessness model of depression.

GABAergic modulation of learned helplessness

Characterization and possible opioid modulation of N-methyl-D-aspartic acid induced increases in serum luteinizing hormone levels in the developing male rat.

Luteinizing hormone releasing action ofN-methyl aspartate is blocked by GABA or taurine but not by dopamine antagonists

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Luteinizing hormone releasing action ofN-methyl aspartate is blocked by GABA or taurine but not by dopamine antagonists