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The effect of D-aspartate on luteinizing hormone-releasing hormone, ??-melanocyte-stimulating hormone, GABA and dopamine release

National University of Cordoba, Argentina, Córdoba, Cordoba, Argentina
Neuroreport (Impact Factor: 1.52). 01/2003; 13(17):2341-4. DOI: 10.1097/01.wnr.0000044986.13025.9d
Source: PubMed

ABSTRACT

Since D-aspartate stimulates prolactin and LH release, our objective was to determine whether D-aspartate modifies the release of hypothalamic and posterior pituitary factors involved in the control of their secretion and whether its effects on these tissues are exerted through NMDA receptors and mediated by nitric oxide. In the hypothalamus, D-aspartate stimulated luteinizing hormone-releasing hormone (LHRH), alpha-melanocyte-stimulating hormone (alpha-MSH) and GABA release and inhibited dopamine release through interaction with NMDA receptors. It increased nitric oxide synthase (NOS) activity, and its effects on LHRH and hypothalamic GABA release were blunted when NOS was inhibited. In the posterior pituitary gland, D-aspartate inhibited GABA release but had no effect on dopamine or alpha-MSH release. We report that D-aspartate differentially affects the release of hypothalamic and posterior pituitary factors involved in the regulation of pituitary hormone secretion.

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    • "It has been observed that D-Asp in rats is capable of eliciting the release of the gonadotropin-releasing hormone (GnRH) from the hypothalamus, the luteinizing hormone (LH) and the growth hormone (GH) from the pituitary gland, and testosterone from the testes [13]. In addition, D-Asp occurs in a high concentration in the pineal gland [14], where it modulates melatonin synthesis in rat pinealocytes [15], and is implicated in the α-melanocyte-stimulating hormone, GABA, and in dopamine release [16]. In sheep, D-Asp is endogenously present in tissues and is electively stored in endocrine glands, such as the pituitary, and in the brain after its administration. "
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    ABSTRACT: D-aspartic acid is an amino acid present in neuroendocrine tissues of invertebrates and vertebrates, including rats and humans. Here we investigated the effect of this amino acid on the release of LH and testosterone in the serum of humans and rats. Furthermore, we investigated the role of D-aspartate in the synthesis of LH and testosterone in the pituitary and testes of rats, and the molecular mechanisms by which this amino acid triggers its action. For humans: A group of 23 men were given a daily dose of D-aspartate (DADAVIT) for 12 days, whereas another group of 20 men were given a placebo. For rats: A group of 10 rats drank a solution of either 20 mM D-aspartate or a placebo for 12 days. Then LH and testosterone accumulation was determined in the serum and D-aspartate accumulation in tissues. The effects of D-aspartate on the synthesis of LH and testosterone were gauged on isolated rat pituitary and Leydig cells. Tissues were incubated with D-aspartate, and then the concentration (synthesis) of LH and cGMP in the pituitary and of testosterone and cAMP in the Leydig cells was determined. In humans and rats, sodium D-aspartate induces an enhancement of LH and testosterone release. In the rat pituitary, sodium D-aspartate increases the release and synthesis of LH through the involvement of cGMP as a second messenger, whereas in rat testis Leydig cells, it increases the synthesis and release of testosterone and cAMP is implicated as second messenger. In the pituitary and in testes D-Asp is synthesized by a D-aspartate racemase which convert L-Asp into D-Asp. The pituitary and testes possesses a high capacity to trapping circulating D-Asp from hexogen or endogen sources. D-aspartic acid is a physiological amino acid occurring principally in the pituitary gland and testes and has a role in the regulation of the release and synthesis of LH and testosterone in humans and rats.
    Full-text · Article · Oct 2009 · Reproductive Biology and Endocrinology
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    ABSTRACT: Probes for the occurrence of endogenous D-aspartic acid (D-Asp) and N-methyl-D-aspartic acid (NMDA) in the neural complex and gonads of a protochordate, the ascidian Ciona intestinalis, have confirmed the presence of these two excitatory amino acids and their involvement in hormonal activity. A hormonal pathway similar to that which occurs in vertebrates has been discovered. In the cerebral ganglion D-Asp is synthesized from L-Asp by an aspartate racemase. Then, D-Asp is transferred through the blood stream into the neural gland where it gives rise to NMDA by means of an NMDA synthase. NMDA, in turn, passes from the neuronal gland into the gonads where it induces the synthesis and release of a gonadotropin-releasing hormone (GnRH). The GnRH in turn modulates the release and synthesis of testosterone and progesterone in the gonads, which are implicated in reproduction.
    Full-text · Article · Oct 2003 · FEBS Letters
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    ABSTRACT: Considerable evidence suggests that the nitric oxide (NO)/cGMP signaling pathway plays an important role in the expression of reproductive behavior and in gonadotropin-releasing hormone (GnRH) release from the hypothalamus The effects of the NO/cGMP pathway on GnRH release and gene expression have also been examined in GT1 cells. However, it is still controversial whether NO/cGMP signaling facilitates or inhibits GnRH release in these cells. The current study examined the effects of estradiol and progesterone on neuronal NO synthase (nNOS), soluble guanylyl cyclase (sGC), and NO-dependent cGMP production in the preoptic area (POA) and hypothalamus (HYP) as well as in GT1-1 cells. Ovariectomized female rats received vehicle, estradiol benzoate (48 h) and/or progesterone (3-4 h) before preparation of brain slices. GT1-1 cells were incubated with vehicle, estradiol (48 h), progesterone (3-4 h), or with both hormones. The combination of estradiol and progesterone increased the expression of nNOS protein in the POA and HYP. Hormones had little effect on the abundance of sGC. Estradiol and progesterone together greatly enhanced NO-stimulated sGC activity in HYP-POA slices. In GT1-1 cells, NO-stimulated sGC activity was significantly increased by estradiol and progesterone, alone or in combination, but sGC expression was not altered by hormones.
    No preview · Article · Aug 2004 · Endocrine
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