Thanks Vaughn. I remember vaguely something about DAA through some sort of cascade increasing melanin production. I will have to research it. Keen to take this, but don't want my skin to darken any more than it already is.
Weird- I noticed the same thing from taking Lit-Up, but I just figured that it had to do more with the L-tyrosine content. DAA does have an effect on MSH release in the hypothalamus, but not the posterior pituitary- DAA and NMDA are both pretty interesting in terms of some of the effects they produce. I also become noticeably darker when I take forskolin as well:
Neuroreport. 2002 Dec 3;13(17):2341-4.
The effect of D-aspartate on luteinizing hormone-releasing hormone, alpha-melanocyte-stimulating hormone, GABA and dopamine release.
Pampillo M,
Scimonelli T,
Bottino MC,
Duvilanski BH,
Rettori V,
Seilicovich A,
Lasaga M.
Source
Centro de Investigaciones en Reproducción, Facultad de Medicina, Piso 10, Universidad de Buenos Aires (C1121ABG), Buenos Aires, Argentina.
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.
Brain Res. 1994 Dec 15;666(2):201-6.
N-methyl-D-aspartate (NMDA) stimulates release of alpha-MSH from the rat hypothalamus through release of nitric oxide.
Wayman CP,
Pike NV,
Wilson JF.
Source
Department of Pharmacology and Therapeutics, University of Wales College of Medicine, Health Park, Cardiff, UK.
Abstract
Superfusion of rat hypothalamic slices with 10(-4) M N-methyl-D-aspartic acid (NMDA) resulted in increased release of alpha-melanocyte-stimulating hormone (alpha-MSH). Peptide release was blocked by 10(-6) M NG-nitro-L-arginine methyl ester (L-NAME) a specific competitive inhibitor of nitric oxide synthase but not by the inactive enantiomer D-NAME at 10(-6) M. The inhibition by L-NAME was reversed by the addition of 10(-5) mM L-arginine, an excess of enzyme substrate. Release of nitric oxide products into tissue superfusates was stimulated by a 50 mM concentration of potassium ions and by 10(-4) M NMDA. Potassium-stimulated release was blocked by L-NAME. Basal, potassium-stimulated and NMDA-stimulated release of nitric oxide products were significantly inhibited by the NMDA-receptor antagonist D(-)-2-amino-5-phosphopentanoic acid (AP5) at 10(-4) M and by the NMDA-channel blocker ketamine at 10(-4) M. We conclude that nitric oxide mediates the stimulatory action of glutamic acid on the release of alpha-MSH from the rat hypothalamus.
