PMID- 11014243
OWN - NLM
STAT- MEDLINE
DCOM- 20001031
LR  - 20131121
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 141
IP  - 10
DP  - 2000 Oct
TI  - The role of D-aspartic acid and N-methyl-D-aspartic acid in the regulation of 
      prolactin release.
PG  - 3862-70
AB  - 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.
FAU - D'Aniello, G
AU  - D'Aniello G
AD  - Laboratory of Neurobiology, Zoological Station of Naples, Italy.
FAU - Tolino, A
AU  - Tolino A
FAU - D'Aniello, A
AU  - D'Aniello A
FAU - Errico, F
AU  - Errico F
FAU - Fisher, G H
AU  - Fisher GH
FAU - Di Fiore, M M
AU  - Di Fiore MM
LA  - eng
GR  - SO6GM45455/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Excitatory Amino Acid Agonists)
RN  - 30KYC7MIAI (Aspartic Acid)
RN  - 6384-92-5 (N-Methylaspartate)
RN  - 9002-62-4 (Prolactin)
SB  - IM
MH  - Animals
MH  - Aspartic Acid/metabolism/pharmacology/*physiology
MH  - Excitatory Amino Acid Agonists/*metabolism/pharmacology
MH  - Hippocampus/metabolism
MH  - Hypothalamus/metabolism
MH  - Male
MH  - N-Methylaspartate/biosynthesis/metabolism/pharmacology/*physiology
MH  - Pituitary Gland/metabolism
MH  - Pituitary Gland, Anterior/metabolism
MH  - Prolactin/*metabolism
MH  - Rats
MH  - Rats, Wistar
EDAT- 2000/10/03 11:00
MHDA- 2001/02/28 10:01
CRDT- 2000/10/03 11:00
PHST- 2000/10/03 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/10/03 11:00 [entrez]
AID - 10.1210/endo.141.10.7706 [doi]
PST - ppublish
SO  - Endocrinology. 2000 Oct;141(10):3862-70. doi: 10.1210/endo.141.10.7706.