Disease relevance of N-methyl-D-aspartic acid

• 6. In mice, (+)-HA-966 antagonized sound and N-methyl-DL-aspartic acid (NMDLA)-induced seizures with ED50 values of 52.6 mg/kg of body weight (i.p.) and 900 mg/kg (i.v.), respectively [1].
• To determine if the LHRH neurons themselves could be prematurely activated to induce such a pattern of plasma LH, and hence lead to precocious puberty, the neuroexcitatory amino acid analog N-methyl-DL-aspartic acid (NMA) was similarly administered [2].
• METHODS: We used an in vivo rat model of brain injury in which N-methyl-DL-aspartic acid (NMA) is injected subcutaneously (s.c.) and c-Fos expression in the arcuate nucleus is used as a measure of injury [3].
• Similarly, the same doses of L. leonurus extract significantly (p < 0.05; Student's t-test) delayed the onset of tonic seizures produced by picrotoxin (8 mg/kg) and N-methyl-DL-aspartic acid (400 mg/kg) [4].

Psychiatry related information on N-methyl-D-aspartic acid

• These results suggest that receptors in the nucleus accumbens, sensitive to kainic and quisqualic acids, play a more important role in the stimulation of locomotor activity than those sensitive to N-methyl-DL-aspartic acid [5].

High impact information on N-methyl-D-aspartic acid

• On d 4, during the final 3 h of the infusion, single boluses of hu metastin 45-54 (10 microg), N-methyl-DL-aspartic acid (NMDA) (10 mg/kg) and GnRH (0.3 microg) were administered to interrogate each element of the metastin-GPR54-GnRH-GnRH receptor cascade [6].
• Comparison of the effects of N-methyl-DL-aspartic acid on gonadotropin and prolactin secretion in anestrous mares and mares exhibiting estrous cycles during anestrus [7].
• After injection into the nucleus accumbens all three amino acids stimulated locomotor activity, with kainic acid being the most potent and N-methyl-DL-aspartic acid the least potent [5].
• We examined the effects of POAH cell loss, produced by microinjection of neurotoxin (N-methyl-DL-aspartic acid), on sleep and thermoregulation in cats [8].
• The selective non-competitive NMDA receptor antagonist, MK-801, potently blocked convulsions induced in the mouse by N-methyl-DL-aspartic acid (NMDLA) with an i.v. ED50 dose of 0.2 mg/kg [9].

Chemical compound and disease context of N-methyl-D-aspartic acid

• Bath application of N-methyl-DL-aspartic acid (NMDA) or D-glutamate increased the occurrence and duration of spontaneous episodes of motor activity [10].

Biological context of N-methyl-D-aspartic acid

• Intracaudate injection of N-methyl-dl-aspartic acid inhibits cortical evoked potentials [11].

Anatomical context of N-methyl-D-aspartic acid

• N-methyl-DL-aspartic acid lesions of the medial preoptic area disrupt ongoing parental behavior in male rats [12].
• Kainate and quisqualate were found to be very potent excitants, while N-methyl-DL-aspartic acid (NMDLA) caused little or no effect on Purkinje cell dendrites [13].

Associations of N-methyl-D-aspartic acid with other chemical compounds

• Since the anesthetic gas xenon behaves as an NMDA antagonist, the present article investigated, by distinct morphological approaches and after different times, the possible neuroprotectant effects of this gas in a model of neuronal damage induced by N-methyl-dl-aspartic acid (NMA) on rat arcuate nucleus [14].
• Methanol extract was also tested for activity against seizures in albino mice induced by pentylenetetrazole (PTZ), bicuculline and N-methyl-DL-aspartic acid (NMDLA) [15].

Analytical, diagnostic and therapeutic context of N-methyl-D-aspartic acid

• Resolution of the neuroexcitatory N-methylaspartic acid (2-methylaminosuccinic acid) enantiomers by ligand-exchange thin-layer chromatography [16].

References