Abstract:
:Kynurenic acid (KYNA) is an antagonist of (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors and it blocks the glycine site of the NMDA receptor preferentially (IC50 = 7.9 microM). KYNA is produced endogenously by transamination of its precursor L-kynurenine (L-KYN). We tested the hypothesis that effects of endogenous, de novo produced KYNA, following bath-application of L-KYN to slices, would be different than effects of commercially-synthesized (exogenous) KYNA. The ability to block spontaneous epileptiform activity, induced by lowering extracellular magnesium, was examined in area CA3 of hippocampus and the entorhinal cortex. At a concentration of 200 microM L-KYN, which produced 0.89 +/- 0.20 microM KYNA, there were fewer slices with spontaneous epileptiform activity than slices exposed to 2 microM exogenous KYNA. The results indicate a more potent neuromodulatory action of endogenous KYNA than has been previously realized.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Scharfman HE,Hodgkins PS,Lee SC,Schwarcz Rdoi
10.1016/s0304-3940(99)00690-4keywords:
subject
Has Abstractpub_date
1999-10-22 00:00:00pages
111-4issue
2eissn
0304-3940issn
1872-7972pii
S0304-3940(99)00690-4journal_volume
274pub_type
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