These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Two pathways of nitric oxide production through glutamate receptors in the rat cerebellum in vivo.
    Author: Yamada K, Nabeshima T.
    Journal: Neurosci Res; 1997 Jun; 28(2):93-102. PubMed ID: 9220466.
    Abstract:
    The effects of N-methyl-D-aspartate (NMDA), (+)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), and trans-(+/-)-1-amino-(1S,3R)-cyclopentanedicarboxylic acid (ACPD) on nitric oxide (NO) production in the cerebellum of conscious rats were investigated by measuring the levels of total NO metabolites (nitrite plus nitrate, NOx-) in dialysates obtained by in vivo microdialysis. All glutamate receptor agonists dose-dependently increased NOx- levels. Pharmacological characterization with various glutamate receptor antagonists indicated that the effects of NMDA, AMPA and ACPD are mediated by NMDA, non-NMDA, and L(+)-2-amino-3-phosphonopropionic acid (L(+)-AP-3)-sensitive metabotropic glutamate receptors, respectively. The NO synthase (NOS) inhibitors, including NG-nitro-L-arginine methyl ester (L-NAME), NG-nitro-L-arginine (L-NA), 7-nitroindazole (7-NI), and NG-monomethyl-L-arginine, inhibited NMDA-induced, but not AMPA- or ACPD-induced, increase in NOx- levels. L-Arginine enhanced NMDA-induced, but not AMPA- or ACPD-induced, increase in NOx- levels. Cytochrome P-450 inhibitors, SKF525A and erythromycin, inhibited the effect of NMDA, but not AMPA or ACPD. These results suggest that AMPA and ACPD may induce NO production through a NOS-independent pathway although NMDA receptor-mediated NO production is dependent on NOS activity in the rat cerebellum in vivo.
    [Abstract] [Full Text] [Related] [New Search]