Nitric Oxide Synthase Inhibition and Glutamate Binding in Quinolinate-Lesioned Rat Hippocampus

Title:

Nitric Oxide Synthase Inhibition and Glutamate Binding in Quinolinate-Lesioned Rat Hippocampus

Creator:

Václav Lisý and František Šťastný

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:d23f426e-f695-4088-aed5-297662c6cf84
uuid:d23f426e-f695-4088-aed5-297662c6cf84
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, Quinolinic acid, NMDA receptor, Membrane binding, Nitric oxide synthase (NOS), Neurodegeneration, 14, and 612

Type:

article, studie, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

a1_The effect of lesions induced by bilateral intracerebroventricular (ICV) injection of quinolinate (250 nmol of QUIN/ventricle), a selective N-methyl-D-aspartate (NMDA) receptor agonist, on [3H]glutamate ([3H]Glu) binding to the main types of both ionotropic and metabotropic glutamate receptors (iGluR and mGluR) was investigated in synaptic membrane preparations from the hippocampi of 50-day-old rats. The membranes from QUIN injured brains revealed significantly lowered binding in iGluR (by 31 %) as well as in mGluR (by 22 %) as compared to the controls. Using selected glutamate receptor agonists as displacers of [3H]Glu binding we found that both the NMDA-subtype of iGluR and group I of mGluR are involved in this decrease of binding. Suppression of nitric oxide (NO) production by NG-nitro-L-arginine (50 nmol of NARG/ventricle) or the increase of NO generation by 3-morpholinylsydnoneimine (5 nmol of SIN-1/ventricle) failed to alter [3H]Glu or [3H]CPP (3-((D)-2-carboxypiperazin-4-yl)-[1,2-3H]-propyl-1-phosphonic acid; NMDA-antagonist) binding declines caused by QUIN-lesions. Thus, our findings indicate that both the NMDA-subtype of iGluR and group I of mGluR are susceptible to the QUIN-induced neurodegeneration in the rat hippocampus. However, the inhibition of NO synthesis did not reveal any protective action in the QUIN-evoked, NMDA-receptor mediated decrease of [3H]Glu binding., a2_Therefore, the additional mechanisms of QUIN action, different from direct NMDA receptor activation/NO production (e.g. lipid peroxidation induced by QUIN-Fe-complexes) cannot be excluded., V. Lisý, F. Šťastný., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2002 Volume:51 | Number:3

Harvested from:

CDK

Metadata only:

false