Clenbuterol enhances the production of kynurenic acid in brain cortical slices and glial cultures.

نویسندگان

  • Elzbieta Luchowska
  • Renata Kloc
  • Sebastian Wnuk
  • Bartosz Olajossy
  • Marian Wielosz
  • Ewa M Urbańska
چکیده

The effect of a beta(2)-adrenergic agonist, clenbuterol on the production of a glutamate receptor antagonist, kynurenic acid was studied in vitro. Clenbuterol enhanced the production of kynurenic acid in brain cortical slices (0.1-1.0 mM) and in glial cultures (1-50 muM). Timolol, a non-selective beta-adrenergic antagonist prevented this effect. The presented data indicate a novel mechanism of action of beta(2)-adrenoceptor agonists and suggest that an increased formation of the endogenous glutamate receptor antagonist, kynurenic acid could partially contribute to their neuroprotective activity.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Thioperamide, antagonist of histamine H3 receptors, increases brain production of kynurenic acid

Brain histamine plays the role of neuromodulator and neurotransmitter in a variety of physiological and pathological processes. Kynurenic acid (KYNA) is an antagonist of the glycine site within the N-methyl-D-aspartate (NMDA) receptor complex, and of nicotinic α7 receptors in the brain of mammals. Here, we report that thioperamide, H3 receptor antagonist/inverse agonist is capable of increasing...

متن کامل

Hyperglycemia enhances the inhibitory effect of mitochondrial toxins and D,L-homocysteine on the brain production of kynurenic acid.

We have evaluated the effect of diabetes-mimicking conditions on the inhibition of kynurenic acid (KYNA) production exerted by mitochondrial toxins: 3-nitropropionic acid (3-NPA) and aminooxyacetic acid (AOAA), by endogenous agonists of glutamate receptors: L-glutamate and L-cysteine sulfinate, and by a risk factor of atherosclerosis, D,L-homocysteine. Hyperglycemia (30 mM; 2 h) itself did not ...

متن کامل

FK506 attenuates 1-methyl-4-phenylpyridinium- and 3-nitropropionic acid-evoked inhibition of kynurenic acid synthesis in rat cortical slices.

Kynurenic acid (KYNA), the only known endogenous glutamate antagonist, is produced in the brain by kynurenine aminotransferases (KATs) I and II. Mitochondrial toxins, 1-methyl-4-phenylpyridinium (MPP +) and 3-nitropropionic acid (3-NPA), were previously shown to reduce KYNA synthesis via interference with KAT I and II. Data presented here demonstrate that immunophilin ligand, FK506 (10-130 micr...

متن کامل

Quinolinate-induced cortical cholinergic damage: modulation by tryptophan metabolites.

Certain products of tryptophan metabolism interact with excitatory amino acid receptors to produce or protect against excitotoxicity. In this study, the action of several tryptophan metabolites, yielded by the kynurenine pathway, on cortical cholinergic toxicity was evaluated following focal injection into the rat nucleus basalis magnocellularis (nbM). Metabolites were injected singly or in com...

متن کامل

N(G)-nitro-L-arginine and its methyl ester inhibit brain synthesis of kynurenic acid possibly via nitric oxide-independent mechanism.

The effect of nitric oxide synthase (NOS) inhibitors on the brain production of endogenous glutamate receptor antagonist, kynurenic acid, was estimated in vitro. Under standard incubation conditions N(G)-nitro-L-arginine, but not N(G)-nitro-L-arginine methyl ester, up to 5 mM, or 7-nitroindazole, up to 100 microM, inhibited de novo synthesis of kynurenic acid in cortical slices. However, during...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Pharmacological reports : PR

دوره 60 4  شماره 

صفحات  -

تاریخ انتشار 2008