TY - JOUR AU - Knyihár-Csillik, E AU - Mihály, András AU - Krisztinné Péva, Beáta AU - Robotka, H AU - Szatmári, István AU - Fülöp, Ferenc AU - Toldi, József AU - Csillik, Bertalan AU - Vécsei, László TI - The kynurenate analog SZR-72 prevents the nitroglycerol-induced increase of c-fos immunoreactivity in the rat caudal trigeminal nucleus: Comparative studies of the effects of SZR-72 and kynurenic acid JF - NEUROSCIENCE RESEARCH J2 - NEUROSCI RES VL - 61 PY - 2008 IS - 4 SP - 429 EP - 432 PG - 4 SN - 0168-0102 DO - 10.1016/j.neures.2008.04.009 UR - https://m2.mtmt.hu/api/publication/1122177 ID - 1122177 AB - Administration of nitroglycerol in a migraine model results in an increased number of c-fos-expressing secondary sensory neurons in the caudal trigeminal nucleus. Since synapses between first- and second-order trigeminal neurons are mediated by excitatory amino acids, NMDA receptors are inhibited by kynurenic acid, though this crosses the blood-brain barrier only poorly. Systemic treatment of rats with SZR-72, a newly synthetized kynurenic acid analog, diminished the nitroglycerol-induced increase of c-fos immunoreactivity in the brain stem highly significantly, while treatment with kynurenic acid resulted in a significantly smaller decrease, proving that SZR-72 is much more effective than kynurenic acid. (C) 2008 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved. LA - English DB - MTMT ER - TY - JOUR AU - Gigler, Gábor AU - Szénási, Gábor AU - Simo, A AU - Lévay, György István AU - Hársing, László Gábor AU - Sas, Katalin AU - Vécsei, László AU - Toldi, József TI - Neuroprotective effect of L-kynurenine sulfate administered before focal cerebral ischemia in mice and global cerebral ischemia in gerbils JF - EUROPEAN JOURNAL OF PHARMACOLOGY J2 - EUR J PHARMACOL VL - 564 PY - 2007 IS - 1-3 SP - 116 EP - 122 PG - 7 SN - 0014-2999 DO - 10.1016/j.ejphar.2007.02.029 UR - https://m2.mtmt.hu/api/publication/1078436 ID - 1078436 N1 - A közleményen Sas Katalin Összehasonlító Élettani Tanszék affiliációja téves intézményi hozzárendelés (EA, SZTE admin5) AB - Excessive stimulation of N-methyl-D-aspartate (NMDA) receptors during ischemia contributes to apoptotic and excitotoxic nerve cell death. Kynurenic acid is a selective antagonist at the glycine co-agonist site of the NMDA receptor complex at low concentration, and it is a broad-spectrum excitatory amino acid receptor blocker at high concentration. Kynurenic acid provides neuroprotection in animal models of cerebral ischemia only at very high doses as it hardly crosses the blood-brain barrier. The neuroprotective effect of L-kynurenine sulfate, a precursor of kynurenic acid, was therefore studied because L-kynurenine readily crosses the blood-brain barrier. L-kynurenine sulfate was administered 15 min before permanent focal cerebral ischemia produced by electrocoagulation of the distal middle cerebral artery in mice. L-kynurenine sulfate induced a small decrease in the surface area of the brain infarction (10%, P<0.05) at 30 mg/kg i.p., and it caused strong reductions in infarct size (24-25%, P<0.01) at 100 and 300 mg/kg i.p. Treatment of gerbils with L-kynurenine sulfate at 300 mg/kg i.p. 2 h before a 3-min bilateral carotid occlusion decreased (40%, P<0.01) the pyramidal cell loss in the CAl area of the hippocampus. Furthermore, L-kynurenine sulfate inhibited the ischemia-induced hypermotility (77%, P<0.001), and decreased (50%, P<0.01) the ischemia-induced deterioration of spontaneous alternation, a measure of spatial memory, without altering the rectal temperature. In conclusion, the administration of L-kynurenine can elevate the brain concentration of kynurenic acid to neuroprotective levels, suggesting the potential clinical usefulness of L-kynurenine for the prevention of neuronal loss. (c) 2007 Elsevier B.V. All rights reserved. LA - English DB - MTMT ER - TY - CONF AU - Farkas, Tamás AU - Juhász-Vedres, G AU - Rózsa, Éva AU - Soós, Katalin AU - Datki, Zsolt László AU - Fülöp, Lívia AU - Kis, Zsolt AU - Penke, Botond AU - Toldi, József ED - Magyariné, Berkó Anikó TI - Különböző peptidek vizsgálata az 1-42 β-amiloid peptid által okozott szinaptotoxicitásban T2 - Magyar Élettani Társaság 70. vándorgyűlése PB - Magyar Élettani Társaság C1 - Budapest PY - 2006 SP - 98 EP - 98 PG - 1 UR - https://m2.mtmt.hu/api/publication/1187537 ID - 1187537 LA - Hungarian DB - MTMT ER - TY - JOUR AU - Marosi, Máté Gábor AU - Rakos, G AU - Robotka, H AU - Nemeth, H AU - Sas, Katalin AU - Kis, Zsolt AU - Farkas, Tamás AU - Lur, G AU - Vécsei, László AU - Toldi, József TI - Hippocampal (CA1) activities in Wistar rats from different vendors Fundamental differences in acute ischemia. JF - JOURNAL OF NEUROSCIENCE METHODS J2 - J NEUROSCI METH VL - 156 PY - 2006 IS - 1-2 SP - 231 EP - 235 PG - 5 SN - 0165-0270 DO - 10.1016/j.jneumeth.2006.03.010 UR - https://m2.mtmt.hu/api/publication/1031334 ID - 1031334 AB - Two-vessel occlusion, a frequently used model of global cerebral ischemia in rats, results in a dysfunction predominantly within the CA1 field of the hippocampus; it induces many processes with different time-scales. However, the great divergence in the results of the studies reported in the literature suggests valuable differences in response to hypoperfusion-induced ischemia among the laboratory rats used in these studies. In the present work, the acute effects of two-carotid occlusion-induced global ischemia (2VO) on the CA3 stimulation-evoked population spike activity in the CA1 region of Wistar rats from different suppliers (Charles-River and Harlan) were compared. In the acute electrophysiological experiments, the hippocampal CA1 responses revealed that the Charles-River rats immediately compensated the 2VO much better than did the Harlan rats. However, 3 days later, no difference could be observed between the CA1 activities of these rats. The presented data show that the Wistar rats from different vendors represent an important source of variability in the results of acute experiments on the hippocampal ischemia. These observations draw attention to the importance of the careful choice of the laboratory rats (both strains and breeds) used in such experiments. LA - English DB - MTMT ER - TY - CHAP AU - Kiss, Csaba AU - Bari, Ferenc AU - Toldi, József AU - Vécsei, László ED - Török, Tamás ED - Klebovich, Imre TI - Kynurenines in the brain: therapeutic perspectives T2 - Monoamine oxidase inhibitors and their role in neurotransmission (drug development) PB - Medicina Könyvkiadó CY - Budapest SN - 963242901X PY - 2004 SP - 79 EP - 114 PG - 36 UR - https://m2.mtmt.hu/api/publication/1816822 ID - 1816822 LA - English DB - MTMT ER - TY - JOUR AU - Nemeth, H AU - Robotka, H AU - Kis, Zsolt AU - Rózsa, Éva AU - Janáky, Tamás AU - Somlai, Csaba AU - Marosi, Máté Gábor AU - Farkas, Tamás AU - Toldi, József AU - Vécsei, László TI - Kynurenine administered together with probenecid markedly inhibits pentylenetetrazol-induced seizures. An electrophysiological and behavioural study JF - NEUROPHARMACOLOGY J2 - NEUROPHARMACOLOGY VL - 47 PY - 2004 IS - 6 SP - 916 EP - 925 PG - 10 SN - 0028-3908 DO - 10.1016/j.neuropharm.2004.06.007 UR - https://m2.mtmt.hu/api/publication/1030160 ID - 1030160 AB - The kynurenine pathway converts tryptophan into various compounds, including L-kynurenine, which in turn can be converted to the excitatory amino acid receptor antagonist kynurenic acid, which may therefore serve as a protective agent in such neurological disorders as epileptic seizures. Kynurenic acid, however, has a very limited ability to cross the blood-brain barrier, whereas kynurenine passes the barrier easily. In this study, we tested the hypothesis that kynurenine administered systemically together with probenecid, which inhibits kynurenic acid excretion from the cerebrospinal fluid, results in an increased level of kynurenic acid in the brain that is sufficiently high to provide protection against the development of pentylentetrazol-induced epileptic seizures. CA3 stimulation-evoked population spike activity was recorded from the pyramidal layer of area CA1 of the rat hippocampus, and in another series of behavioural experiments, water maze and open-field studies were carried out to test the presumed protective effect of kynurenine + probenecid pre-treatment against pentylenetetrazol-induced seizures. This study has furnished the first electrophysiological proof that systemic kynurenine (300 mg/kg, i.p.) and probenecid (200 mg/kg, i.p.) administration protects against pentylenetetrazol-induced (60 mg/kg, i.p.) epileptic seizures. (C) 2004 Elsevier Ltd. All rights reserved. LA - English DB - MTMT ER -