@article{MTMT:1122177,
	title = {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},
	url = {https://m2.mtmt.hu/api/publication/1122177},
	author = {Knyihár-Csillik, E and Mihály, András and Krisztinné Péva, Beáta and Robotka, H and Szatmári, István and Fülöp, Ferenc and Toldi, József and Csillik, Bertalan and Vécsei, László},
	doi = {10.1016/j.neures.2008.04.009},
	journal-iso = {NEUROSCI RES},
	journal = {NEUROSCIENCE RESEARCH},
	volume = {61},
	unique-id = {1122177},
	issn = {0168-0102},
	abstract = {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.},
	year = {2008},
	eissn = {1872-8111},
	pages = {429-432},
	orcid-numbers = {Mihály, András/0000-0002-6802-0169; Szatmári, István/0000-0002-8571-5229; Fülöp, Ferenc/0000-0003-1066-5287; Toldi, József/0000-0001-7355-0503; Vécsei, László/0000-0001-8037-3672}
}

@article{MTMT:1078436,
	title = {Neuroprotective effect of L-kynurenine sulfate administered before focal cerebral ischemia in mice and global cerebral ischemia in gerbils},
	url = {https://m2.mtmt.hu/api/publication/1078436},
	author = {Gigler, Gábor and Szénási, Gábor and Simo, A and Lévay, György István and Hársing, László Gábor and Sas, Katalin and Vécsei, László and Toldi, József},
	doi = {10.1016/j.ejphar.2007.02.029},
	journal-iso = {EUR J PHARMACOL},
	journal = {EUROPEAN JOURNAL OF PHARMACOLOGY},
	volume = {564},
	unique-id = {1078436},
	issn = {0014-2999},
	abstract = {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.},
	year = {2007},
	eissn = {1879-0712},
	pages = {116-122},
	orcid-numbers = {Szénási, Gábor/0000-0002-7350-6091; Hársing, László Gábor/0000-0003-1670-8591; Vécsei, László/0000-0001-8037-3672; Toldi, József/0000-0001-7355-0503}
}

@CONFERENCE{MTMT:1187537,
	title = {Különböző peptidek vizsgálata az 1-42 β-amiloid peptid által okozott szinaptotoxicitásban},
	url = {https://m2.mtmt.hu/api/publication/1187537},
	author = {Farkas, Tamás and Juhász-Vedres, G and Rózsa, Éva and Soós, Katalin and Datki, Zsolt László and Fülöp, Lívia and Kis, Zsolt and Penke, Botond and Toldi, József},
	booktitle = {Magyar Élettani Társaság 70. vándorgyűlése},
	unique-id = {1187537},
	year = {2006},
	pages = {98-98},
	orcid-numbers = {Datki, Zsolt László/0000-0002-2537-4741; Fülöp, Lívia/0000-0002-8010-0129; Kis, Zsolt/0000-0002-6896-5883; Penke, Botond/0000-0003-0938-0567; Toldi, József/0000-0001-7355-0503}
}

@article{MTMT:1031334,
	title = {Hippocampal (CA1) activities in Wistar rats from different vendors Fundamental differences in acute ischemia.},
	url = {https://m2.mtmt.hu/api/publication/1031334},
	author = {Marosi, Máté Gábor and Rakos, G and Robotka, H and Nemeth, H and Sas, Katalin and Kis, Zsolt and Farkas, Tamás and Lur, G and Vécsei, László and Toldi, József},
	doi = {10.1016/j.jneumeth.2006.03.010},
	journal-iso = {J NEUROSCI METH},
	journal = {JOURNAL OF NEUROSCIENCE METHODS},
	volume = {156},
	unique-id = {1031334},
	issn = {0165-0270},
	abstract = {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.},
	year = {2006},
	eissn = {1872-678X},
	pages = {231-235},
	orcid-numbers = {Kis, Zsolt/0000-0002-6896-5883; Vécsei, László/0000-0001-8037-3672; Toldi, József/0000-0001-7355-0503}
}

@{MTMT:1816822,
	title = {Kynurenines in the brain: therapeutic perspectives},
	url = {https://m2.mtmt.hu/api/publication/1816822},
	author = {Kiss, Csaba and Bari, Ferenc and Toldi, József and Vécsei, László},
	booktitle = {Monoamine oxidase inhibitors and their role in neurotransmission (drug development)},
	unique-id = {1816822},
	year = {2004},
	pages = {79-114},
	orcid-numbers = {Toldi, József/0000-0001-7355-0503; Vécsei, László/0000-0001-8037-3672}
}

@article{MTMT:1030160,
	title = {Kynurenine administered together with probenecid markedly inhibits pentylenetetrazol-induced seizures. An electrophysiological and behavioural study},
	url = {https://m2.mtmt.hu/api/publication/1030160},
	author = {Nemeth, H and Robotka, H and Kis, Zsolt and Rózsa, Éva and Janáky, Tamás and Somlai, Csaba and Marosi, Máté Gábor and Farkas, Tamás and Toldi, József and Vécsei, László},
	doi = {10.1016/j.neuropharm.2004.06.007},
	journal-iso = {NEUROPHARMACOLOGY},
	journal = {NEUROPHARMACOLOGY},
	volume = {47},
	unique-id = {1030160},
	issn = {0028-3908},
	abstract = {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.},
	year = {2004},
	eissn = {1873-7064},
	pages = {916-925},
	orcid-numbers = {Kis, Zsolt/0000-0002-6896-5883; Janáky, Tamás/0000-0002-6466-8283; Toldi, József/0000-0001-7355-0503; Vécsei, László/0000-0001-8037-3672}
}