@article{MTMT:1235938,
	title = {Effect of MPTP on the brain amino acid concentrations},
	url = {https://m2.mtmt.hu/api/publication/1235938},
	author = {Klivényi, Péter and Kékesi, Adrienna Katalin and Hartai, ZS and Juhász, Gábor Dénes and Vécsei, László},
	journal-iso = {MOVEMENT DISORD},
	journal = {MOVEMENT DISORDERS},
	volume = {21},
	unique-id = {1235938},
	issn = {0885-3185},
	year = {2006},
	eissn = {1531-8257},
	pages = {S68-S68},
	orcid-numbers = {Klivényi, Péter/0000-0002-5389-3266; Kékesi, Adrienna Katalin/0000-0003-3042-4878; Juhász, Gábor Dénes/0000-0002-0849-6931; Vécsei, László/0000-0001-8037-3672}
}

@article{MTMT:1294676,
	title = {The acute effects of 3-nitropropionic acid on the behavior and spontaneous cortical electrical activity of rats},
	url = {https://m2.mtmt.hu/api/publication/1294676},
	author = {Lukács, Anita and Szabó, Andrea and Vezér, Tünde and Papp, András},
	journal-iso = {ACTA NEUROBIOL EXP},
	journal = {ACTA NEUROBIOLOGIAE EXPERIMENTALIS},
	volume = {66},
	unique-id = {1294676},
	issn = {0065-1400},
	abstract = {In this study, the acute effects of 3-nitropropionic acid was investigated on open field and startle behavior of rats, and on their cortical electrical activity. Spontaneous locomotor activity, acoustic startle response, and pre-pulse inhibition of acoustic startle were measured in male Wistar rats (10 weeks old, 180-200g body weight) after a single dose of 10 or 20 mg/kg i.p. 3-nitropropionic acid. After the behavioral tests, the rats were anaesthetized, and spontaneous cortical electrical activity was recorded. The vertical, horizontal and local open field performance showed dose-dependent deterioration in the rats treated with 3-nitropropionic acid. The number of “noise-positive” startle responses showed non-significant changes, but the inhibition by pre-pulse was significantly reduced in the high dose animals. High dose also increased the proportion of low-frequencies in the cortical activity. Three-nitropropionic acid, known primarily to act in repeated doses (e.g., in animal models of Huntington’s disease) had also some clear-cut acute effects on behavioral and electrophysiological parameters of the treated rats.},
	year = {2006},
	eissn = {1689-0035},
	pages = {227-233},
	orcid-numbers = {Lukács, Anita/0000-0002-0746-8920; Papp, András/0000-0003-0485-0806}
}

@article{MTMT:1032192,
	title = {Effects of mitochondrial toxins on the brain amino acid concentrations},
	url = {https://m2.mtmt.hu/api/publication/1032192},
	author = {Klivényi, Péter and Kékesi, Adrienna Katalin and Hartai, Z and Juhász, Gábor Dénes and Vécsei, László},
	doi = {10.1007/s11064-005-8512-x},
	journal-iso = {NEUROCHEM RES},
	journal = {NEUROCHEMICAL RESEARCH},
	volume = {30},
	unique-id = {1032192},
	issn = {0364-3190},
	abstract = {In the pathogenesis of Parkinson's disease and Huntington's disease excitotoxicity may play an important role. The common toxin model for Parkinson's disease is MPTP, while for Huntington's disease it is 3-NP. These toxins inhibit the mitochondrial respiratory chain, resulting in an energy deficit. In the central nervous system, the amino acids act as neurotransmitters and neuromodulators. The energy deficit caused by these neurotoxins may alter the concentrations of amino acids. Thus, it can be claimed that the aminoacidergic neurotransmission can be changed by neurotoxins. To test this hypothesis we studied the amino acid concentrations in different brain regions following MPTP or 3-NP administration. The two toxins were found to produce similar changes. We detected marked decreases in most of the amino acid concentrations in the striatum and in the cortex, while the levels in the cerebellum increased significantly. The decreased amino acid levels can be explained by the reduced levels of ATP produced by these neurotoxins. In the cerebellum, where there is no detectable ATP loss, the elevated amino acid levels may reflect a compensation of the altered neurotransmission.},
	year = {2005},
	eissn = {1573-6903},
	pages = {1421-1427},
	orcid-numbers = {Klivényi, Péter/0000-0002-5389-3266; Kékesi, Adrienna Katalin/0000-0003-3042-4878; Juhász, Gábor Dénes/0000-0002-0849-6931; Vécsei, László/0000-0001-8037-3672}
}