Alterations in the cortical and peripheral somatosensory evoked activity of rats treated with 3-nitropropionic acid

被引:3
作者
Szabó, A [1 ]
Papp, A [1 ]
Nagymajtényi, L [1 ]
Vezér, T [1 ]
机构
[1] Univ Szeged, Dept Publ Hlth, Dom Ter 10, H-6720 Szeged, Hungary
关键词
3-nitropropionic acid; somatosensory system; cortical evoked activity; peripheral evoked activity; rat;
D O I
10.1016/j.toxlet.2005.07.006
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
In this study, the action of 3-nitropropionic acid (3-NP) on the parameters of the cortical and peripheral evoked potentials was investigated in rats in different administration schemes (20 mg/kg i.p. during recording or 24 h before, and 5 x 15 mg/kg daily 28 days before recording) to elucidate some neurophysiological effects of the substance. Responses in the somatosensory cortex and in the tail nerve, evoked by peripheral electric stimulation, were recorded in acute preparation under urethane anaesthesia. Amplitude, latency, and duration of the responses were measured. In rats treated 28 days before recording, latency of the cortical response was significantly (and the duration slightly) increased by 3-NP. The frequency dependence of the tail nerve response was more pronounced than that of the cortical response. After acute administration of 3-NP, the amplitude of the somatosensory evoked potential decreased. With double stimuli, the ratio of the amplitudes of the two responses (relative fatigue) was treatment-dependent. The relative refractory period of the tail nerve was altered both by acute and subacute 3-NP treatment. These results may be relevant in 3-NP based disease models but it needs further studies to find possible connections between the known biochemical effects of 3-NP and the functional neurotoxical changes described. The mode of evoked response analysis used is, theoretically, applicable for other neurotoxic effects and can be the base of development of functional biomarkers. (c) 2005 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:212 / 217
页数:6
相关论文
共 25 条
[1]   3-NITROPROPIONIC ACID INDUCES APOPTOSIS IN CULTURED STRIATAL AND CORTICAL-NEURONS [J].
BEHRENS, MI ;
KOH, J ;
CANZONIERO, LMT ;
SENSI, SL ;
CSERNANSKY, CA ;
CHOI, DW .
NEUROREPORT, 1995, 6 (03) :545-548
[2]  
Brouillet E, 1998, J NEUROCHEM, V70, P794
[3]   Replicating Huntington's disease phenotype in experimental animals [J].
Brouillet, E ;
Condé, F ;
Beal, MF ;
Hantraye, P .
PROGRESS IN NEUROBIOLOGY, 1999, 59 (05) :427-468
[4]   Inhibition of mitochondrial complex II induces a long-term potentiation of NMDA-mediated synaptic excitation in the striatum requiring endogenous dopamine [J].
Calabresi, P ;
Gubellini, P ;
Picconi, B ;
Centonze, D ;
Pisani, A ;
Bonsi, P ;
Greengard, P ;
Hipskind, RA ;
Borrelli, E ;
Bernardi, G .
JOURNAL OF NEUROSCIENCE, 2001, 21 (14) :5110-5120
[5]  
COLES CJ, 1979, J BIOL CHEM, V254, P5161
[6]   Electrophysiological biomarkers of an organophosphorous pesticide, dichlorvos [J].
Dési, I ;
Nagymajtényi, L .
TOXICOLOGY LETTERS, 1999, 107 (1-3) :55-64
[7]   Visually evoked potentials in respiratory chain disorders [J].
Finsterer, J .
ACTA NEUROLOGICA SCANDINAVICA, 2001, 104 (01) :31-35
[8]   Delayed dystonia with striatal CT lucencies induced by a mycotoxin (3-nitropropionic acid) [J].
He, FS ;
Zhang, SL ;
Qian, FY ;
Zhang, CL .
NEUROLOGY, 1995, 45 (12) :2178-2183
[9]  
JAMES LF, 1980, AM J VET RES, V41, P377
[10]   Maternal copper deficiency impairs the developmental expression of protein kinase c α, β and γ isoforms in neonatal rat brain [J].
Johnson, WT ;
Thomas, AC ;
Lozano, AA .
NUTRITIONAL NEUROSCIENCE, 2000, 3 (02) :113-122