The aim of this research was to investigate the variations of P50 auditory sensory gating(P50)in normal healthy adults and the first onset schizophrenics.By using the American Nicolet Bravo electromyography/evoked pot...The aim of this research was to investigate the variations of P50 auditory sensory gating(P50)in normal healthy adults and the first onset schizophrenics.By using the American Nicolet Bravo electromyography/evoked potential(EMG/EP)system,P50 was measured with conditioning-testing paradigm(paired-click stimuli S1 and S2 were used)in 58 first onset schizophrenics and 108 healthy adults,and the Positive and Negative Syndrome Scale(PANSS)was applied.The following three conclusions have been reached.(1)In normal control(NC)group,measured from central,anterior and posterior zone(Cz,Fz and Pz respectively),there were no statistical differences(P>0.05)between S1 and S2 evoked P50 peak latencies(S1-P50 and S2-P50);the ampli-tudes of S2-P50[(2.2P1.4),(2.3P1.5)and(2.1P1.4)μV respectively]reduced significantly as compared with S1-P50[(5.6P3.3),(5.6P3.9)and(4.9P2.8)μV respectively](P<0.01);the S2/S1 ration,S1-S2 difference,and 100(1-S2/S1)had no statistical differences(P>0.05).(2)Compared with NC,the schizophrenic group significantly showed lower S1-P50 amplitudes(P<0.01,except at Pz in whichZ=2.030,P=0.042),higher S2-P50 amplitudes,higher S2/S1 ratio,lower S1-S2 difference,and more decreased 100(1-S2/S1)(P<0.01)at Cz,Fz and Pz.(3)No significant correlations were found among S2/S1 ratio,S1-S2,100(1-S2/S1)of sen-sory gating and PANSS(P>0.05)in schizophrenic group.The first onset schizophrenics had sensory gating deficits,which could be quantified by P50.展开更多
Background The neonatal ventral hippocampal lesion （NVHL） rat model has been proposed as an experimental model for schizophrenia. NVHL rats display impaired central nervous system （CNS） inhibition, which may lead ...Background The neonatal ventral hippocampal lesion （NVHL） rat model has been proposed as an experimental model for schizophrenia. NVHL rats display impaired central nervous system （CNS） inhibition, which may lead to a phenomenon similar to P50 sensory gating deficits observed in schizophrenic patients. In this study, we investigated whether sensory gating deficits occurred in the NVHL rat as a model for schizophrenia. Methods We created the NVHL rat model using ibotenate. The P20 and N40 were measured to assess sensory response and gating in NVHL and sham rats. Epidural electrodes recorded evoked potentials （EPs）, from which latencies, amplitudes, difference scores （$1-$2）, and gating ratios （$2/$1） were assessed. Results Compared with sham controls, prolonged S1 N40 latency and decreased S2 N40 amplitude were detected in the NVHL group. In neither difference scores nor gating ratios, a significant difference was found between NVHL group and sham controls. Conclusions NVHL rats may be a valid animal model for schizophrenia. This strategy will be useful in future neurobiological studies investigating the etiology of schizophrenia.展开更多
基金supported by the National Natural Science Foundation of China(Grant No.0470626).
文摘The aim of this research was to investigate the variations of P50 auditory sensory gating(P50)in normal healthy adults and the first onset schizophrenics.By using the American Nicolet Bravo electromyography/evoked potential(EMG/EP)system,P50 was measured with conditioning-testing paradigm(paired-click stimuli S1 and S2 were used)in 58 first onset schizophrenics and 108 healthy adults,and the Positive and Negative Syndrome Scale(PANSS)was applied.The following three conclusions have been reached.(1)In normal control(NC)group,measured from central,anterior and posterior zone(Cz,Fz and Pz respectively),there were no statistical differences(P>0.05)between S1 and S2 evoked P50 peak latencies(S1-P50 and S2-P50);the ampli-tudes of S2-P50[(2.2P1.4),(2.3P1.5)and(2.1P1.4)μV respectively]reduced significantly as compared with S1-P50[(5.6P3.3),(5.6P3.9)and(4.9P2.8)μV respectively](P<0.01);the S2/S1 ration,S1-S2 difference,and 100(1-S2/S1)had no statistical differences(P>0.05).(2)Compared with NC,the schizophrenic group significantly showed lower S1-P50 amplitudes(P<0.01,except at Pz in whichZ=2.030,P=0.042),higher S2-P50 amplitudes,higher S2/S1 ratio,lower S1-S2 difference,and more decreased 100(1-S2/S1)(P<0.01)at Cz,Fz and Pz.(3)No significant correlations were found among S2/S1 ratio,S1-S2,100(1-S2/S1)of sen-sory gating and PANSS(P>0.05)in schizophrenic group.The first onset schizophrenics had sensory gating deficits,which could be quantified by P50.
基金This study was supported by the grants from the National Key Basic Research Science Foundation （973 Project, No. 2010CB529605） and the National Natural Science Foundation of China （No. 81000581 and No.30971046）.
文摘Background The neonatal ventral hippocampal lesion （NVHL） rat model has been proposed as an experimental model for schizophrenia. NVHL rats display impaired central nervous system （CNS） inhibition, which may lead to a phenomenon similar to P50 sensory gating deficits observed in schizophrenic patients. In this study, we investigated whether sensory gating deficits occurred in the NVHL rat as a model for schizophrenia. Methods We created the NVHL rat model using ibotenate. The P20 and N40 were measured to assess sensory response and gating in NVHL and sham rats. Epidural electrodes recorded evoked potentials （EPs）, from which latencies, amplitudes, difference scores （$1-$2）, and gating ratios （$2/$1） were assessed. Results Compared with sham controls, prolonged S1 N40 latency and decreased S2 N40 amplitude were detected in the NVHL group. In neither difference scores nor gating ratios, a significant difference was found between NVHL group and sham controls. Conclusions NVHL rats may be a valid animal model for schizophrenia. This strategy will be useful in future neurobiological studies investigating the etiology of schizophrenia.
