Gamma band oscillation（GBO） and sensory gating（SG） are associated with many cognitive functions.Ketamine induces deficits of GBO and SG in the prefrontal cortex（PFC）. However, the time-courses of the effects of ...Gamma band oscillation（GBO） and sensory gating（SG） are associated with many cognitive functions.Ketamine induces deficits of GBO and SG in the prefrontal cortex（PFC）. However, the time-courses of the effects of different doses of ketamine on GBO power and SG are poorly understood. Studies have indicated that GBO power and SG have a common substrate for their generation and abnormalities. In this study, we found that（1） ketamine administration increased GBO power in the PFC in rats differently in the low-and high-dose groups;（2） auditory SG was significantly lower than baseline in the 30 mg/kg and 60 mg/kg groups, but not in the 15 mg/kg and 120 mg/kg groups; and（3） changes in SG and basal GBO power were significantly correlated in awake rats. These results indicate a relationship between mechanisms underlying auditory SG and GBO power.展开更多
Background Depressive disorder is a well-known chronic, recurrent and disabling mental disease with high direct and indirect costs to society in both western and eastern cultures. Approximately 40% of depressed patien...Background Depressive disorder is a well-known chronic, recurrent and disabling mental disease with high direct and indirect costs to society in both western and eastern cultures. Approximately 40% of depressed patients show only partial or no response to initial or even multiple antidepressant medications and are usually called treatment-resistant depression （TRD） patients. The present work was to measure the features of sensory gating （SG） P50 in TRD patients with the intent of understanding the characteristics of this disease. Methods In 50 TRD patients, 39 non-treatment-resistant depression （NTRD） patients and 51 healthy controls （HC）, auditory evoked potential P50 was measured using the conditioning/testing paradigm presented with auditory double clicks stimuli, and 36 TRD patients had repeated measurements after an 8-week venlafaxine treatment course. Results All the depressive disorder patients, including the TRD and NTRD groups, showed an increased testing stimulus wave （$2-P50） amplitude compared to controls （P 〈0.01 and P 〈0.05）, but there was no significant difference between the TRD and NTRD groups （P 〉0.05）. There were significant differences in the ratio of testing stimulus （S2） and conditioning stimulus （S1） （S2/S1） and in the value of 100 × （1-S2/S1） among the three groups. Compared to the baseline, TRD patients had no significant changes of features and different expression of P50 after acute treatment （P 〉0.05）. Meanwhile, a statistically significant positive correlation of S2/S1 with the scores of the 17-item Hamilton Rating Scale for Depression （HAMD-17） （P 〈0.01）, and a significantly negative correlation of S1-S2, 100 × （1-S2/S1） with the scores of HAMD-17 （P 〈0.01） were observed in the TRD patients＇ baseline measurement, but there was no correlation after venlafaxine treatment （P 〉0.05）. Conclusions Both the TRD and NTRD patients had obvious SG deficits, with a more severe deficit in TRD patients. Although, with a correlated relationship to the severity of depressive symptoms, SG P50 deficit might be suggested as a trait marker for TRD, and a combination of S2/S1 ratio, S1-S2 and 100 × （1-S2/S1）, was recommended for electrophysiological measurement in TRD patients.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
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
Objective To investigate the variation of auditory evoked potential P50 in first-episode schizo- phrenia. Methods P50 was recorded from 66 schizophrenics and 92 normal controls with American Brova instrument, and asse...Objective To investigate the variation of auditory evoked potential P50 in first-episode schizo- phrenia. Methods P50 was recorded from 66 schizophrenics and 92 normal controls with American Brova instrument, and assessing their psychotic symptoms with PANSS. Results Compared with NC, schizophrenics showed sensory gating deficit, reflecting by increased S2/S1 ratio (NC: 42±21% , Sch:81±40% ,P <0. 01). No significant correlation was found between PANSS score and the three markers for assessing the sensory gating, such as the S2/S1 ratio, S2-S1, and 100 (1 -S2/S1) (P > 0. 05). Schizophrenics showed no differences with P50 markers between the 5 weeks and 12 weeks of treatment. Conclusion P50 might be biological trait marker of schizophrenia.展开更多
基金supported by a grant from the First Affiliated Hospital of Kunming Medical University (2015BS015)grants from the joint projects of Yunnan Province (40215003, H-201639 and 2017FE468(-250))a grant from the Ministry of Science and Technology of the People’s Republic of China (2011BAK04B04)
文摘Gamma band oscillation（GBO） and sensory gating（SG） are associated with many cognitive functions.Ketamine induces deficits of GBO and SG in the prefrontal cortex（PFC）. However, the time-courses of the effects of different doses of ketamine on GBO power and SG are poorly understood. Studies have indicated that GBO power and SG have a common substrate for their generation and abnormalities. In this study, we found that（1） ketamine administration increased GBO power in the PFC in rats differently in the low-and high-dose groups;（2） auditory SG was significantly lower than baseline in the 30 mg/kg and 60 mg/kg groups, but not in the 15 mg/kg and 120 mg/kg groups; and（3） changes in SG and basal GBO power were significantly correlated in awake rats. These results indicate a relationship between mechanisms underlying auditory SG and GBO power.
文摘Background Depressive disorder is a well-known chronic, recurrent and disabling mental disease with high direct and indirect costs to society in both western and eastern cultures. Approximately 40% of depressed patients show only partial or no response to initial or even multiple antidepressant medications and are usually called treatment-resistant depression （TRD） patients. The present work was to measure the features of sensory gating （SG） P50 in TRD patients with the intent of understanding the characteristics of this disease. Methods In 50 TRD patients, 39 non-treatment-resistant depression （NTRD） patients and 51 healthy controls （HC）, auditory evoked potential P50 was measured using the conditioning/testing paradigm presented with auditory double clicks stimuli, and 36 TRD patients had repeated measurements after an 8-week venlafaxine treatment course. Results All the depressive disorder patients, including the TRD and NTRD groups, showed an increased testing stimulus wave （$2-P50） amplitude compared to controls （P 〈0.01 and P 〈0.05）, but there was no significant difference between the TRD and NTRD groups （P 〉0.05）. There were significant differences in the ratio of testing stimulus （S2） and conditioning stimulus （S1） （S2/S1） and in the value of 100 × （1-S2/S1） among the three groups. Compared to the baseline, TRD patients had no significant changes of features and different expression of P50 after acute treatment （P 〉0.05）. Meanwhile, a statistically significant positive correlation of S2/S1 with the scores of the 17-item Hamilton Rating Scale for Depression （HAMD-17） （P 〈0.01）, and a significantly negative correlation of S1-S2, 100 × （1-S2/S1） with the scores of HAMD-17 （P 〈0.01） were observed in the TRD patients＇ baseline measurement, but there was no correlation after venlafaxine treatment （P 〉0.05）. Conclusions Both the TRD and NTRD patients had obvious SG deficits, with a more severe deficit in TRD patients. Although, with a correlated relationship to the severity of depressive symptoms, SG P50 deficit might be suggested as a trait marker for TRD, and a combination of S2/S1 ratio, S1-S2 and 100 × （1-S2/S1）, was recommended for electrophysiological measurement in TRD patients.
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.
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Supported by the National Nature Science Foundation of China (30470626)
文摘Objective To investigate the variation of auditory evoked potential P50 in first-episode schizo- phrenia. Methods P50 was recorded from 66 schizophrenics and 92 normal controls with American Brova instrument, and assessing their psychotic symptoms with PANSS. Results Compared with NC, schizophrenics showed sensory gating deficit, reflecting by increased S2/S1 ratio (NC: 42±21% , Sch:81±40% ,P <0. 01). No significant correlation was found between PANSS score and the three markers for assessing the sensory gating, such as the S2/S1 ratio, S2-S1, and 100 (1 -S2/S1) (P > 0. 05). Schizophrenics showed no differences with P50 markers between the 5 weeks and 12 weeks of treatment. Conclusion P50 might be biological trait marker of schizophrenia.
