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,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
药物成瘾被认为是药物长期作用于脑而产生的一种慢性复吸性脑疾病，长期反复的药物（如吗啡）滥用会导致一系列严重后果，如药物依赖、药物耐受、强迫性药物寻求等。本实验利用条件化位置偏好（conditioned place preference，CPP）模...药物成瘾被认为是药物长期作用于脑而产生的一种慢性复吸性脑疾病，长期反复的药物（如吗啡）滥用会导致一系列严重后果，如药物依赖、药物耐受、强迫性药物寻求等。本实验利用条件化位置偏好（conditioned place preference，CPP）模型来检测大鼠对吗啡依赖和心理渴求等过程；采用双声刺激听觉诱发电位来研究大鼠在慢性吗啡给予、戒断以及再给药过程中海马感觉门控（N40）的动态变化。吗啡组大鼠注射吗啡（10mg／kg，i．p．）12d，经历第一次戒断12d，再次注射吗啡（2．5mg／kg，i．P．）1d，之后经历第二次戒断2d；对照组大鼠注射同体积生理盐水，其余实验条件与吗啡组相同。CPP实验表明，这种药物给予方法促使大鼠对吗啡产生药物依赖和心理渴求。双声刺激诱发电位实验表明，吗啡组大鼠在吗啡给予期间海马感觉门控受到损伤；第一次戒断期的第1～2天海马感觉门控能力减弱，第3天增强，第4～12天逐渐恢复到正常水平；再次给予吗啡后海马感觉门控能力与对照组相比显著降低，并且随后2d的戒断期内海马感觉门控能力也一直保持较低水平，表明再次给药使大鼠海马感觉门控对吗啡更加敏感化。结果提示，长期反复的吗啡给予及再给药干扰了海马的感觉门控能力，吗啡成瘾对大脑可能产生长期影响。展开更多
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,
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the National Natural Science Foundation of China(No.3047055330530270)+1 种基金Science Foundationof the Chinese Academy of Sciences(No.KSCX2-SW-217-03)the National Basic Research Development Program of China(No.2005CB522803)
文摘药物成瘾被认为是药物长期作用于脑而产生的一种慢性复吸性脑疾病，长期反复的药物（如吗啡）滥用会导致一系列严重后果，如药物依赖、药物耐受、强迫性药物寻求等。本实验利用条件化位置偏好（conditioned place preference，CPP）模型来检测大鼠对吗啡依赖和心理渴求等过程；采用双声刺激听觉诱发电位来研究大鼠在慢性吗啡给予、戒断以及再给药过程中海马感觉门控（N40）的动态变化。吗啡组大鼠注射吗啡（10mg／kg，i．p．）12d，经历第一次戒断12d，再次注射吗啡（2．5mg／kg，i．P．）1d，之后经历第二次戒断2d；对照组大鼠注射同体积生理盐水，其余实验条件与吗啡组相同。CPP实验表明，这种药物给予方法促使大鼠对吗啡产生药物依赖和心理渴求。双声刺激诱发电位实验表明，吗啡组大鼠在吗啡给予期间海马感觉门控受到损伤；第一次戒断期的第1～2天海马感觉门控能力减弱，第3天增强，第4～12天逐渐恢复到正常水平；再次给予吗啡后海马感觉门控能力与对照组相比显著降低，并且随后2d的戒断期内海马感觉门控能力也一直保持较低水平，表明再次给药使大鼠海马感觉门控对吗啡更加敏感化。结果提示，长期反复的吗啡给予及再给药干扰了海马的感觉门控能力，吗啡成瘾对大脑可能产生长期影响。
