Blindness provides an unparalleled opportunity to study plasticity of the nervous system in humans.Seminal work in this area examined the often dramatic modifications to the visual cortex that result when visual input...Blindness provides an unparalleled opportunity to study plasticity of the nervous system in humans.Seminal work in this area examined the often dramatic modifications to the visual cortex that result when visual input is completely absent from birth or very early in life（Kupers and Ptito,2014）.More recent studies explored what happens to the visual pathways in the context of acquired blindness.This is particularly relevant as the majority of diseases that cause vision loss occur in the elderly.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 National Institutes of Health Contracts P30-EY008098 and T32-EY017271-06(BethesdaMD)+14 种基金United States Department of Defense DM090217(ArlingtonVA)Alcon Research Institute Young Investigator Grant(Fort WorthTX)Eye and Ear Foundation(PittsburghPA)Research to Prevent Blindness(New YorkNY)Aging Institute Pilot Seed GrantUniversity of Pittsburgh(PittsburghPA)Postdoctoral Fellowship Program in Ocular Tissue Engineering and Regenerative OphthalmologyLouis J.Fox Center for Vision RestorationUniversity of Pittsburgh and UPMC(PittsburghPA)
文摘Blindness provides an unparalleled opportunity to study plasticity of the nervous system in humans.Seminal work in this area examined the often dramatic modifications to the visual cortex that result when visual input is completely absent from birth or very early in life（Kupers and Ptito,2014）.More recent studies explored what happens to the visual pathways in the context of acquired blindness.This is particularly relevant as the majority of diseases that cause vision loss occur in the elderly.
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.
