Current rodent models of the complete congenital stationary night blindness (CSNB1) were time- consuming in breeding and validation, which makes it imperative to find a more “easily handle” animal model to broaden o...Current rodent models of the complete congenital stationary night blindness (CSNB1) were time- consuming in breeding and validation, which makes it imperative to find a more “easily handle” animal model to broaden our understanding of this disorder. In the present study, a light-deprivation (LD) mouse model was made to validate whether it was a more “suitable” animal mode for investigating the pathogenesis of the CSNB1. Compared with controls, the LD mice exhibited a remarkable reduction in the amplitude of the dark-adapted electroretinogram (ERG) b-wave, the Max-ERG b-wave and also the oscillatory potentials (Ops), indicating an abnormal activity of rod bipolar cells in the retina. However, the ERG a-wave was relatively normal in the LD mice, which was quite consistent with what was confirmed in previously reported animal models of the CSNB1 and CSNB patients. Taken together, the LD mouse model showed CSNB1-like negative ERG responses as evidenced by the abnormal b-wave. Our study will provide a potentially useful animal model to decipher the pathogenesis of the CSNB1.展开更多
Depression leads to a large social burden because of its substantial impairment and disability in everyday activities. The prevalence and considerable impact of this disorder call for a better understanding of its pat...Depression leads to a large social burden because of its substantial impairment and disability in everyday activities. The prevalence and considerable impact of this disorder call for a better understanding of its pathophysiology to improve the diagnosis, treatment and prevention. Though productive animal models and pathophysiological theories have been documented, it is still very far to uncover the complex array of symptoms caused by depression. Moreover, the neural circuitry mechanism underlying behavioral changes in some depression-like behavior animals is still limited. Changes in the neural circuitry of amygdala, dorsal raphe nucleus, ventral tegmental area, hippocampus, locus coeruleus and nucleus accumbens are related to depression. However, the interactions between individual neural circuitry of different brain areas, have not yet been fully elucidated. The purpose of the present review is to examine and summarize the current evidence for the pathophysiological mechanism of depression, with a focus on the neural circuitry, and emphasize the necessity and importance of integrating individual neural circuitry in different brain regions to understand depression.展开更多
文摘Current rodent models of the complete congenital stationary night blindness (CSNB1) were time- consuming in breeding and validation, which makes it imperative to find a more “easily handle” animal model to broaden our understanding of this disorder. In the present study, a light-deprivation (LD) mouse model was made to validate whether it was a more “suitable” animal mode for investigating the pathogenesis of the CSNB1. Compared with controls, the LD mice exhibited a remarkable reduction in the amplitude of the dark-adapted electroretinogram (ERG) b-wave, the Max-ERG b-wave and also the oscillatory potentials (Ops), indicating an abnormal activity of rod bipolar cells in the retina. However, the ERG a-wave was relatively normal in the LD mice, which was quite consistent with what was confirmed in previously reported animal models of the CSNB1 and CSNB patients. Taken together, the LD mouse model showed CSNB1-like negative ERG responses as evidenced by the abnormal b-wave. Our study will provide a potentially useful animal model to decipher the pathogenesis of the CSNB1.
文摘Depression leads to a large social burden because of its substantial impairment and disability in everyday activities. The prevalence and considerable impact of this disorder call for a better understanding of its pathophysiology to improve the diagnosis, treatment and prevention. Though productive animal models and pathophysiological theories have been documented, it is still very far to uncover the complex array of symptoms caused by depression. Moreover, the neural circuitry mechanism underlying behavioral changes in some depression-like behavior animals is still limited. Changes in the neural circuitry of amygdala, dorsal raphe nucleus, ventral tegmental area, hippocampus, locus coeruleus and nucleus accumbens are related to depression. However, the interactions between individual neural circuitry of different brain areas, have not yet been fully elucidated. The purpose of the present review is to examine and summarize the current evidence for the pathophysiological mechanism of depression, with a focus on the neural circuitry, and emphasize the necessity and importance of integrating individual neural circuitry in different brain regions to understand depression.
