Experimental Neurobiology最新文献

Alzheimer's disease (AD) is the most common cause of dementia, characterized by prominent episodic memory dysfunction. Recent studies have suggested that there is a sequential mechanism in the memory deficit, with long-term ones preceding short-term ones. However, there is lack of explanation for these symptoms. Interaction between the hippocampus and retrosplenial cortex (RSC) during slow-wave sleep (SWS) is a crucial step for successful long-term memory formation. In particular, sharp-wave ripple (SWR) is a principal hippocampus oscillation that coordinates with RSC activity. To determine the relationship between memory dysfunction and SWR-related oscillation changes in AD, we implanted local field potential electrodes in the hippocampus and RSC of AD model mice (APP/PS1). We found that the SWR-coupled ripple wave increased in the RSC, while the amplitude of the SWR was preserved. In addition, the corresponding delta power in hippocampus and RSC was elevated, together with altered delta synchrony in AD mice. All these findings showed a significant correlation with long-term memory deficits measured in contextual fear conditions. Our study suggests that altered SWR-coupled oscillations are a possible underlying mechanism of episodic memory dysfunction in AD mice.

Insomnia has become a common central nervous system disease. At present, the pathogenesis of insomnia is not clear. Animal models can help us understand the pathogenesis of the disease and can be used in transformational medicine. Therefore, it is very necessary to establish an appropriate model of insomnia. Clinical data show that insomnia patients with high levels of thyroxine and often accompanied by cardiovascular problems, a common mechanism underlying all of these physiological disruptions is the sympathetic nervous system. Combined with the characteristics of chronic onset of clinical insomnia, an insomnia model induced by long-term intraperitoneal injection of thyroid hormone has been created in our laboratory. In this paper, the insomnia-like state of the model was evaluated based on three validity criteria. Face validity has been demonstrated in metabolism, the Morris water maze, electrocardiogram (ECG) and electroencephalogram (EEG). Structure validity has been proved by the results of targeted metabolomics. After treatment with diazepam, a commonly used clinical anti-insomnia drug, the above physiological and pathological disorders were reversed. The results of comprehensive analysis show that the established thyrotoxicosis-associated insomnia model meets the validity requirement to establish an appropriate animal model of insomnia. The model presented in this article might help to study pathogenetic mechanisms of clinical insomnia, as well as to test promising methods of insomnia treatment.

Many studies have reported structural or functional brain changes in patients with alcohol-dependence (ADPs). However, there has been an insufficient number of studies that were able to identify functional changes along with structural abnormalities in ADPs. Since neuronal cell death can lead to abnormal brain function, a multimodal approach combined with structural and functional studies is necessary to understand definitive neural mechanisms. Here, we explored regional difference in cortical thickness and their impact on functional connection along with clinical relevance. Fifteen male ADPs who have been diagnosed by the Diagnostic and Statistical Manual of Mental Disorders 5 (DSM-5) underwent highresolution T1 and resting-state functional magnetic resonance imaging (MRI) scans together with 15 male healthy controls (HCs). The acquired MRI data were post-processed using the Computational Anatomy Toolbox (CAT 12) and CONN-fMRI functional connectivity (FC) toolbox with Statistical Parametric Mapping (SPM 12). When compared with male HCs, the male ADPs showed significantly reduced cortical thickness in the left postcentral gyrus (PoCG), an area responsible for altered resting-state FC patterns in male ADPs. Statistically higher FCs in PoCG-cerebellum (Cb) and lower FCs in PoCG-supplementary motor area (SMA) were observed in male ADPs. In particular, the FCs with PoCG-Cb positively correlated with alcohol use disorders identification test (AUDIT) scores in male ADPs. Our findings suggest that the association of brain structural abnormalities and FC changes could be a characteristic difference in male ADPs. These findings can be useful in understanding the neural mechanisms associated with anatomical, functional and clinical features of individuals with alcoholism.