Cross-Modal Plasticity during Self-Motion Perception.

To maintain stable and coherent perception in an ever-changing environment, the brain needs to continuously and dynamically calibrate information from multiple sensory sources, using sensory and non-sensory information in a flexible manner. Here, we review how the vestibular and visual signals are recalibrated during self-motion perception. We illustrate two different types of recalibration: one long-term cross-modal (visual-vestibular) recalibration concerning how multisensory cues recalibrate over time in response to a constant cue discrepancy, and one rapid-term cross-modal (visual-vestibular) recalibration concerning how recent prior stimuli and choices differentially affect subsequent self-motion decisions. In addition, we highlight the neural substrates of long-term visual-vestibular recalibration, with profound differences observed in neuronal recalibration across multisensory cortical areas. We suggest that multisensory recalibration is a complex process in the brain, is modulated by many factors, and requires the coordination of many distinct cortical areas. We hope this review will shed some light on research into the neural circuits of visual-vestibular recalibration and help develop a more generalized theory for cross-modal plasticity.

A preliminary study on abnormal brain function and autistic behavior in mice caused by dcf1 deletion.

Autism is one of the urgent problems in neuroscience. Early research in our laboratory found that dcf1 gene-deficient mice exhibited autistic behavior. Reviewing the literature, we know that the caudate putamen (CPu) brain region is closely related to the occurrence of autism. In this study, we observed that the electrical signal in the abnormal brain region of adult mice was enhanced by using field potential detection for the corresponding brain region. We then used retrovirus markers to track neurons in the CPu brain region and found that there are neural projections in the hippocampus-CPu brain region. Therefore, we selected DREADDs (Designer receptors exclusively activated by designer drugs) to inhibit the abnormal brain region of the mouse and found, through behavioral testing, that this can inhibit the autistic behavior of mice. This research provides new evidence for the understanding of the cause of autism and has accumulated new basis for the treatment of autism. It has theoretical significance and potential application value for the understanding and treatment of autism.