40 Hz light flicker stimulation is deemed to hold considerable promise in the treatment of Alzheimer’s disease (AD). However, whether its long-term effect can improve working memory and its related mechanisms remains to be further explored. In this study, 21 adult Wistar rats were randomly divided into the AD light-stimulation group, the AD group and the control group. AD models were established in the first two of these groups, with the light-stimulation group receiving long-term 40 Hz light flicker stimulation. Working memory performance across groups was subsequently evaluated using the T-maze task. To investigate the potential neural mechanisms underlying the effects of 40 Hz light stimulation on working memory, we examined changes in neuronal excitability within the hippocampus (HPC) and medial prefrontal cortex (mPFC), as well as alterations in inter-regional synchronization of neural activity. The findings demonstrated that prolonged 40 Hz light stimulation significantly improved working memory performance in AD model rats. Furthermore, the intervention enhanced the synchronization of neural activity between the hippocampus (HPC) and medial prefrontal cortex (mPFC), as well as the efficiency of information transfer, primarily mediated by theta and low-frequency gamma oscillations. This study provides theoretical support for exploring the mechanisms of 40 Hz light flicker stimulation and its further clinical application in the prevention and treatment of Alzheimer’s disease.
The transmission and interaction of neural information between the hippocampus and the prefrontal cortex play an important role in learning and memory. However, the specific effects of learning memory-related tasks on the connectivity characteristics between these two brain regions remain inadequately understood. This study employed in vivo microelectrode recording to obtain local field potentials (LFPs) from the ventral hippocampus (vHPC) and medial prefrontal cortex (mPFC) in eight rats during the performance of a T-maze task, assessed both before and after task learning. Additionally, dynamic causal modeling (DCM) was utilized to analyze alterations in causal connectivity between the vHPC and the mPFC during memory task execution pre- and post-learning. Results indicated the presence of forward connections from vHPC to mPFC and backward connections from mPFC to vHPC during the T-maze task. Moreover, the forward connection between these brain regions was slightly enhanced after task learning, whereas the backward connection was diminished. These changes in connectivity corresponded with the observed trends when the rats correctly performed the T-maze task. In conclusion, this study may facilitate future investigations into the underlying mechanisms of learning and memory from the perspective of connectivity characteristics between distinct brain regions.
