â… ) Retrieving Early Associative Fear Memory Prevents Subsequent Storage For Long-Term Memory â…¡) The Dependence Of Sensory-Evoked Hippocampal Responses On Sensory Cortical Activity

Memory has a critical function for humans and animals to have a better life. Various forms of memory in different individuals determine different style of lives. Inevitably, some mental and psychological memories such as post-traumatic stress disorder (PTSD) may do harm to us. Therefore, eliminating the destructive memory has important clinical and social significance. It is thought that memory can be divided in four distinct temporal stages: acquisition, consolidation, retrieval, and reconsolidation. Retrieval of a memory trace can induce an additional labile phase that requires an active process named reconsolidation to stabilize memory. In the time window of reconsolidation, the use of certain behavioral and pharmacological approaches can specifically erase the retrieved memory, leaving other memories unchanged. However, we have little understanding whether a simple memory retrieval by itself can sufficiently erase the retrieved memory, without combinations of other approaches. On the basis of associative fear memory, we have conducted several experiments to investigate this issue.Associative fear conditioning is a widely used learning paradigm in the research of the neural mechanism underlying learning and memory. In this study, we trained rats in an associative fear conditioning task, during which a flash visual stimulus was used as a conditioned stimulus (CS), which was paired with a subsequent presence of electrical shock (unconditioned stimulus, US). In our experiments, animals could memorize the flash CS after the learning and exhibited freezing responses when receiving this stimulus, and this memory lasted for at least 3 weeks. We found that the subsequent memory retrieval during an early phase after learning (within 5 days) was able to erase the fear memory. The erasure effect was most significant when the memory was retrieved at day 5, an effect that was further found to be weakened by a proceeding memory retrieval conducted on day 3. The study of the above questions can deepen our understanding of the mechanism of memory extinction, consolidation and reconsolidation. Within certain time window, a simple memory retrieval by itself can sufficiently erase the retrieved memory. The neural mechanisms and clinical significance of this issue remain to be researched furtherly.As part of the limbic system, hippocampus can encode sensory information and has a temporary role in memory storage. Hippocampus can also accept the input information from the sensory cortex and sensory thalamus.Given the substantial differences in information processing between aforementioned two types of projection in the sensory system, the sensory information to hippocampal function may also differ. However, we have no ideas whether the hippocampal response to sensory stimulation receives the projection of sensory cortex. In our experiments, hippocampal CA1 local field potential (LFP) induced by visual stimuli (flash) were recored with glass electrode, exploring the dependence of the evoked activity changes on the visual cortex. The results show that inactivating the bilateral visual cortex by lidocaine (blocker of sodium channel) will lead to the significant reduction of CA1 LFP amplitude which was induced by visual stimulus, although the electrical activity has not been completely blocked. We therefore predict that hippocampal LFP response has certain dependence on sensory cortex.