Nature Sub-Journal: The seahorse circadian clock reveals the role of time in regulating memory recovery.

Have you ever been familiar with something but suddenly can't remember it? Especially in the afternoon or in the evening, our memory seems to be controlled by people, recovering more slowly.recently, a report published in nature communications showed that memory recovery may indeed be controlled by the hippocampal clock controlled by circadian rhythm dependent transcription factor BMAL1.is a protein that regulates the expression of many other genes, and usually fluctuates between low levels before waking up (zt1-12) and high levels before going to bed (12-24).in this study, BMAL1 deficient mice and normal mice were asked to explore a new object within a few minutes, and a "recall" experiment was conducted 24 hours later.the results showed that the mice without BMAL1 were even more forgetful before waking up, which proved that the activity of BMAL1 regulated the memory recovery ability of mice.subsequently, the researchers traced the role of BMAL1 in memory retrieval to the hippocampus, and found that the memory retrieval ability of BMAL1 deficient mice was related to the down-regulation of dopamine cAMP signal in hippocampus, and the crosstalk between D1 / d5r and cAMP signal controlled by the hippocampal biological clock affected the time rule of memory retrieval, and BMAL1 mediated Da D1/ D5r and cAMP signal transduction can enhance memory retrieval by targeting GluA1 s845 phosphorylation.(circadian rhythm regulation model of memory retrieval) this study proves that the biological clock is regulating the retrieval mechanism of memory.however, the molecular mechanism of regulating memory retrieval is still unclear. If we can find a way to promote memory recovery through BMAL1 pathway, we may consider its application in the treatment of human memory retrieval defects, such as dementia and Alzheimer's disease.end References: [1] forgetfully reliable on time of day [2] hippocampalclock regulations memory retrieval via dopamine and PKA induced GluA1 phosphorylation