Taken together, our findings suggest that, in C280/289V mice, the abnormal increase in presynaptic release probability in the resting-state caused invalid activation of the postsynaptic release, which displayed an increasing trend in phosphorylation level, leading to receptor desensitization and difficulty in further activation.
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S-nitros(yl)ation of CaMKIIα and its precision redox regulation by SNOTAC plays a critical role in learning and memory.
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