Review demonstrates translational control impacts memory in excitatory and inhibitory neurons, suggesting implications for neurological disorders.
Synaptic plasticity and memory formation require de novo protein synthesis. The mechanistic/mammalian target of rapamycin complex 1 (mTORC1) promotes mRNA translation initiation in the central nervous system. Recent research has uncovered that excitatory neurons, inhibitory neurons, and glia play distinct roles in modulating synaptic strength and encoding long‐term memory via mTORC1 signaling. In this review, we discuss the mechanisms by which mTORC1 regulates translation initiation in the brain and its cell type‐specific roles in shaping distinct forms of synaptic plasticity and memory. We also consider how dysregulated translational control contributes to neurological disorders and explore emerging technologies for therapeutic modulation of the mTORC1 pathway.
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Huang et al. (2025) studied this question.
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