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Early postsynaptic potentiation in hippocampal somatostatin interneurons is mTORC1-dependent and disrupted in Fmr1−/y mice
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DOI：10.1016/j.neuroscience.2025.12.033.png)
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Abstract
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• Rapamycin prevents early synaptic potentiation (SP) in somatostatin interneurons. • mTORC1 is necessary for early SP in somatostatin interneurons. • Intrinsic excitability does not change during early SP in somatostatin interneurons. • Early SP in somatostatin interneurons is dysregulated in Fmr1−/y mice. • Excitatory synaptic currents are reduced in somatostatin interneurons in Fmr1−/y mice.
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