GluN2B-containing NMDA receptors contribute to the beneficial effects of hydrogen sulfide on cognitive and synaptic plasticity deficits in APP/PS1 transgenic mice
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文摘

Elevating hippocampal H2S ameliorates cognitive deficits in APP/PS1 mice.

H2S elevation restores hippocampal NMDAR-dependent LTP in APP/PS1 mice.

Elevation of H2S restores synaptic GluN2B expression and response in APP/PS1 mice.

Elevation of H2S enhances NMDAR-dependent signaling in APP/PS1 mice.

Blockade of GluN2B abolishes the beneficial effects of H2S elevation in APP/PS1 mice.

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