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PRECLINICAL PUBLICATION · 2011

Microglial Ca(2+)-activated K(+) channels are possible molecular targets for the analgesic effects of S-ketamine on neuropathic pain.

Mouse / Other

Evidence by therapy association

Study details and outcomes are extracted in the context of a specific intervention. Separate associations are retained rather than silently merged.

PMID 22131399 ↗2011Reported benefit

Microglial Ca(2+)-activated K(+) channels are possible molecular targets for the analgesic effects of S-ketamine on neuropathic pain.

MouseOtherTransgenic mice (line not stated) and cultured microgliaMaleIntrathecal administration used for charybdotoxin; route for S-ketamine not stated in abstractDuring development of tactile allodynia after nerve injury

Model: Peripheral (spinal) nerve injury producing tactile allodynia and spinal microglial hyperactivation

S-ketamine preferentially suppressed nerve injury-induced tactile allodynia and spinal microglial hyperactivation and inhibited BK currents induced by nerve injury or NS1619. Intrathecal charybdotoxin inhibited allodynia, P2X4 receptor expression and brain-derived neurotrophic factor synthesis. NS1…

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