Key result
Anoxia induced a sustained outward current and hyperpolarization in 40% of dorsal vagal neurons, which was mediated by the activation of ATP-sensitive K+ (KATP) channels.
The sustained anoxia-induced outward current in rat dorsal vagal neurons is mediated by the activation of ATP-sensitive K+ (KATP) channels.
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No immediate clinical implications; leaves open KATP role in human anoxic vagal neuron responses.
Trapp et al. (1995) studied Anoxia (n=142). Anoxia vs. Baseline/normoxia was evaluated on Anoxia-induced outward current (AOC). Anoxia induced a sustained outward current and hyperpolarization in 40% of dorsal vagal neurons, which was mediated by the activation of ATP-sensitive K+ (KATP) channels.
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