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Neurotransmitters modulate sodium channel availability through activation of G protein-coupled receptors,cAMP-dependent protein kinase (PKA),and protein kinase C (PKC).Voltage-dependent slow inactivation also controls sodium channel availability,synaptic integration,and neuronal firing.Here we show by analysis of sodium channel mutants that neuromodulation via PKA and PKC enhances intrinsic slow inactivation of sodium channels,making them unavailable for activation.