Our results suggested that blocking M currents might facilitate the PA in AI-L5 pyramidal neurons, which underlies auditory plasticity. Blocking M currents facilitated PA by increasing the plateau potential and enhancing intrinsic excitability. Our results also showed that blocking M currents with XE991 switched the neuronal firing patterns in the AI-L5 pyramidal neurons from regular spiking to intrinsic bursting. The active threshold and threshold intensity were significantly reduced, indicating that intrinsic excitability was enhanced. We found that blocking M currents with XE991 depolarized the AI-L5 pyramidal neurons, which significantly increased the input resistance. We used in vitro whole cell patch-clamp recordings in isolated mouse brain slices to investigate the effects of M currents on the PA in pyramidal neurons in layer V of the primary auditory cortex (AI-L5). Further study is needed to determine whether M currents affect the PA of auditory central neurons and provide additional analysis of the variations in electrophysiological properties. Potassium efflux through M channels produces potassium currents, called M currents, that play an essential role in regulating neural excitability and synaptic plasticity. Many studies have reported that muscarinic receptor agonists inhibit muscarinic-sensitive potassium channels (M channels). However, the mechanism is not clearly understood.
PA is presumed to be associated with learning-related auditory plasticity at the cellular level.
PA can be induced in neurons in the mouse auditory nucleus by activating cholinergic receptors with carbachol (CCh), a dual muscarinic and nicotinic receptor agonist.
Neuronal persistent activity (PA) is a common phenomenon observed in many types of neurons.
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