LAUSR

Neuronal persistent activity (PA) is a common phenomenon observed in many types of neurons. 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. PA is presumed to be associated with learning-related auditory plasticity at the cellular level. However, the mechanism is not clearly understood. Many studies have reported that muscarinic cholinergic receptor agonists inhibit muscarinic-sensitive potassium channels (M channels). Potassium influx through M channels produces potassium currents, called M currents, which play an essential role in regulating neural excitability and synaptic plasticity. 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. 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). We found that blocking M currents with XE991 depolarized the AI-L5 pyramidal neurons, which significantly increased the input resistance. The active threshold and threshold intensity were significantly reduced, indicating that the intrinsic excitability was enhanced. 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. Blocking M currents facilitated PA by increasing the plateau potential and enhancing intrinsic excitability. Our results suggested that blocking M currents might facilitate the PA in AI-L5 pyramidal neurons, which underlies auditory plasticity.