Abstract
Release of acetylcholine (ACh) in neocortex is important for learning, memory and attention tasks. The primary source of ACh in neocortex is axons ascending from the basal forebrain. Release of ACh from these axons evokes changes in the cortical local field potential (LFP), including a decline in low-frequency spectral power that is often referred to as desynchronization of the LFP and is thought to result from the activation of muscarinic ACh receptors. Using channelrhodopsin-2, we selectively stimulated the axons of only cholinergic basal forebrain neurons in primary somatosensory cortex of the urethane-anesthetized mouse while monitoring the LFP. Cholinergic stimulation caused desynchronization and two brief increases in higher-frequency power at stimulus onset and offset. Desynchronization (1-6 Hz) was localized, extending ≤ 1 mm from the edge of stimulation, and consisted of both nicotinic and muscarinic receptor-mediated components that were inhibited by mecamylamine and atropine, respectively. Hence we have identified a nicotinic receptor-mediated component to desynchronization. The increase in higher-frequency power (>10 Hz) at stimulus onset was also mediated by activation of nicotinic and muscarinic receptors. However, the increase in higher-frequency power (10-20 Hz) at stimulus offset was evoked by activation of muscarinic receptors and inhibited by activation of nicotinic receptors. We conclude that the activation of nicotinic and muscarinic ACh receptors in neocortex exerts several effects that are reflected in distinct frequency bands of the cortical LFP in urethane-anesthetized mice.