Nicotine modulates the facial stimulation-evoked responses in cerebellar granule cell layer in vivo in mice

Nicotinic acetylcholine receptors are cationic channels that mediate fast excitatory transmission in the central nervous system. Several nicotinic acetylcholine receptor subunits have been detected within cerebellar granule cell layer (GCL), and activation of these receptors may have a significant influence on neuronal synaptic transmission of the cerebellum. The aim of present study was to better understand the roles of nicotinic acetylcholine receptors during the sensory stimulation-evoked synaptic transmission in the cerebellar GCL. Our results showed that cerebellar surface perfusion of nicotine significantly facilitated the cerebellar GCL field potential responses evoked by air-puff stimulation of ipsilateral whisker pad, which exhibited increases in amplitude and area under the curve (AUC) of both stimulus onset responses (N1) and stimulus offset responses (N2). The nicotine-induced increase in AUC of facial stimulation-evoked N1 was dose-dependent with a 50% effective concentration (EC50) of 32.6 mu M. Application of either a selective alpha 4 beta 2 nicotinic acetylcholine receptors antagonist, DH beta E (1 mu M) or a selective alpha 7 nicotinic acetylcholine receptors antagonist, MLA (1 mu M) alone attenuated, but not completely abolished the nicotine-induced increases in the amplitude and AUC of the facial stimulation-evoked N1. However, simultaneous blockade of alpha 7 and alpha 4 beta 2 nicotinic acetylcholine receptor subunits abolished the nicotine-induced increase in the amplitude of N1. These results indicate that nicotine activates alpha 7 and alpha 4 beta 2 nicotinic acetylcholine receptor subunits, resulting in an enhancement of facial stimulation - evoked responses in mouse cerebellar GCL. Our results suggest that nicotine modulates the sensory information processing in the cerebellar GCL through alpha 7 and alpha 4 beta 2 subunits nicotinic acetylcholine receptors.