Alternative TitleNicotinic regulation of tone-evoked flavoprotein autofluorescence responses and neural circuits of thalamorecipient layers in mouse auditory cortex
Note (General)Systemic nicotine administration regulates neuronal activities in mouse auditory cortex but how nicotine regulates the spread of the activities across auditory cortical areas is not well known. We investigated this phenomenon by using flavoprotein fluorescence imaging. Nicotine exposure expanded the activated area and enhanced sound-evoked fluorescence intensity at optimal frequency peak site in AI. Intracortical administration of DHβE, an inhibitor of nicotine acetylcholine receptors composed of α4 and β2 subunits (α4β2*-nAChR), blocked nicotine-induced enhancement in the fluorescence intensity peak site, but it did not affect to the expansion of activated area. In the primary auditory system, acute nicotine exposure is known to induce sensory filtering to synchronize thalamocortical axon excitability and increase synaptic activity in AI. However, cell type and mechanism of nicotinic regulation remains unclear. We prepared in vitro auditory thalamocortical slice and investigated reduction of thalamocortical-indued action potentials in excitatory neurons in the thalamorecepient layer in AI. Moreover, we revealed a reduction in thalamocortical input to fast-spiking (FS) inhibitory cells, but not significant reduction in direct inhibitory postsynaptic potentials (IPSCs) onto cortical excitatory cells. Additionally, thalamocortical induced excitatory and inhibitory balance shifted towards excitatory dominance. These results suggest that nicotine exposure reduced cortical circuit activity but consequently increase excitatory dominance.
Collection (particular)国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文
Date Accepted (W3CDTF)2023-10-11T15:41:07+09:00
Data Provider (Database)国立国会図書館 : 国立国会図書館デジタルコレクション