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 i...
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Published in | European journal of pharmacology Vol. 843; pp. 126 - 133 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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Elsevier B.V
15.01.2019
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Abstract | 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 μM. Application of either a selective α4β2 nicotinic acetylcholine receptors antagonist, DHβE (1 μM) or a selective α7 nicotinic acetylcholine receptors antagonist, MLA (1 μM) 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 α7 and α4β2 nicotinic acetylcholine receptor subunits abolished the nicotine-induced increase in the amplitude of N1. These results indicate that nicotine activates α7 and α4β2 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 α7 and α4β2 subunits nicotinic acetylcholine receptors. |
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AbstractList | 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 (EC
) of 32.6 μM. Application of either a selective α4β2 nicotinic acetylcholine receptors antagonist, DHβE (1 μM) or a selective α7 nicotinic acetylcholine receptors antagonist, MLA (1 μM) 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 α7 and α4β2 nicotinic acetylcholine receptor subunits abolished the nicotine-induced increase in the amplitude of N1. These results indicate that nicotine activates α7 and α4β2 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 α7 and α4β2 subunits nicotinic acetylcholine receptors. 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 μM. Application of either a selective α4β2 nicotinic acetylcholine receptors antagonist, DHβE (1 μM) or a selective α7 nicotinic acetylcholine receptors antagonist, MLA (1 μM) 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 α7 and α4β2 nicotinic acetylcholine receptor subunits abolished the nicotine-induced increase in the amplitude of N1. These results indicate that nicotine activates α7 and α4β2 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 α7 and α4β2 subunits nicotinic acetylcholine receptors. |
Author | Xu, Yin-Hua Qiu, De-Lai Cui, Song-Biao Chu, Chun-Ping Zhang, Bin-Bin Su, Wen-Hao Li, Yu-Zi Bing, Yan-Hua Wu, Mao-Cheng |
Author_xml | – sequence: 1 givenname: Yin-Hua surname: Xu fullname: Xu, Yin-Hua organization: Key Laboratory of Cellular Function and Pharmacology of Jilin Province, Yanbian University, Yanji, Jilin Province, China – sequence: 2 givenname: Bin-Bin surname: Zhang fullname: Zhang, Bin-Bin organization: Key Laboratory of Cellular Function and Pharmacology of Jilin Province, Yanbian University, Yanji, Jilin Province, China – sequence: 3 givenname: Wen-Hao surname: Su fullname: Su, Wen-Hao organization: Department of Neurology, Affiliated Hospital of Yanbian University, Yanji, Jilin Province, China – sequence: 4 givenname: Mao-Cheng surname: Wu fullname: Wu, Mao-Cheng organization: Key Laboratory of Cellular Function and Pharmacology of Jilin Province, Yanbian University, Yanji, Jilin Province, China – sequence: 5 givenname: Yan-Hua surname: Bing fullname: Bing, Yan-Hua organization: Key Laboratory of Cellular Function and Pharmacology of Jilin Province, Yanbian University, Yanji, Jilin Province, China – sequence: 6 givenname: Song-Biao surname: Cui fullname: Cui, Song-Biao organization: Department of Neurology, Affiliated Hospital of Yanbian University, Yanji, Jilin Province, China – sequence: 7 givenname: Chun-Ping surname: Chu fullname: Chu, Chun-Ping organization: Key Laboratory of Cellular Function and Pharmacology of Jilin Province, Yanbian University, Yanji, Jilin Province, China – sequence: 8 givenname: Yu-Zi surname: Li fullname: Li, Yu-Zi email: liyuzi@ybu.edu.cn organization: Department of Cardiology, Affiliated Hospital of Yanbian University, Yanji, Jilin Province, China – sequence: 9 givenname: De-Lai surname: Qiu fullname: Qiu, De-Lai email: dlqiu@ybu.edu.cn organization: Key Laboratory of Cellular Function and Pharmacology of Jilin Province, Yanbian University, Yanji, Jilin Province, China |
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Keywords | Sensory stimulation Cerebellar granule cell layer Nicotinic acetylcholine receptors Field potential recording |
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SubjectTerms | Animals Cerebellar granule cell layer Cerebellum - cytology Cerebellum - physiology Face Female Field potential recording Male Mice, Inbred ICR Nicotine - pharmacology Nicotinic acetylcholine receptors Nicotinic Agonists - pharmacology Physical Stimulation Receptors, Nicotinic - physiology Sensory stimulation Synaptic Transmission |
Title | Nicotine modulates the facial stimulation-evoked responses in cerebellar granule cell layer in vivo in mice |
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