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Propofol facilitates excitatory inputs of cerebellar Purkinje cells by depressing molecular layer interneuron activity during sensory information processing in vivo in mice

He, Yuan-Yuana,b,*; Jin, Ria,c,*; Jin, Wen-Zhea,d; Liu, Henga,b; Chu, Chun-Pinga; Qiu, De-Laia,b

doi: 10.1097/WNR.0000000000000449
CELLULAR, MOLECULAR AND DEVELOPMENTAL NEUROSCIENCE

Propofol is a rapid-acting sedative-hypnotic medication that has been widely used for the induction and maintenance of anesthesia; it has specific actions on different areas of the brain, such as sensory information transmission in the somatosensory cortex. However, the effects of propofol on the properties of sensory stimulation-evoked responses in cerebellar Purkinje cells (PCs) are currently unclear. In the present study, we studied the effects of propofol on facial stimulation-evoked responses in cerebellar PCs and molecular level interneurons (MLIs) in urethane-anesthetized mice using electrophysiological and pharmacological methods. Our results showed that cerebellar surface perfusion with propofol induced a decrease in the amplitude of the gamma-aminobutyric acid (GABA)-ergic component (P1) in a dose-dependent manner, but induced a significant increase in the amplitude of the excitatory response (N1). The IC50 of propofol-induced inhibition of P1 was 217.3 μM. In contrast, propofol (100 μM) depressed the spontaneous activity and tactile-evoked responses in MLIs. In addition, blocking GABAA receptor activity abolished the propofol (300 μM)-induced inhibition of the tactile-evoked inhibitory response and the increase in the sensory stimulation-evoked spike firing rate of PCs. These results indicated that propofol depressed the tactile stimulation-evoked spike firing of MLIs, resulting in a decrease in the amplitude of the tactile-evoked inhibitory response and an increase in the amplitude of the excitatory response in the cerebellar PCs of mice. Our results suggest that propofol modulates sensory information processing in cerebellar cortical PCs and MLIs through the activation of GABAA receptors.

aCellular Function Research Center

bDepartment of Physiology and Pathophysiology, College of Medicine, Yanbian University

cDepartment of Osteology

dDepartment of Pain, Affiliated Hospital of Yanbian University, Yanji City, Jilin Province, China

* Yuan-Yuan He and Ri Jin contributed equally to the writing of this article.

Correspondence to De-Lai Qiu, MD, PhD, Cellular Function Research Center, YanBian University, 977, GongYuan Road, Yanji City, Jilin Province, China Tel: +86 433 243 5050; fax: +86 433 243 5051; e-mail: cpchu@ybu.edu.cn

Received August 4, 2015

Accepted August 6, 2015

© 2015 Wolters Kluwer Health | Lippincott Williams & Wilkins