Propofol enhances facial stimulation-evoked responses in the cerebellar granule cell layer via NMDA receptor activation in mice in vivo.
We recently reported that propofol depressed facial stimulation-evoked gamma-aminobutyric acid (GABA) transmission at cerebellar molecular layer interneuron-Purkinje cell (PC) synapses in mice in vivo, but facilitated excitatory parallel fiber inputs onto PCs. Here, we examine the effects of propofol on cerebellar granule cell layer (GCL) responses to facial stimulation in urethane-anesthetized mice, using electrophysiological and pharmacological methods. Cerebellar surface perfusion of propofol (50-1000μM) facilitated field potentials evoked in the cerebellar GCL by air-puff stimulation of the ipsilateral whisker pad, shown by increases in the half-width and area under the curve (AUC) of the stimulus onset response (Ron). Propofol also significantly increased the amplitude of the stimulus offset response (Roff) and Roff/Ron ratio. The propofol-induced increase in Ron AUC was dose-dependent, with a 50% effective concentration (EC50) of 242.4µM. Application of the GABAA receptor antagonist gabazine (20μM) significantly increased the amplitude, half-width, rise tau and AUC of Ron, but these parameters were further increased by additional application of propofol (300µM). Notably, application of the N-methyl-d-aspartate (NMDA) receptor blocker D-APV (250µM) significantly attenuated the half-width and AUC of Ron and the amplitude of Roff, without significantly changing the amplitude of Ron. These results indicate that propofol enhanced facial stimulation-evoked responses in the cerebellar GCL via NMDA receptor activation, which resulted in the facilitation of excitatory parallel fiber inputs onto cerebellar PCs in mice in vivo.
Cellular Function Research Center, Yanbian University, Yanji, Jilin Province, China; Department of Physiology and Pathophysiology, College of Medicine, Yanbian University, Yanji, Jilin Province, China; Department of Pain, Affiliated Hospital of Yanbian University, Yanji City, Jilin Province, China.
Wen-Zhe
WZ
Jin
Cellular Function Research Center, Yanbian University, Yanji, Jilin Province, China; Department of Physiology and Pathophysiology, College of Medicine, Yanbian University, Yanji, Jilin Province, China.
Heng
H
Liu
Department of physiology, Jilin Medical College, Jilin City, Jinlin Province, China.
Peng
P
Wan
Cellular Function Research Center, Yanbian University, Yanji, Jilin Province, China. Electronic address: cpchu@ybu.edu.cn.
Chun-Ping
CP
Chu
Cellular Function Research Center, Yanbian University, Yanji, Jilin Province, China; Department of Physiology and Pathophysiology, College of Medicine, Yanbian University, Yanji, Jilin Province, China; Key Laboratory of Natural Resource of the Changbai Mountain and Functional Molecular of the Ministry of Education, Yanbian University, Yanji City, China. Electronic address: dlqiu@ybu.edu.cn.
De-Lai
DL
Qiu
D000818:Animals; D002531:Cerebellum / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D005071:Evoked Potentials / Q000187:drug effects*; D005145:Face; D051379:Mice; D008813:Mice, Inbred ICR; D010812:Physical Stimulation; D015742:Propofol / Q000494:pharmacology*; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors / Q000378:metabolism*
D016194:Receptors, N-Methyl-D-Aspartate; D015742:Propofol
Cerebellar granule cell layer (GCL); Field potential recording; GABA(A) receptor; NMDA receptor; Propofol; Sensory stimulation