Suppression of the nociceptive jaw-opening reflex by stimulation of the red nucleus

2012 ◽  
Vol 1473 ◽  
pp. 124-130 ◽  
Author(s):  
Eriko Yajima ◽  
Yoshihide Satoh ◽  
Ken’Ichi Ishizuka ◽  
Shin-ichi Iwasaki ◽  
Kazuto Terada
2006 ◽  
Vol 1083 (1) ◽  
pp. 145-150 ◽  
Author(s):  
Yoshihide Satoh ◽  
Ken'Ichi Ishizuka ◽  
Diana Oskutyte ◽  
Toshiki Murakami

2013 ◽  
Vol 97 ◽  
pp. 24-31 ◽  
Author(s):  
Yoshihide Satoh ◽  
Eriko Yajima ◽  
Ken’Ichi Ishizuka ◽  
Yasuhiro Nagamine ◽  
Shin-ichi Iwasaki

2016 ◽  
Vol 110 ◽  
pp. 29-36 ◽  
Author(s):  
Yoshihide Satoh ◽  
Ken’Ichi Ishizuka ◽  
Mutsumi Takahashi ◽  
Shin-ichi Iwasaki

2011 ◽  
Vol 1391 ◽  
pp. 44-53 ◽  
Author(s):  
Takako Fukuhara ◽  
Takanori Tsujimura ◽  
Yuka Kajii ◽  
Kensuke Yamamura ◽  
Makoto Inoue

2004 ◽  
Vol 92 (6) ◽  
pp. 3332-3337 ◽  
Author(s):  
Jens Ellrich

Long-term depression (LTD) of somatosensory processing has been demonstrated in slice preparations of the spinal dorsal horn. Although LTD could be reliably induced in vitro, inconsistent results were encountered when the same types of experiments were conducted in adult animals in vivo. We addressed the hypothesis that LTD of orofacial sensorimotor processing can be induced in mice under general anesthesia. The effects of electric low- and high-frequency conditioning stimulation of the tongue on the sensorimotor jaw-opening reflex (JOR) elicited by electric tongue stimulation were investigated. Low-frequency stimulation induced a sustained decrease of the reflex integral for ≥1 h after the end of conditioning stimulation. After additional high-frequency stimulation, the reflex partly recovered from LTD. High-frequency stimulation alone induced a transient increase of the JOR integral for <10 min. The LTD of the sensorimotor jaw-opening reflex in anesthetized mice may be an appropriate model to investigate the central mechanisms and the pharmacology of synaptic plasticity in the orofacial region. The application of electrophysiological techniques in mice provides the opportunity to include adequate knock-out models to elucidate the neurobiology of LTD.


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