Effects of MK-801 on the expression of serine racemase and d-amino acid oxidase mRNAs and on the d-serine levels in rat brain

2007 ◽  
Vol 555 (1) ◽  
pp. 17-22 ◽  
Author(s):  
Atsushi Hashimoto ◽  
Masanobu Yoshikawa ◽  
Hidehiro Andoh ◽  
Hiroshi Yano ◽  
Hideo Matsumoto ◽  
...  
2006 ◽  
Vol 540 (1-3) ◽  
pp. 82-86 ◽  
Author(s):  
Kazuhide Takeyama ◽  
Masanobu Yoshikawa ◽  
Tetsuo Oka ◽  
Mitsuru Kawaguchi ◽  
Toshiyasu Suzuki ◽  
...  

2004 ◽  
Vol 131 (1-2) ◽  
pp. 141-144 ◽  
Author(s):  
Masanobu Yoshikawa ◽  
Tetsuo Oka ◽  
Mitsuru Kawaguchi ◽  
Atsushi Hashimoto

2005 ◽  
Vol 525 (1-3) ◽  
pp. 94-97 ◽  
Author(s):  
Masanobu Yoshikawa ◽  
Hidehiro Andoh ◽  
Kenji Ito ◽  
Toshiyasu Suzuki ◽  
Mitsuru Kawaguchi ◽  
...  

Author(s):  
Hong Wei ◽  
Zuyue Chen ◽  
Ari Koivisto ◽  
Antti Pertovaara

Abstract Background Earlier studies show that endogenous sphingolipids can induce pain hypersensitivity, activation of spinal astrocytes, release of proinflammatory cytokines and activation of TRPM3 channel. Here we studied whether the development of pain hypersensitivity induced by sphingolipids in the spinal cord can be prevented by pharmacological inhibition of potential downstream mechanisms that we hypothesized to include TRPM3, σ1 and NMDA receptors, gap junctions and D-amino acid oxidase. Methods Experiments were performed in adult male rats with a chronic intrathecal catheter for spinal drug administrations. Mechanical nociception was assessed with monofilaments and heat nociception with radiant heat. N,N-dimethylsphingosine (DMS) was administered to induce pain hypersensitivity. Ononetin, isosakuranetin, naringenin (TRPM3 antagonists), BD-1047 (σ1 receptor antagonist), carbenoxolone (a gap junction decoupler), MK-801 (NMDA receptor antagonist) and AS-057278 (inhibitor of D-amino acid oxidase, DAAO) were used to prevent the DMS-induced hypersensitivity, and pregnenolone sulphate (TRPM3 agonist) to recapitulate hypersensitivity. Results DMS alone produced within 15 min a dose-related mechanical hypersensitivity that lasted at least 24 h, without effect on heat nociception. Preemptive treatments with ononetin, isosakuranetin, naringenin, BD-1047, carbenoxolone, MK-801 or AS-057278 attenuated the development of the DMS-induced hypersensitivity, but had no effects when administered alone. Pregnenolone sulphate (TRPM3 agonist) alone induced a dose-related mechanical hypersensitivity that was prevented by ononetin, isosakuranetin and naringenin. Conclusions Among spinal pronociceptive mechanisms activated by DMS are TRPM3, gap junction coupling, the σ1 and NMDA receptors, and DAAO.


2021 ◽  
Vol 1751 ◽  
pp. 147202
Author(s):  
Shunsuke Takagi ◽  
Darrick T. Balu ◽  
Joseph T. Coyle

2007 ◽  
Vol 26 (6) ◽  
pp. 1657-1669 ◽  
Author(s):  
Louise Verrall ◽  
Mary Walker ◽  
Nancy Rawlings ◽  
Isabel Benzel ◽  
James N. C. Kew ◽  
...  

2014 ◽  
Vol 5 (9) ◽  
pp. 848-854 ◽  
Author(s):  
Gabriel E. Romero ◽  
Amber D. Lockridge ◽  
Catherine W. Morgans ◽  
Dipankar Bandyopadhyay ◽  
Robert F. Miller

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