scholarly journals Mechanism for Noncompetitive Inhibition by Novel GluN2C/D N-Methyl-d-aspartate Receptor Subunit-Selective Modulators

2011 ◽  
Vol 80 (5) ◽  
pp. 782-795 ◽  
Author(s):  
Timothy M. Acker ◽  
Hongjie Yuan ◽  
Kasper B. Hansen ◽  
Katie M. Vance ◽  
Kevin K. Ogden ◽  
...  
Keyword(s):  
Receptor Subunit ◽  
Noncompetitive Inhibition ◽  
Aspartate Receptor

Expression of N-Methyl-D-Aspartate receptor subunit mRNAs in the human brain: Hippocampus and cortex

1998 ◽  
Vol 390 (1) ◽  
pp. 75-90 ◽  
Author(s):  
Clemens R. Scherzer ◽  
G. Bernhard Landwehrmeyer ◽  
Julie A. Kerner ◽  
Timothy J. Counihan ◽  
Christoph M. Kosinski ◽  
...  
Keyword(s):  
Human Brain ◽  
Receptor Subunit ◽  
Aspartate Receptor

The role of N-methyl-d -aspartate receptor subunit NR2B in spinal cord in cancer pain

2010 ◽  
Vol 14 (5) ◽  
pp. 496-502 ◽  
Author(s):  
XiaoPing Gu ◽  
Juan Zhang ◽  
ZhengLiang Ma ◽  
JunHua Wang ◽  
XiaoFang Zhou ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cancer Pain ◽  
Receptor Subunit ◽  
Aspartate Receptor

scholarly journals Intrathecal Injection of the ς1Receptor Antagonist BD1047 Blocks Both Mechanical Allodynia and Increases in Spinal NR1 Expression during the Induction Phase of Rodent Neuropathic Pain

2008 ◽  
Vol 109 (5) ◽  
pp. 879-889 ◽  
Author(s):  
Dae-Hyun Roh ◽  
Hyun-Woo Kim ◽  
Seo-Yeon Yoon ◽  
Hyoung-Sig Seo ◽  
Young-Bae Kwon ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Dorsal Horn ◽  
Mechanical Allodynia ◽  
Maintenance Phase ◽  
Spinal Cord Dorsal Horn ◽  
Induction Phase ◽  
Receptor Subunit ◽  
Aspartate Receptor ◽  
Spinal Cord Dorsal

Background Selective blockade of spinal sigma(1) receptors (Sig-1R) suppresses nociceptive behaviors in the mouse formalin test. The current study was designed to verify whether intrathecal Sig-1R antagonists can also suppress chronic neuropathic pain. Methods Neuropathic pain was produced by chronic constriction injury (CCI) of the right sciatic nerve in rats. The Sig-1R antagonist BD1047 was administered intrathecally twice daily from postoperative days 0 to 5 (induction phase of neuropathic pain) or from days 15 to 20 (maintenance phase). Western blot and immunohistochemistry were performed to determine changes in Sig-1R expression and to examine the effect of BD1047 on N-methyl-D-aspartate receptor subunit 1 expression and phosphorylation in spinal cord dorsal horn from neuropathic rats. Results BD1047 administered on postoperative days 0-5 significantly attenuated CCI-induced mechanical allodynia, but not thermal hyperalgesia, and this suppression was blocked by intrathecal administration of the Sig-1R agonist PRE084. In contrast, BD1047 treatment during the maintenance phase of neuropathic pain had no effect on mechanical allodynia. Sig-1R expression significantly increased in the ipsilateral spinal cord dorsal horn from days 1 to 3 after CCI. Importantly, BD1047 (30 nmol) administered intrathecally during the induction, but not the maintenance phase, blocked the CCI-induced increase in N-methyl-D-aspartate receptor subunit 1 expression and phosphorylation. Conclusions These results demonstrate that spinal Sig-1Rs play a critical role in both the induction of mechanical allodynia and the activation of spinal N-methyl-d-aspartate receptors in CCI rats and suggest a potential therapeutic role for the use of Sig-1R antagonists in the clinical management of neuropathic pain.

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