Potentiation by calcium ions of [3H]MK-801 binding to an ion channel associated with the N-methyl-d-aspartate receptor complex in rat brain

1995 ◽  
Vol 26 (1) ◽  
pp. 59-68 ◽  
Author(s):  
Daiken Han ◽  
Kiyokazu Ogita ◽  
Yukio Yoneda
Keyword(s):  
Ion Channel ◽  
Rat Brain ◽  
Calcium Ions ◽  
Receptor Complex ◽  
Mk 801 ◽  
Aspartate Receptor

scholarly journals Ion Channel Involvement in Anoxic Depolarization Induced by Cardiac Arrest in Rat Brain

1995 ◽  
Vol 15 (4) ◽  
pp. 587-594 ◽  
Author(s):  
Yaxia Xie ◽  
Elke Zacharias ◽  
Patricia Hoff ◽  
Frank Tegtmeier
Keyword(s):  
Cardiac Arrest ◽  
Ion Channel ◽  
Rat Brain ◽  
Ion Homeostasis ◽  
Rapid Decline ◽  
Channel Blockers ◽  
Mk 801 ◽  
Anoxic Depolarization ◽  
Ion Activity ◽  
Cellular Ca

Anoxic depolarization (AD) and failure of ion homeostasis play an important role in ischemia-induced neuronal injury. In the present study, different drugs with known ion-channel-modulating properties were examined for their ability to interfere with cardiac-arrest-elicited AD and with the changes in the extracellular ion activity in rat brain. Our results indicate that only drugs primarily blocking membrane Na+ permeability (NBQX, R56865, and flunarizine) delayed the occurrence of AD, while compounds affecting cellular Ca2+ load (MK-801 and nimodipine) did not influence the latency time. The ischemia-induced [Na+]e reduction was attenuated by R56865. Blockade of the ATP-sensitive K+ channels with glibenclamide reduced the [K+]e increase upon ischemia, indicating an involvement of the KATP channels in ischemia-induced K+ efflux. The KATP channel opener cromakalim did not affect the AD or the [K+]e concentration. The ischemia-induced rapid decline of extracellular calcium was attenuated by receptor-operated Ca2+ channel blockers MK-801 and NBQX, but not by the voltage-operated Ca2+ channel blocker nimodipine, R56865, and flunarizine.

(+)-3-[123I]Iodo-MK-801: Synthesis and characterization of binding to the N-methyl-D-aspartate receptor complex

Life Sciences ◽  
1990 ◽  
Vol 46 (15) ◽  
pp. 1103-1110 ◽  
Author(s):  
Richard W. Ransom ◽  
Wai-si Eng ◽  
H.Donald Burns ◽  
Raymond E. Gibson ◽  
Howard F. Solomon
Keyword(s):  
Synthesis And Characterization ◽  
Receptor Complex ◽  
Mk 801 ◽  
Aspartate Receptor

Alterations in the N-Methyl-D-Aspartate Receptor Complex following Focal Cerebral Ischemia

1989 ◽  
Vol 9 (5) ◽  
pp. 709-712 ◽  
Author(s):  
D. Dewar ◽  
M. C. Wallace ◽  
A. Kurumaji ◽  
J. McCulloch
Keyword(s):  
Cerebral Cortex ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Artery Occlusion ◽  
Receptor Complex ◽  
Ischemic Insult ◽  
Mk 801 ◽  
Aspartate Receptor ◽  
Cerebral Artery Occlusion ◽  
The Brain

The functional integrity of the N-methyl-d-aspartate receptor complex following focal cerebral ischemia in the rat has been examined at a time when brain tissue is irreversibly damaged. Twelve hours after unilateral permanent middle cerebral artery occlusion, [3H]-MK-801 binding was not significantly altered in the ischemic cerebral cortex compared to sham-operated animals. Moreover, the enhancement of [3H]MK-801 binding by exogenous glutamate was preserved in an area of the brain that was permanently damaged by the ischemic insult.

Sign in / Sign up

Export Citation Format

Share Document