Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1073/pnas.0701149104 http://scihub22266oqcxt.onion/10.1073/pnas.0701149104 C2042205!2042205!17913893     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Proc+Natl+Acad+Sci+U+S+A 2007 ; 104 (41): 16323-8 Nephropedia Template TP {{tp|p=17913893|t=2007. TRPM7 channels in hippocampal neurons detect levels of extracellular divalent cations |pdf=|usr=}}{{17913893}} gab.com Text TRPM7 channels in hippocampal neurons detect levels of extracellular divalent cations JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=17913893 #FOAvip Exposure to low Ca2+ and/or Mg2+ is tolerated by cardiac myocytes, astrocytes, and neurons, but restoration to normal divalent cation levels paradoxically causes Ca2+ overload and cell death. This phenomenon has been called the ?Ca2+ paradox? of ischemia?reperfusion. The mechanism by which a decrease in extracellular Ca2+ and Mg2+ is ?detected? and triggers subsequent cell death is unknown. Transient periods of brain ischemia are characterized by substantial decreases in extracellular Ca2+ and Mg2+ that mimic the initial condition of the Ca2+ paradox. In CA1 hippocampal neurons, lowering extracellular divalents stimulates a nonselective cation current. We show that this current resembles TRPM7 currents in several ways. Both (i) respond to transient decreases in extracellular divalents with inward currents and cell excitation, (ii) demonstrate outward rectification that depends on the presence of extracellular divalents, (iii) are inhibited by physiological concentrations of intracellular Mg2+, (iv) are enhanced by intracellular phosphatidylinositol 4,5-bisphosphate (PIP2), and (v) can be inhibited by G?q-linked G protein-coupled receptors linked to phospholipase C ?1-induced hydrolysis of PIP2. Furthermore, suppression of TRPM7 expression in hippocampal neurons strongly depressed the inward currents evoked by lowering extracellular divalents. Finally, we show that activation of TRPM7 channels by lowering divalents significantly contributes to cell death. Together, the results demonstrate that TRPM7 contributes to the mechanism by which hippocampal neurons ?detect? reductions in extracellular divalents and provide a means by which TRPM7 contributes to neuronal death during transient brain ischemia. Twit Text FOAVip TRPM7 channels in hippocampal neurons detect levels of extracellular divalent cations ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=17913893 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=17913893 #FOAvip English Wikipedia <ref>{{Cite pmid|17913893}}</ref> TRPM7 channels in hippocampal neurons detect levels of extracellular divalent cations #MMPMID17913893 Wei WL; Sun HS; Olah ME; Sun X; Czerwinska E; Czerwinski W; Mori Y; Orser BA; Xiong ZG; Jackson MF; Tymianski M; MacDonald JF Proc Natl Acad Sci U S A 2007[Oct]; 104 (41): 16323-8 PMID17913893show ga Exposure to low Ca2+ and/or Mg2+ is tolerated by cardiac myocytes, astrocytes, and neurons, but restoration to normal divalent cation levels paradoxically causes Ca2+ overload and cell death. This phenomenon has been called the ?Ca2+ paradox? of ischemia?reperfusion. The mechanism by which a decrease in extracellular Ca2+ and Mg2+ is ?detected? and triggers subsequent cell death is unknown. Transient periods of brain ischemia are characterized by substantial decreases in extracellular Ca2+ and Mg2+ that mimic the initial condition of the Ca2+ paradox. In CA1 hippocampal neurons, lowering extracellular divalents stimulates a nonselective cation current. We show that this current resembles TRPM7 currents in several ways. Both (i) respond to transient decreases in extracellular divalents with inward currents and cell excitation, (ii) demonstrate outward rectification that depends on the presence of extracellular divalents, (iii) are inhibited by physiological concentrations of intracellular Mg2+, (iv) are enhanced by intracellular phosphatidylinositol 4,5-bisphosphate (PIP2), and (v) can be inhibited by G?q-linked G protein-coupled receptors linked to phospholipase C ?1-induced hydrolysis of PIP2. Furthermore, suppression of TRPM7 expression in hippocampal neurons strongly depressed the inward currents evoked by lowering extracellular divalents. Finally, we show that activation of TRPM7 channels by lowering divalents significantly contributes to cell death. Together, the results demonstrate that TRPM7 contributes to the mechanism by which hippocampal neurons ?detect? reductions in extracellular divalents and provide a means by which TRPM7 contributes to neuronal death during transient brain ischemia. äTRPM7 channels in hippocampal neurons detect levels of extracellular d(epmc).pdf DeepDyve Pubget Overpricing