Tolbutamide attenuates diazoxide-induced aggravation of hypoxic cell injury

Pissarek, Margit; Reichelt, C.; Krauss, Gerhard; Illéš, Peter

doi:10.1016/s0006-8993(98)01001-4

Cited by 6 publications

(3 citation statements)

References 36 publications

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“…Assuming that under physiological conditions [ATP] t in neurons makes up 80 -90% of this value (Pissarek et al 1998;Plaschke et al 1998), the estimate of [ATP] t in Retzius neurons would be in the range of 4.6 to 5.1 mM, which, considering the inaccuracies of the two methods, is in good agreement with the values estimated from the H ϩ -injection experiments.…”

Section: Intracellular Concentration Of Adenosine Phosphates In Retzisupporting

confidence: 72%

Apparent Intracellular Mg2+ Buffering in Neurons of the Leech Hirudo medicinalis

Günzel

Zimmermann

Durry

et al. 2001

Biophysical Journal

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The apparent intracellular Mg2+ buffering, or muffling (sum of processes that damp changes in the free intracellular Mg2+ concentration, [Mg2+](i), e.g., buffering, extrusion, and sequestration), was investigated in Retzius neurons of the leech Hirudo medicinalis by iontophoretic injection of H+, OH-, or Mg2+. Simultaneously, changes in intracellular pH and the intracellular Mg2+, Na+, or K+ concentration were recorded with triple-barreled ion-selective microelectrodes. Cell volume changes were monitored measuring the tetramethylammonium (TMA) concentration in TMA-loaded neurons. Control measurements were carried out in electrolyte droplets (diameter 100-200 microm) placed on a silver wire under paraffin oil. Droplets with or without ATP, the presumed major intracellular Mg2+ buffer, were used to quantify the pH dependence of Mg2+ buffering and to determine the transport index of Mg2+ during iontophoretic injection. The observed pH dependence of [Mg2+](i) corresponded to what would be expected from Mg2+ buffering through ATP. The quantity of Mg2+ muffling, however, was considerably larger than what would be expected if ATP were the sole Mg2+ buffer. From the decrease in Mg2+ muffling in the nominal absence of extracellular Na+ it was estimated that almost 50% of the ATP-independent muffling is due to the action of Na+/Mg2+ antiport.

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Section: Intracellular Concentration Of Adenosine Phosphates In Retzisupporting

confidence: 72%

Apparent Intracellular Mg2+ Buffering in Neurons of the Leech Hirudo medicinalis

Günzel

Zimmermann

Durry

et al. 2001

Biophysical Journal

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“…However, in thymocytes, Hughes and Cidlowski, [258], have shown that it is necessary but not sufficient for apoptosis to occur. Furthermore, they have shown in vitro that caspase activity is inhibited at [K + ] i which are similar to those estimated in apoptotic thymocytes (~35 mM) [260]. The question remains, 'Is the route of K + efflux important to apoptosis or is the critical factor the efflux of K + itself?'…”

Section: Potassium Channelsmentioning

confidence: 55%

“…This is in contrast to the protective role of K ATP channel activation in numerous neuronal and cardiac in vitro models of ischaemia [259][260][261][262][263]. In primary cortical murine cultures, apoptotic neuronal death, induced by either staurosporine or serum deprivation, was preceded by an increase in a TEA-sensitive K + efflux measured using whole-cell recordings [251].…”

Section: Potassium Channelsmentioning

confidence: 99%

Ion channels involved in stroke

Small

2001

Emerging Therapeutic Targets

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Ion channels are membrane proteins that flicker open and shut to regulate the flow of ions down their electrochemical gradient across the membrane and consequently regulate cellular excitability. Every living cell expresses ion channels, as they are critical life-sustaining proteins. Ion channels are generally either activated by voltage or by ligand interaction. For each group of ion channels the channels' molecular biology and biophysics will be introduced and the pharmacology of that group of channels will be reviewed. The in vitro and in vivo literature will be reviewed and, for ion channel groups in which clinical trials have been conducted, the efficacy and therapeutic potential of the neuroprotective compounds will be reviewed. A large part of this article will deal with glutamate receptors, focusing specifically on N-methyl-D-aspartate (NMDA) receptors. Although the outcome of clinical trials for NMDA receptor antagonists as therapeutics for acute stroke is disappointing, the culmination of these failed trials was preceded by a decade of efforts to develop these agents. Sodium and calcium channel antagonists will be reviewed and the newly emerging efforts to develop therapeutics targeting potassium channels will be discussed. The future development of stroke therapeutics targeting ion channels will be discussed in the context of the failures of the last decade in hopes that this decade will yield successful stroke therapeutics.

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