On-Line Microdialysis-Graphite Furnace Atomic Absorption Spectrometry in the Determination of Brain Magnesium Levels in Gerbils Subjected to Cerebral Ischemia/Reperfusion

Lin, Ming‐Cheng; Huang, Yeou‐Lih; Liu, Hong‐Wen; Yang, Dar-Yu; Lee, Chien-Pin; Yang, Lin‐Lan; Cheng, Fu‐Chou

doi:10.1080/07315724.2004.10719404

Cited by 28 publications

(25 citation statements)

References 17 publications

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“…Although this regulation has been proposed to control opening of hemichannels under normal conditions (298) it might be more prominent under pathological conditions. In agreement with this possibility, an ∼10-fold reduction in extracellular concentration of divalent cations (Ca 2+ and Mg 2+ ) occurs in ischemic brain (187, 188, 210, 264). Moreover, in low [Ca 2+ ] o , biologically relevant signaling molecules ( e.g.…”

Section: Introductionmentioning

confidence: 53%

Modulation of Brain Hemichannels and Gap Junction Channels by Pro-Inflammatory Agents and Their Possible Role in Neurodegeneration

Orellana

Saéz

Shoji

et al. 2009

Antioxidants & Redox Signaling

204

190

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In normal brain, neurons, astrocytes, and oligodendrocytes, the most abundant and active cells express pannexins and connexins, protein subunits of two families forming membrane channels. Most available evidence indicates that in mammals endogenously expressed pannexins form only hemichannels and connexins form both gap junction channels and hemichannels. Whereas gap junction channels connect the cytoplasm of contacting cells and coordinate electric and metabolic activity, hemichannels communicate the intra- and extracellular compartments and serve as a diffusional pathway for ions and small molecules. A subthreshold stimulation by acute pathological threatening conditions (e.g., global ischemia subthreshold for cell death) enhances neuronal Cx36 and glial Cx43 hemichannel activity, favoring ATP release and generation of preconditioning. If the stimulus is sufficiently deleterious, microglia become overactivated and release bioactive molecules that increase the activity of hemichannels and reduce gap junctional communication in astroglial networks, depriving neurons of astrocytic protective functions, and further reducing neuronal viability. Continuous glial activation triggered by low levels of anomalous proteins expressed in several neurodegenerative diseases induce glial hemichannel and gap junction channel disorders similar to those of acute inflammatory responses triggered by ischemia or infectious diseases. These changes are likely to occur in diverse cell types of the CNS and contribute to neurodegeneration during inflammatory process. Antiox. Redox Signal. 11, 369–399.

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Section: Introductionmentioning

confidence: 53%

Modulation of Brain Hemichannels and Gap Junction Channels by Pro-Inflammatory Agents and Their Possible Role in Neurodegeneration

Orellana

Saéz

Shoji

et al. 2009

Antioxidants & Redox Signaling

204

190

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“…These occur as a result of the excitotoxic release of glutamate and consequent membrane depolarization, which act in concert to activate two major influx pathways for Ca 2ϩ , namely NMDA receptors and voltage-dependent Ca 2ϩ channels (3)(4)(5). A large reduction in the extracellular concentration of Mg 2ϩ (6) was recently shown to occur in the ischemic brain, confirming that both extracellular Ca 2ϩ and Mg 2ϩ are simultaneously reduced. The precise mechanism by which neurons respond to changes in the extracellular concentration of divalent cations remains unclear.…”

mentioning

confidence: 73%

TRPM7 channels in hippocampal neurons detect levels of extracellular divalent cations

Wei¹,

Sun

Olah³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

100

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Exposure to low Ca 2؉ and/or Mg 2؉ is tolerated by cardiac myocytes, astrocytes, and neurons, but restoration to normal divalent cation levels paradoxically causes Ca 2؉ overload and cell death. This phenomenon has been called the ''Ca 2؉ paradox'' of ischemiareperfusion. The mechanism by which a decrease in extracellular Ca 2؉ and Mg 2؉ is ''detected'' and triggers subsequent cell death is unknown. Transient periods of brain ischemia are characterized by substantial decreases in extracellular Ca 2؉ and Mg 2؉ that mimic the initial condition of the Ca 2؉ 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 Mg 2؉ , (iv) are enhanced by intracellular phosphatidylinositol 4,5-bisphosphate (PIP 2), 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.calcium paradox ͉ divalent cation sensing ͉ siRNA ͉ ischemia

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“…Furthermore, the higher atom density and longer residence time in the graphite tube improve ETAAS detection limits by a factor of up to 1,000-fold-down to the submicrogram-per-liter range-compared to flame AAS. In view of its advantages, several on-line and off-line methods based on the combination of microdialysis sampling and ETAAS have been developed for in vivo determination of Zn, Mn, Cu, Fe, and Pt (cisplatin) (Nakashima et al, 1997;Tokunaga et al, 2000;Leveque et al, 2001Leveque et al, , 2003Lin et al, 2004Yang et al, 2004). Because only small-volume microdialysates that contain very low concentrations of analyte ions are required for analyses, and because it always takes a long time to collect the data for biokinetics studies for in vivo animal experiments, the resulting reduction in contamination and losses of analyte species and minimized complexity of the operation procedures are key factors that lead to the attractiveness of in vivo determination of trace metal ions.…”

Section: Atomic Spectrometric Detectionmentioning

confidence: 99%

In vivomonitoring of the transfer kinetics of trace elements in animal brains with hyphenated inductively coupled plasma mass spectrometry techniques

Su¹,

Sun²,

Tzeng³

et al. 2009

Mass Spectrom. Rev.

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The roles of metal ions to sustain normal function and to cause dysfunction of neurological systems have been confirmed by various studies. However, because of the lack of adequate analytical method to monitor the transfer kinetics of metal ions in the brain of a living animal, research on the physiopathological roles of metal ions in the CNS remains in its early stages and more analytical efforts are still needed. To explicitly model the possible links between metal ions and physiopathological alterations, it is essential to develop in vivo monitoring techniques that can bridge the gap between metalloneurochemistry and neurophysiopathology. Although inductively coupled plasma mass spectrometry (ICP-MS) is a very powerful technique for multiple trace element analyses, when dealing with chemically complex microdialysis samples, the detection capability is largely limited by instrumental sensitivity, selectivity, and contamination that arise from the experimental procedure. As a result, in recent years several high efficient and clean on-line sample pretreatment systems have been developed and combined with microdialysis and ICP-MS for the continuous and in vivo determination of the concentration-time profiles of metal ions in the extracellular space of rat brain. This article reviews the research relevant to the development of analytical techniques for the in vivo determination of dynamic variation in the concentration levels of metal ions in a living animal.

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On-Line Microdialysis-Graphite Furnace Atomic Absorption Spectrometry in the Determination of Brain Magnesium Levels in Gerbils Subjected to Cerebral Ischemia/Reperfusion

Cited by 28 publications

References 17 publications

Modulation of Brain Hemichannels and Gap Junction Channels by Pro-Inflammatory Agents and Their Possible Role in Neurodegeneration

Modulation of Brain Hemichannels and Gap Junction Channels by Pro-Inflammatory Agents and Their Possible Role in Neurodegeneration

TRPM7 channels in hippocampal neurons detect levels of extracellular divalent cations

In vivomonitoring of the transfer kinetics of trace elements in animal brains with hyphenated inductively coupled plasma mass spectrometry techniques

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