Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Microdialysis-perfusion of the urethane-anesthetized rat hippocampus was performed to assess the effects of acidosis on extracellular amino acids. Perfusion with Krebs-Ringer bicarbonate buffer at pH 6.9 produced a selective decrease in taurine. A further reduction of pH to 6.4 induced diminished glutamate levels. The Cl-/HCO3- exchange inhibitor 4,4'-diisothiocyano-2,2'-disulfonic acid stilbene (DIDS) did not affect interstitial taurine during perfusion, but there was a rebound increase in taurine levels upon withdrawal of the agent. In contrast, glutamate concentrations were elevated during DIDS administration, and decreased upon reperfusion with standard buffer. The reduction of extracellular taurine and glutamate concentrations caused by low pH was inhibited by DIDS. The results suggest that taurine and glutamate uptake and/or release in vivo is pH-dependent, and that the effects of acidosis possibly are mediated by the Cl-/HCO3- antiporter. The decrease in extracellular glutamate brought about by low pH may have pathophysiologic implications in conditions associated with disturbed pH homeostasis such as cerebral ischemia and spreading depression.
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PMID:In vivo acidosis reduces extracellular concentrations of taurine and glutamate in the rat hippocampus. 791 39

Sodium dynamics are essential for regulating functional processes in glial cells. Indeed, glial Na(+) signaling influences and regulates important glial activities, and plays a role in neuron-glia interaction under physiological conditions or in response to injury of the central nervous system (CNS). Emerging studies indicate that Na(+) pumps and Na(+) -dependent ion transporters in astrocytes, microglia, and oligodendrocytes regulate Na(+) homeostasis and play a fundamental role in modulating glial activities in neurological diseases. In this review, we first briefly introduced the emerging roles of each glial cell type in the pathophysiology of cerebral ischemia, Alzheimer's disease, epilepsy, Parkinson's disease, Amyotrophic Lateral Sclerosis, and myelin diseases. Then, we discussed the current knowledge on the main roles played by the different glial Na(+) -dependent ion transporters, including Na(+) /K(+) ATPase, Na(+) /Ca(2+) exchangers, Na(+) /H(+) exchangers, Na(+) -K(+) -Cl(-) cotransporters, and Na(+) - HCO3- cotransporter in the pathophysiology of the diverse CNS diseases. We highlighted their contributions in cell survival, synaptic pathology, gliotransmission, pH homeostasis, and their role in glial activation, migration, gliosis, inflammation, and tissue repair processes. Therefore, this review summarizes the foundation work for targeting Na(+) -dependent ion transporters in glia as a novel strategy to control important glial activities associated with Na(+) dynamics in different neurological disorders. GLIA 2016;64:1677-1697.
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PMID:Glial Na(+) -dependent ion transporters in pathophysiological conditions. 2745 21


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