5-(N-ethyl-N-isopropyl)amiloride and mild acidosis protect cultured cerebellar granule cells against glutamate-induced delayed neuronal death

Andreeva, N. A.; Bi, Khodorov; Stelmashook, E. V.; Sokolova, S. N.; Cragoe, Edward J.; Victorov, Ilya V.

doi:10.1016/0306-4522(92)90085-g

Cited by 34 publications

(10 citation statements)

References 25 publications

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“…Our findings contradict reports that amiloride may be neuroprotective [12]. In these in vitro studies, amiloride was shown to protect primary cerebellar granule cells from glutamateinduced delayed neuronal death, presumably by inhibiting glutamate n-methyl-D-aspartate receptor activity.…”

Section: Discussioncontrasting

confidence: 79%

Amiloride Increases Neuronal Damage after Traumatic Brain Injury in Rats

Turner

Heuvel

Vink

2004

Journal of the American College of Nutrition

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Section: Discussioncontrasting

confidence: 79%

Amiloride Increases Neuronal Damage after Traumatic Brain Injury in Rats

Turner

Heuvel

Vink

2004

Journal of the American College of Nutrition

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“…This view has recently been challenged (Sapolsky et al, 1996), following the demonstration that mild acidosis protects against NMDA toxicity in cortical cultures and against glutamate toxicity in cortical and cerebellar cultures (Andreeva et al, 1992;Kaku et al, 1993). This effect is at least partly explained by the depression of NMDA receptormediated currents by acidity (Traynelis and Cull Candy, 1990).…”

Section: Discussionmentioning

confidence: 93%

Lactate reduces glutamate‐induced neurotoxicity in rat cortex

Ros

Pecinska

Alessandri

et al. 2001

J of Neuroscience Research

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Experiments were carried out to test the hypothesis that lactate reduces the neurotoxicity of glutamate in vivo. MAP2 immunohistochemistry was used to measure lesion size, and microdialysis to measure the changes in glucose and lactate in the extracellular compartment. After implantation of a microdialysis probe 100 mM glutamate with or without 6 mM lactate was added to the perfusion medium and infused into the cortex of unanesthetized rats. Infusion of 100 mM glutamate for a period of 30 min produced a lesion of 6.05 +/- 0.64 mm(3), an increase in lactate of 124 +/- 19% above basal and a 21 +/- 9% reduction of glucose below basal level. When 6mM L-lactate was perfused together with 100 mM glutamate there was a significant reduction in the size of the lesion and there was no reduction in dialysate glucose. When L-lactate was replaced with D-lactate the lesion size and the increase in dialysate lactate were greater than after glutamate alone. The neuroprotective role of L-lactate is attributed to its ability to meet the increased energy demands of neurones exposed to high concentrations of glutamate.

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“…This Na + -induced Ca 2+ i overload triggers a cascade of deleterious events that lead to tissue dysfunction (e.g., cardiac arrhythmias, altered synaptic transmission) and ultimately tissue damage, including free radical toxicity, cellular edema, apoptosis and necrosis (reviewed in [61,111,159]). Persuasive evidence for NHE1 involvement is provided by numerous studies using selective NHE1 antagonists that significantly reduce Na + i and Ca 2+ i overloads and effectively mitigate cardiac [23, 61] and neural [4,57] injuries associated with ischemia-reperfusion both in vitro and in vivo.…”

Section: Involvement In Pathophysiological Statesmentioning

confidence: 99%

Diversity of the mammalian sodium/proton exchanger SLC9 gene family

Orlowski

Grinstein

2004

Pfl�gers Archiv European Journal of Physiology

594

584

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Sodium/proton antiporters or exchangers (NHE) are integral membrane proteins present in most, if not all, living organisms. In mammals, these transporters chiefly catalyze the electroneutral exchange of Na(+) and H(+) down their respective concentration gradients and are crucial for numerous physiological processes, ranging from the fine control of intracellular pH and cell volume to systemic electrolyte, acid-base and fluid volume homeostasis. NHE activity also facilitates the progression of other cellular events such as adhesion, migration, and proliferation. Thus far, eight distinct NHE genes (NHE1/SLC9A1-NHE8/SLC9A8) and several pseudogenes have been identified in the human genome. The functional genes encode proteins of varying primary sequence identity (25-70%), but share a common predicted secondary structure comprising 12 conserved membrane-spanning segments at the amino-terminus and a more divergent, cytoplasmically-oriented, carboxy-terminus. They show considerable heterogeneity in their patterns of tissue/cell expression and membrane localization. Functional studies have revealed further differences in their kinetic properties, sensitivity to pharmacological antagonists, and regulation by diverse hormonal and mechanical stimuli. Altered NHE activity has been linked to the pathogenesis of several diseases, including essential hypertension, congenital secretory diarrhea, diabetes, and tissue damage caused by ischemia/reperfusion. Further characterization of their functional properties should lead to a better understanding of their unique contributions to human health and disease.

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5-(N-ethyl-N-isopropyl)amiloride and mild acidosis protect cultured cerebellar granule cells against glutamate-induced delayed neuronal death

Cited by 34 publications

References 25 publications

Amiloride Increases Neuronal Damage after Traumatic Brain Injury in Rats

Amiloride Increases Neuronal Damage after Traumatic Brain Injury in Rats

Lactate reduces glutamate‐induced neurotoxicity in rat cortex

Diversity of the mammalian sodium/proton exchanger SLC9 gene family

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