Major differences in Ca2+i response to anoxia between neonatal and adult rat CA1 neurons: role of Ca2+o and Na+o (2024)

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Sodium influx pathways during and after anoxia in rat hippocampal neurons

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Mechanisms that contribute to Na+ influx during and immediately after 5 min anoxia were investigated in cultured rat hippocampal neurons loaded with the Na+-sensitive fluorophore sodium-binding benzofuran isophthalate. During anoxia, an influx of Na+ in the face of reduced Na+,K+-ATPase activity caused a rise in [Na+]i. After the return to normoxia, Na+,K+-ATPase activity mediated the recovery of [Na+]i despite continued Na+ entry. Sodium influx during and after anoxia occurred through multiple pathways and increased the longer neurons were maintained in culture. Under the experimental conditions used, Na+ entry during anoxia did not reflect the activation of ionotropic glutamate receptors, TTX- or lidocaine-sensitive Na+ channels, plasmalemmal Na+/Ca2+ exchange, Na+/H+ exchange, or HCO3--dependent mechanisms; rather, contributions were received from a Gd3+-sensitive pathway activated by reactive oxygen species and Na+/K+/2Cl- cotransport in neurons maintained for 6-10 and 11-14 d i...

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Anoxia-evoked intracellular pH and Ca2+ concentration changes in cultured postnatal rat hippocampal neurons

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Claire Sheldon

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Oxygen deprivation activates an ATP-inhibitable K+ channel in substantia nigra neurons

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Gabriel Haddad

Depending on its severity and duration, O2 deprivation activates mechanisms that can lead to profound deleterious changes in neuronal structure and function. Hypoxia also evokes inherent adaptive mechanisms that can possibly delay injury and increase neuronal survival. One of these neuronal adaptive mechanisms is believed to be the activation of K+ channels, but direct evidence for their activation is lacking. We performed experiments to test the hypothesis that hypoxia induces activation of K+ channels via changes in cytosolic and membrane factors such as ATP, Ca2+, and membrane potential. The effect of hypoxia on single-channel currents was studied in rat substantia nigra neurons, since these have a high density of glibenclamide binding sites. In cell-attached patches, hypoxia or cyanide reversibly activated an outward current. This hypoxia-activated current in excised inside-out patches was K+ selective and voltage dependent, and had a high sensitivity to internal ATP, ADP, and A...

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An obligate role for oxygen in the early stages of glutamate-induced, delayed neuronal death

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In vitro models of hypoxic/hypoglycemic injury reveal common mechanisms with glutamate excitotoxicity, but glutamate-induced toxicity in the absence of oxygen has never been directly addressed. Therefore, we assessed neuronal survival and intracellular calcium concentrations ([Ca2+]i) in neonatal hippocampal cultures in response to glutamate in the presence and absence of oxygen. Twenty-four hours of hypoxia alone killed 40% of the initial population, attributable to glutamate receptor-stimulated osmotic lysis. A 5 min glutamate exposure in ambient air killed 80% of the initial population by 24 hr later. When cultures were deprived of oxygen during and for 2-24 hr after excitotoxin exposure, glutamate did not cause additional neuronal death beyond that induced by oxygen depletion alone. Toxicities caused by activation of NMDA, AMPA, or kainate receptors were each ameliorated by oxygen depletion. In the absence of oxygen, glutamate evoked normal increases in [Ca2+]i, indicating that ...

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Differential fall in ATP accounts for effects of temperature on hypoxic damage in rat hippocampal slices

2000 •

Georgina Chambers

Intracellular recordings, ATP and cytosolic calcium measurements from CA1 pyramidal cells in rat hippocampal slices were used to examine the mechanisms by which temperature alters hypoxic damage. Hypothermia (34 degrees C) preserved ATP (1.7 vs. 0.8 nM/mg) and improved electrophysiologic recovery of the CA1 neurons after hypoxia; 58% of the neurons subjected to 10 min of hypoxia (34 degrees C) recovered their resting and action potentials, while none of the neurons at 37 degrees C recovered. Increasing the glucose concentration from 4 to 6 mM during normothermic hypoxia improved ATP (1.3 vs. 0.8 nM/mg) and mimicked the effects of hypothermia; 67% of the neurons recovered their resting and action potentials. Hypothermia attenuated the membrane potential changes and the increase in intracellular Ca(2+) (212 vs. 384 nM) induced by hypoxia. Changing the glucose concentration in the artificial cerebrospinal fluid primarily affects ATP levels during hypoxia. Decreasing the glucose concent...

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Pharmacology & Therapeutics

Hypoxia and Neuronal Function under in Vitro Conditions

1999 •

Karen Nieber

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European Journal of Pharmacology

MEK inhibition exacerbates ischemic calcium imbalance and neuronal cell death in rat cortical cultures

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Pietro Giusti, Stephen Skaper

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Major differences in Ca2+i response to anoxia between neonatal and adult rat CA1 neurons: role of Ca2+o and Na+o (2024)
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