The early events of oxygen and glucose deprivation: setting the scene for neuronal death?

Martin, Rosemary; Lloyd, H.G.E.; Cowan, Anna I.

doi:10.1016/0166-2236(94)90008-6

Cited by 337 publications

(219 citation statements)

References 65 publications

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“…The resultant loss of ATP-dependent ionic segregation and subsequent failure to maintain the normal ionic gradient triggers inappropriate membrane depolarization. Consequently, voltage-dependent calcium channels are activated resulting in intracellular calcium accumulation and eventually neuronal death (Martin et al, 1994;Dimagl et al, 1999;Lee et al, 1999).…”

Section: Cellular Theoriesmentioning

confidence: 99%

Impaired cognitive function and mental performance in mild dehydration

2003

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Dehydration is a reliable predictor of impaired cognitive status. Objective data, using tests of cortical function, support the deterioration of mental performance in mildly dehydrated younger adults. Dehydration frequently results in delirium as a manifestation of cognitive dysfunction. Although, the occurrence of delirium suggests transient acute global cerebral dysfunction, cognitive impairment may not be completely reversible. Animal studies have identified neuronal mitochondrial damage and glutamate hypertransmission in dehydrated rats. Additional studies have identified an increase in cerebral nicotinamide adenine dinucleotide phosphate-diaphorase activity (nitric oxide synthase, NOS) with dehydration. Available evidence also implicates NOS as a neurotransmitter in long-term potentiation, rendering this a critical enzyme in facilitating learning and memory. With ageing, a reduction of NOS activity has been identified in the cortex and striatum of rats. The reduction of NOs synthase activity that occurs with ageing may blunt the rise that occurs with dehydration, and possibly interfere with memory processing and cognitive function. Dehydration has been shown to be a reliable predictor of increasing frailty, deteriorating mental performance and poor quality of life. Intervention models directed toward improving outcomes in dehydration must incorporate strategies to enhance prompt recognition of cognitive dysfunction.

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Section: Cellular Theoriesmentioning

confidence: 99%

Impaired cognitive function and mental performance in mild dehydration

2003

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“…This evidence might also support the idea that the inconsistency between the reversal potential of the aglycemia-induced current and the equilibrium potential for Na ϩ ions is explained by a second, opposing K ϩ current. Interestingly, an increase of the extracellular K ϩ concentration associated with a decreased intracellular concentration of this ion has been reported in some neuronal subtypes during energy deprivation (Jiang and Haddad, 1991; for review, see Martin et al, 1994). Conversely, the participation of chloride ions in the aglycemia-induced inward current is ruled out, because the reversal potential of this current is not changed by using microelectrodes filled with K ϩ acetate instead of K ϩ chloride.…”

Section: Spiny Neurons Are Depolarized By Glucose Deprivationmentioning

confidence: 99%

“…Extracellular levels of adenosine increase during energy deprivation caused by either anoxia or aglycemia (Martin et al, 1994). Because adenosine has been reported to hyperpolarize various neuronal subtypes by activating K ϩ channels (Greene and Haas, 1991), we have studied the possible involvement of endogenous adenosine in the aglycemia-induced membrane hyperpolarization.…”

Section: Large Aspiny Interneurons Are Hyperpolarized By Glucose Deprmentioning

confidence: 99%

Opposite Membrane Potential Changes Induced by Glucose Deprivation in Striatal Spiny Neurons and in Large Aspiny Interneurons

et al. 1997

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We have studied the electrophysiological effects of glucose deprivation on morphologically identified striatal neurons recorded from a corticostriatal slice preparation. The large majority of the recorded cells were spiny neurons and responded to aglycemia with a slow membrane depolarization coupled with a reduction of the input resistance. In voltage-clamp experiments aglycemia caused an inward current. This current was associated with a conductance increase and reversed at Ϫ40 mV. The aglycemia-induced membrane depolarization was not affected by tetrodotoxin ( TTX ) or 6-cyano-7-nitroquinoxaline-2,3-dione plus aminophosphonovalerate, antagonists acting respectively on AMPA and NMDA glutamate receptors. Also, the intracellular injection of bis(2-aminophenoxy)ethane-N,N,NЈ,NЈ-tetra-acetic acid, a calcium (Ca 2ϩ ) chelator, and low Ca 2ϩ /high Mg 2ϩ -containing solutions failed to reduce this phenomenon. Conversely, it was reduced by lowering external sodium (Na ϩ ) concentration.A minority of the recorded cells had the morphological characteristics of large aspiny interneurons and the electrophysiological properties of "long-lasting afterhyperpolarization (L A) cells." These cells responded to aglycemia with a membrane hyperpolarization/outward current that was coupled with an increased conductance. This current was not altered by TTX, blockers of ATP-dependent potassium (K ϩ ) channels, and adenosine A1 receptor antagonists, whereas it was reduced by solutions containing low Ca 2ϩ /high Mg 2ϩ . This current reversed at Ϫ105 mV and was blocked by barium, suggesting the involvement of a K ϩ conductance. We suggest that the opposite membrane responses of striatal neuronal subtypes to glucose deprivation might account for their differential neuronal vulnerability to aglycemia and ischemia.

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“…One of the first consequences of oxygen and glucose deprivation during cerebral ischemia is membrane depolarization, the rapid depletion of cellular ATP, and the accumulation of extracellular excitatory amino acids. During these events, there is a progressive increase in extracellular K ϩ and an increase in intracellular Na ϩ , Cl Ϫ , and Ca 2ϩ , accompanied by suppression of neuronal activity and synaptic transmission (for review, see Martin et al, 1994;Kristian and Siesjo, 1998;Lipton, 1999).…”

Section: Introductionmentioning

confidence: 99%