Calcium, magnesium, and long-term recovery from hypoxia in hippocampal tissue slices
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Cited by (16)
Neurotransmitters in the mediation of cerebral ischemic injury
2018, NeuropharmacologyCitation Excerpt :Excessive activation of glutamate receptors and the consequent overload of intracellular calcium is one of the excitotoxic triggers that leads to cell death (Sims and Zaidan, 1995). Cell swelling and entry of sodium and chloride into neurons, during SD-like depolarization are also triggers for neuronal cell death (Young et al., 1991). During ischemia, energy depletion generates a reduction in ATPase activity, which cannot counteract the influx of large cations.
NADH hyperoxidation correlates with enhanced susceptibility of aged rats to hypoxia
2008, Neurobiology of AgingCitation Excerpt :In the case of hypoxia/ischemia, mitochondria sequester the calcium, but become damaged once the levels of Ca2+ are in excess of their buffering capacity. The reduction or removal of calcium from the experimental media in adult rat hippocampal slice preparations during both brief and prolonged hsd improved the recovery of rat hippocampal slices compared to slices perfused with normal concentrations of calcium (Amagasa et al., 1990; Balestrino and Somjen, 1986; Roberts and Sick, 1988; Young et al., 1991). In addition, a relationship has been demonstrated between the mitochondrial redox status (i.e. NADH levels), synaptic activity and cytosolic calcium levels in adult hippocampal slices.
Effects of prolonged elevation of potassium on hippocampus of anesthetized rats
1993, Brain Research