Elsevier

Brain Research

Volume 548, Issues 1–2, 10 May 1991, Pages 343-345
Brain Research

Calcium, magnesium, and long-term recovery from hypoxia in hippocampal tissue slices

https://doi.org/10.1016/0006-8993(91)91146-RGet rights and content

Abstract

Ortho- and antidromic responses recovered and remained robust for 5 h in slices exposed to transient hypoxia in low calcium, while responses remained depressed in slices made hypoxic in normal calcium. Elevating magnesium in addition to reducing calcium did not improve recovery compared to reducing calcium alone. Spreading depression-like hypoxic depolarization occurred earlier in low calcium than in control fluid. We conclude that loss of function was triggered by calcium uptake by neurons and not by cell swelling, and that activation of NMDA receptors probably played no part.

References (23)

  • DingledineR.

    Brain Slices

    (1984)
  • Cited by (16)

    • Neurotransmitters in the mediation of cerebral ischemic injury

      2018, Neuropharmacology
      Citation 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 Aging
      Citation 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.

    View all citing articles on Scopus
    View full text