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Reverse NCX Attenuates Cellular Sodium Loading in Metabolically Compromised Cortex.

Niklas J Gerkau1, Cordula Rakers2, Simone Durry1

  • 1Institute of Neurobiology, Faculty of Mathematics and Natural Sciences, Heinrich Heine University Duesseldorf, Universitaetsstrasse 1, Duesseldorf, Germany.

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Peri-infarct depolarizations (PIDs) in ischemic stroke involve propagating sodium elevations in neurons and astrocytes. Inhibiting sodium/calcium exchange (NCX) reduced associated calcium loads, suggesting a neuroprotective role for NCX in stroke.

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Area of Science:

  • Neuroscience
  • Ischemic Stroke Research
  • Cellular Physiology

Background:

  • Ischemic stroke core regions experience ionic gradient breakdown, leading to cell death.
  • The penumbra region's recovery post-reperfusion is hindered by peri-infarct depolarizations (PIDs).
  • Sodium influx is implicated in PIDs, but in vivo data on sodium accumulation are lacking.

Purpose of the Study:

  • To investigate in vivo sodium elevations during PIDs in the mouse neocortex.
  • To elucidate the role of sodium influx and sodium/calcium exchange (NCX) in PIDs and subsequent calcium overload.
  • To provide quantitative data on peri-infarct sodium dynamics in vivo.

Main Methods:

  • Utilized in vivo imaging in mouse neocortex to detect sodium elevations during PIDs.
  • Induced transient sodium elevations in acute tissue slices via chemical ischemia.
  • Manipulated NMDA-receptors, glutamate transport, and NCX activity in both in vivo and in vitro models.

Main Results:

  • PIDs in vivo were associated with propagating sodium elevations in both neurons and astrocytes.
  • Blocking NMDA-receptors reduced neuronal sodium and calcium loads in slices.
  • Inhibiting glutamate transport affected sodium influx differently in astrocytes and neurons.
  • Inhibition of NCX increased sodium transients but significantly reduced calcium transients in both cell types, confirmed in vivo.

Conclusions:

  • PIDs drive sodium influx, leading to sodium/calcium exchanger (NCX) reversal and secondary calcium overload.
  • NCX activity may be neuroprotective in stroke by dampening ischemia-induced sodium loading.
  • This study provides the first in vivo quantitative data on sodium elevations in peri-infarct regions.