Sodium homeostasis in rat hippocampal slices during oxygen and glucose deprivation: role of voltage-sensitive sodium channels.
The breakdown in brain ionic homeostasis during energy deprivation (anoxic depolarization [AD]) is intimately linked to neuronal injury. We studied the role of one particular route of Na+ influx, voltage-sensitive Na+ channels, in the AD induced by O2 and/or glucose deprivation. We recorded extracellular Na+ concentration ([Na+]e) and direct current potential (DCP) in the CA1 stratum pyramidale of hippocampal slices using Na+-selective microelectrodes. Tetrodotoxin (0.1-1 microM) delayed the occurrence of AD and reduced the peak change in both [Na+]e and DCP during AD. However the tetrodotoxin effects were overcome by a concomitant reduction in extracellular glucose during anoxia. We conclude that: (1) the activation of voltage-gated Na+ channels is involved in the triggering of AD; (2) there may be a critical level of energy depletion when AD occurs and different mechanisms may underlie AD during hypoxia, compared to O2 and glucose deprivation.
Fung
M L
ML
Department of Physiology, The University of Hong Kong, Pokfulam.
Croning
M D
MD
Haddad
G G
GG
D000818:Animals; D015687:Cell Hypoxia; D005071:Evoked Potentials; D005947:Glucose / Q000172:deficiency*; D006624:Hippocampus / Q000378:metabolism* / Q000502:physiology; D006706:Homeostasis; D066298:In Vitro Techniques; D015640:Ion Channel Gating; D008839:Microelectrodes; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000378:metabolism*; D015222:Sodium Channels / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology
D015222:Sodium Channels; D013779:Tetrodotoxin; D012964:Sodium; D005947:Glucose