Selective vulnerability of synaptic transmission in hippocampus to ex-vivo ischemia: effects of extracellular ionic substitution in the postischemic period.
After 10-60 min of normothermic complete ischemia, hippocampal slices were prepared and allowed to recover for 60 min. The presence or absence of an evoked transsynaptic response was measured in CA1, CA3, and dentate gyrus. A selective vulnerability of the field excitatory postsynaptic potential to ischemia was found (CA1 greater than CA3 greater than dentate gyrus). Recovery of synaptic transmission in CA1 and CA3 was significantly improved by decreasing extracellular Ca2+ and increasing Mg2+ after ischemia. Addition of an N-methyl-D-aspartate antagonist further improved functional recovery. Postischemic reduction in extracellular Cl- increased recovery in CA1 and CA3, whilst reduction in Na+ was deleterious.
Ashton
D
D
Department of Neuropsychopharmacology, Janssen Research Foundation, Beerse, Belgium.
Willems
R
R
Wauquier
A
A
D000818:Animals; D002118:Calcium / Q000378:metabolism / Q000502:physiology*; D003986:Dibenzocycloheptenes / Q000494:pharmacology; D016291:Dizocilpine Maleate; D006168:Guinea Pigs; D006624:Hippocampus / Q000187:drug effects / Q000503:physiopathology*; D066298:In Vitro Techniques; D002546:Ischemic Attack, Transient / Q000378:metabolism / Q000503:physiopathology*; D008274:Magnesium / Q000378:metabolism / Q000502:physiology*; D008297:Male; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter / Q000187:drug effects / Q000502:physiology; D009435:Synaptic Transmission
D003986:Dibenzocycloheptenes; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter; D016291:Dizocilpine Maleate; D008274:Magnesium; D002118:Calcium