Transient ischemia attenuates neuronal afterdischarges induced in the absence of synaptic transmission.
In vitro hippocampal slices were prepared from animals previously subjected to a 10-min period of transient forebrain ischemia. Electrophysiological responses were examined in the selectively vulnerable CA1 region in the presence of standard (2.0 mM) and reduced (0.2 mM) calcium concentrations. Synaptic responses evoked by orthodromic stimulation in standard calcium were intact following ischemia. In contrast, repetitive neuronal discharges, which are normally evoked by antidromic stimulation in the presence of low calcium concentrations, were attenuated or eliminated following ischemia. The possible contributions of presynaptic and postsynaptic mechanisms to post-ischemic hyperexcitability are discussed.
Lee
K S
KS
Department of Neurological Surgery, University of Virginia Health Sciences Center, Charlottesville 22908.
Brooks
P
P
Lowenkopf
T
T
D000818:Animals; D002118:Calcium / Q000502:physiology; D004558:Electric Stimulation; D004566:Electrodes; D004594:Electrophysiology; D005071:Evoked Potentials / Q000502:physiology; D005849:Gerbillinae; D006624:Hippocampus / Q000166:cytology / Q000502:physiology*; D066298:In Vitro Techniques; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D009474:Neurons / Q000502:physiology*; D011712:Pyramidal Tracts / Q000166:cytology / Q000502:physiology; D013569:Synapses / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology
D002118:Calcium