Responses of rat hippocampal slices in a high-K+ medium following in vivo global ischaemia.
1. We hypothesized that burst activity induced in rat hippocampal tissue by a high-K+ medium in vitro would be increased by a previous episode of global ischaemia, severe enough to induce persistent neurological dysfunction. 2. Male Wistar rats that were subjected to 9 min of chest compression, sufficient to reduce blood pressure (BP) to zero, showed evidence of neurological damage attributed to a global ischaemic insult. Hindlimb function was impaired for 24-48 h and a susceptibility to sound-induced seizures was induced in 25 to 35 rats. The seizure susceptibility cleared spontaneously within 2 weeks in 10 of 25 rats. 3. Hippocampal slices from postischaemic rats were prepared, tested for viability and were then exposed to an 8.0 mmol/L K+ artificial cerebrospinal fluid in vitro. Spontaneous epileptiform bursting activity in the high-K+ medium was not increased. Instead, burst size decreased with time after ischaemia. 4. The decrement in bursting activity is attributed to loss of cellular activity or integrity. These changes correlate with functional changes described by others, but not necessarily to histologically verifiable cell death. The time course of these changes was remarkably long, continuing for almost 3 weeks. Thus, a less-than-lethal ischaemia appears to induce neuronal changes, possibly reversible, that continue for at least 20 days after the global ischaemic insult.
Laboratory for Cellular Neuroscience, University of Louisville School of Medicine, Kentucky, USA. elsabban@medicine.med.um.edu.my
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D000818:Animals; D002545:Brain Ischemia / Q000503:physiopathology*; D004594:Electrophysiology; D006614:Hindlimb / Q000502:physiology; D006624:Hippocampus / Q000187:drug effects / Q000503:physiopathology*; D066298:In Vitro Techniques; D007696:Kindling, Neurologic; D008297:Male; D011188:Potassium / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar
D011188:Potassium