Abnormal action-potential bursts and synchronized, GABA-mediated inhibitory potentials in an in vitro model of focal epilepsy.
Focal, freeze-induced lesions were made in isolated hemispheres of turtle cerebral cortex in vitro, permitting the investigation of epileptiform discharges in a preparation with preserved intracortical circuitry. Freeze lesions resulted in interictal discharges and occasional ictal-like events. The interictal discharges were dependent upon activation of non-NMDA excitatory amino acid receptors and were affected by but did not require NMDA receptor activation. Voltage clamp and current clamp recordings revealed abnormal bursts of low-amplitude action potentials in 36% of recorded neurons, while large, repetitive inhibitory potentials, mediated by GABAA receptors, were recorded in 90% of the neurons. Thus, prominent findings in this model include abnormalities of both excitatory and inhibitory activity. Since these changes in neuronal excitability resulted from a localized physical injury, they may resemble the changes that occur in acute posttraumatic epilepsy.
Troyer
M D
MD
Department of Neurology and Neurological Sciences, Stanford University School of Medicine, California.
Blanton
M G
MG
Kriegstein
A R
AR
D000200:Action Potentials; D000818:Animals; D002540:Cerebral Cortex / Q000293:injuries* / Q000503:physiopathology; D003344:Cortical Synchronization; D004569:Electroencephalography; D004828:Epilepsies, Partial / Q000209:etiology / Q000503:physiopathology*; D004834:Epilepsy, Post-Traumatic / Q000503:physiopathology; D005615:Freezing; D006801:Humans; D066298:In Vitro Techniques; D008959:Models, Neurological; D009433:Neural Inhibition; D014426:Turtles / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D005680:gamma-Aminobutyric Acid