Electrophysiological response dynamics during focal cortical infarction.
While the intracellular processes of hypoxia-induced necrosis and the intercellular mechanisms of post-ischemic neurotoxicity associated with stroke are well documented, the dynamic electrophysiological (EP) response of neurons within the core or periinfarct zone remains unclear. The present study validates a method for continuous measurement of the local EP responses during focal cortical infarction induced via photothrombosis. Single microwire electrodes were acutely implanted into the primary auditory cortex of eight rats. Multi-unit neural activity, evoked via a continuous 2 Hz click stimulus, was recorded before, during and after infarction to assess neuronal function in response to local, permanent ischemia. During sham infarction, the average stimulus-evoked peak firing rate over 20 min remained stable at 495.5+/-14.5 spikes s-1, indicating temporal stability of neural function under normal conditions. Stimulus-evoked peak firing was reliably reduced to background levels (firing frequency in the absence of stimulus) following initiation of photothrombosis over a period of 439+/-92 s. The post-infarction firing patterns exhibited unique temporal degradation of the peak firing rate, suggesting a variable response to ischemic challenge. Despite the inherent complexity of cerebral ischemia secondary to microvascular occlusion, complete loss of EP function consistently occurred 300-600 s after photothrombosis. The results suggest that microwire recording during photothrombosis provides a simple and highly efficacious strategy for assessing the electrophysiological dynamics of cortical infarction.
Chiganos
Terry C
TC
Department of Bioengineering, University of Illinois at Chicago, Science and Engineering Offices (SEO), Room 218, 851 South Morgan Street, Chicago, IL 60607, USA. tchiganos@gmail.com
Jensen
Winnie
W
Rousche
Patrick J
PJ
D000161:Acoustic Stimulation; D000818:Animals; D001303:Auditory Cortex / Q000502:physiology; D002545:Brain Ischemia / Q000503:physiopathology; D002544:Cerebral Infarction / Q000503:physiopathology*; D004567:Electrodes, Implanted; D004594:Electrophysiology; D005336:Fiber Optic Technology; D009473:Neuronal Plasticity / Q000502:physiology; D009474:Neurons / Q000473:pathology / Q000502:physiology; D051381:Rats