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Cortical hypoxia secondary to stroke produces an ischemic lesion with two functionally distinct regions. The central zone of necrosis, or infarct core, contains neurons irreversibly damaged from the initial perfusion deficit. Surrounding the infarctMoreCortical hypoxia secondary to stroke produces an ischemic lesion with two functionally distinct regions. The central zone of necrosis, or infarct core, contains neurons irreversibly damaged from the initial perfusion deficit. Surrounding the infarct core, the peri-lesional zone contains neurons that may be functionally altered due to moderate ischemia or network effects, but remain viable beyond the primary injury phase. An understanding of the electrophysiological (EP) profile of neuron clusters within the infarct core and peri-lesional zone may help to better define the therapeutic window for the acute management of stroke.-To compare the continuous electrical signals from core (n = 8) and peri-lesional (n = 8) neuron clusters, microwire electrodes were acutely implanted into the primary auditory cortex of 16 anaesthetized rats. Neural activity was recorded before, during and after an induced focal infarction. For infarct core studies, a single microwire electrode recorded the electrical signals from one neuron cluster located at the center of a focal ischemic lesion. 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. Despite the inherent complexity of cerebral ischemia secondary to microvascular occlusion, complete loss of EP function consistently occurred 300-600 s after photothrombosis.-For peri-lesional studies, a four-channel linear array was implanted into primary auditory cortex such that the microwires were located 0.5--2.0 mm from the border of the lesion. Peri-lesional neuron clusters exhibited a worsening decrease of electrical function up to 6 h following infarction. Furthermore, the nature of the response degradation was dependent on location relative to the lesion border. Laser-doppler blood flow measurements within the infarct core confirmed a decrease of local tissue perfusion, in correlation with electrical function loss. The degradation of electrical responses in the penumbra, however, may be due to spreading vasogenic edema or the physiological result of disrupting local circuitry. The differing core and penumbra responses likely reflect the respective mechanisms of damage. The continuous recording/focal infarction technique will be useful for long-term cortical function analysis during stroke recovery and optimization of treatment regimens.