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Selective functional vulnerability of cortical neurons following transient MCA-occlusion in the cat.
Author(s) -
Gerd Rosner,
Rudolf Graf,
Keisuke Kataoka,
Wolf-Dieter Heiß
Publication year - 1986
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/01.str.17.1.76
Subject(s) - medicine , ischemia , electrophysiology , occlusion , cortical neurons , microelectrode , cats , cerebral blood flow , neuron , blood flow , anesthesia , middle cerebral artery , neuroscience , cardiology , electrode , chemistry , biology , psychiatry
Simultaneous recordings of several cortical neurons were obtained before, during and after transient 15 min occlusion of the middle cerebral artery in cats. With the use of a multiple electrode array consisting of 4-7 platinum/iridium microelectrodes, the cortical pericellular blood flow was concurrently measured by means of the hydrogen clearance technique. Hydrogen clearance measurements revealed a homogeneous blood flow distribution throughout all phases of the experiment in the area covered by the different microelectrodes. Considering only the results of experiments with low residual blood flow during ischemia (less than 0.1 ml/g/min), single unit activity ceased immediately after occlusion and remained so during the ischemic period. The recovery time of action potentials after reperfusion ranged from 10 min to 3 hours depending on the examined neuron. Lower values for discharge rates of the individual cells were generally observed after reoccurrence, although some units exhibited temporarily an even higher spike frequency. Furthermore, the spike form usually changed in that the hyperpolarizing afterpotentials were enlarged after recirculation. However, some cells with a nearly unchanged spike form were found as well. The results indicate that the recovery of cell function largely depends on the individual neuron which supports the idea of a selective functional vulnerability of cortical neurons in response to ischemia.

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