Abstract
The effect of tetrodotoxin (TTX) on cerebral tissue impedance was studied in the cat, as was the effect of TTX on impedance changes induced by calcium and asphyxiation. Impedance measurements were made at 1.0 kHz, in focal volumes of approximately 1.0 mm 3, using a Wheatstone bridge technique. In cats with chronically implanted electrodes, introduction of 1–250 ng of TTX in 0.5 μl CSF into the lateral geniculate body caused no change in cerebral tissue impedance. In acute experiments, topical applications of 0.05–50 μg of TTX in 0.1 ml CSF markedly reduced the amplitude of the cortical EEG without altering cortical tissue impedance. When asphyxiation was preceded by treatment of cortex with TTX, postasphyxial increases in both resistive and reactive impedance were delayed by 4–6 min. A similar delay, together with a marked reduction in the postasphyxial resistance increase, has been shown previously to occur following treatment of the cortex with CaCl 2. The application of CaCl 2 to the cortex prior to asphyxiation did not interfere with the postasphyxial reactance rise. When TTX treatment of the cortex was followed by applications of CaCl 2, the resulting cortical impedance increases were indistinguishable from those following application of CaCl 2 without prior TTX treatment. Postasphyxial resistance changes in calcium treated cortices were inversely related to the resistance changes induced by the calcium prior to asphyxiation. However, when the cortex was treated with TTX followed by CaCl 2 prior to asphyxiation, this inverse relation was lost. The postasphyxial impedance change following cortical pretreatment with TTX and calcium were delayed as with TTX alone. In terms of models of cerebral tissue impedance the results suggest that conductivity changes in hydrated extracellular macromolecules may play an important role in cerebral tissue impedance changes.
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