Summary
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1.
In cats under Dial, multiple micro-electrodes were used to analyze the changes in membrane potential and conductance of cortical neurones produced by inhibition (evoked by surface shocks) and by microiontophoretic applications of GABA.
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2.
IPSPs are associated with a marked but variable increase in membrane conductance. At the peak, the conductance may rise 3–4 fold. 52 estimates gave a mean increase of 54.0% (S.D. 77%).
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The time course of the main increase in conductance coincides approximately with the time course of the IPSP and the period of reduced excitability. After an initial phase of very high conductance, the conductance diminishes exponentially with a time constant of about 50 msec.
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4.
GABA causes a very striking increase in membrane conductance and, in most cases, a negative shift in membrane potential.
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5.
Estimates of the reversal potential of the action of GABA (EGAB) agree well with estimates of the reversal potential for IPSPs (EI) obtained before or after the application of GABA. There was a strong positive correlation between values of EI and EGAB, and the slope of the line describing EI vs EGAB, did not differ significantly from 1.0
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These observations therefore greatly reinforce previous evidence of a close identity between the actions of GABA and of the normal transmitter of cortical IPSPs.
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7.
The increase in conductance produced by GABA shows an initial peak (mean 17.1 n-mho/nA GABA current, S.E. 4.50, n=41) and then tends to fall, after 10–20 sec, to a relatively stable level (mean 9.31 n-mho/nA (S.E. 2.38, n=32)). This phenomenon is particularly evident with large doses of GABA.
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8.
A maintained application of GABA is usually associated with a change in EI towards greater positivity, probably owing to a large influx of Cl−.
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Receiving financial support from the Medical Research Council of Canada and the United Cerebral Palsy Research and Educational Foundation.
Wellcome Fellow, on leave from Edinburgh University
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Dreifuss, J.J., Kelly, J.S. & Krnjević, K. Cortical inhibition and γ-aminobutyric acid. Exp Brain Res 9, 137–154 (1969). https://doi.org/10.1007/BF00238327
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DOI: https://doi.org/10.1007/BF00238327