Abstract
1. In cats either decerebrated or anaesthetized with sodium pentobarbitone, strychnine released by iontophoresis from electrodes containing a 5 mM solution in 165 mM of NaCl, abolished the action of glycine and β-alanine on cuneo-thalamic relay cells without disturbing their response to equally effective applications of γ-aminobutyric acid (GABA) and β-guanidino-propionic acid.
2. The loss of glycine sensitivity appeared to increase as long as the strychnine release continued until even the largest currents tolerated by the electrode were unable to eject effective amounts of glycine. Parallel shifts of the glycine log-current response curves, equivalent to an equipotent dose-ratio of about 2·0 only occurred when the duration of the strychnine applications by current in excess of 28 nA was restricted to a few minutes.
3. Without modifying either the frequency of the spike discharge or the amplitude or shape of the action potential, currents larger than 28 nA occasionally caused a loss of GABA sensitivity.
4. Strychnine administered either intravenously (0·2 mg/kg) or applied topically to the surface of the cuneate (0·5 mM) blocked the response to glycine without any obvious effect on the response to GABA.
5. It was concluded that the discovery of a strychnine-sensitive component of the inhibitory potentials recorded from the cuneate nucleus will reveal the physiological role of the glycine receptors on cuneo-thalamic relay cells.
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Selected References
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