1. Caesium ions (Cs+), applied extracellularly, caused a decrease in the input resistance of cultured spinal cord (s.c.) neurones and depolarized the neurones when they contained 140 mM‐CsCl. 2. The reversal potential for Cs+‐activated currents shifted 56 mV on average for a 10‐fold reduction in the intracellular chloride ion (Cl‐) activity, indicating that the Cs+‐activated currents were specific to Cl‐. 3. The activation of Cl‐ currents by Cs+ was not due to the depolarization‐evoked release of neurotransmitter from presynaptic terminals. We therefore suggest that Cs+ were acting directly on the extracellular surface of the s.c. neurones to activate Cl‐ currents. 4. Cs+‐activated currents showed desensitization in the presence of 140 mM‐Cs+. 5. The log‐log plot of the dose‐response data could be fitted with a straight line with a slope of 1.7 +/‐ 0.4 (n = 6), indicating that at least 2 Cs+ were needed to activate a single Cl‐ channel. The KD of the Cs+‐induced response was greater than 69 mM. 6. In outside‐out patches Cs+ activated single Cl‐ channels. These channels were not activated by sodium or potassium ions. 7. The Cs+‐activated channels displayed a total of five distinct conductance states which had mean conductances of 20, 30, 43, 66 and 92 pS. The 30 and 43 pS states were the most frequently occurring states. 8. The conductance states of the Cs+‐activated channel have the same conductances as those reported for gamma‐aminobutyric acid (GABA)‐ and glycine‐activated channels in rat s.c. neurones. We therefore conclude that Cs+ activate the same type of Cl‐ channel as GABA and glycine through an unidentified receptor.
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