Inhibitory post-synaptic currents in rat hippocampal CA1 neurones.
Spontaneous synaptic currents were recorded in voltage-clamped CA1 neurones in rat hippocampal slices at room temperature (21-25 degrees C). The currents, which could be seen at the resting membrane potential only when cells were loaded with chloride ions, were blocked by bicuculline. It was concluded that they were inhibitory post-synaptic currents (i.p.s.c.s) generated by the opening of chloride-selective channels activated by gamma-aminobutyric acid (GABA). In twenty-nine cells, ten to forty-five i.p.s.c.s were recorded at a potential between -75 and -85 mV. In every cell, i.p.s.c.s varied widely in amplitude with an average coefficient of variation of 28.7%. The mean amplitude varied from 0.22 to 1.16 nA with an average of 0.52 nA. Reversed (outward) currents could be recorded from cells voltage clamped at positive potentials. Null potentials varied between -20 and +20 mV, the variability being attributed to differences in chloride loading. Most currents had a rapid growth phase with a mean growth time (20-80% of peak) of 1.1 ms followed by a slower decay phase. The decay phase was exponential with a single time constant. The average decay time constant (tau D) ranged from 8.3 to 16.2 ms with a mean value of 11.0 ms. The rate of decay of currents was affected by membrane potential. tau D decreased exponentially with hyperpolarization in the range from +40 to -120 mV with an average volt constant (H value) of 146 +/- 9.6 mV (mean +/- 1 S.E. of mean, n = 17). The mean value of tau D at 0 mV was 19 ms. In some cells, growth times also decreased with hyperpolarization. The decay of currents was faster at higher temperatures but remained exponential. At 32 degrees C, the average tau D at 0 mV was 8.3 ms (n = 5) giving a Q10 value of 3.3 for the decay time constant at 0 mV. The frequency and mean amplitude of i.p.s.c.s were reduced by tetrodotoxin (TTX) or cadmium, indicating that many of the currents were generated by action potentials in presynaptic terminals. The spontaneous 'miniatures' remaining had the same time course and voltage sensitivity as currents recorded in normal solutions. Pentobarbitone (50-100 microM) greatly prolonged the decay of i.p.s.c.s but had no discernible effect on their amplitude or growth phase.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D002712:Chlorides / Q000502:physiology; D006624:Hippocampus / Q000187:drug effects / Q000502:physiology*; D066298:In Vitro Techniques; D008297:Male; D009433:Neural Inhibition; D010424:Pentobarbital / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D017981:Receptors, Neurotransmitter / Q000187:drug effects / Q000502:physiology*; D013997:Time Factors
D002712:Chlorides; D017981:Receptors, Neurotransmitter; D010424:Pentobarbital; D001640:Bicuculline