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Voltage dependence of Ia reciprocal inhibitory currents in cat spinal motoneurones
1Division of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra, ACT.
Insights
This study characterizes inhibitory postsynaptic currents (IPSCs) in cat motoneurons, revealing their kinetics and reversal potential. Findings suggest voltage-dependent glycine channel gating influences synaptic current decay.
Area of Science:
- Neuroscience
- Synaptic Physiology
- Motor Control
Background:
- Reciprocal inhibition is crucial for motor control.
- Inhibitory postsynaptic currents (IPSCs) mediate this inhibition.
- Understanding IPSC kinetics and properties is essential for motor system function.
Purpose of the Study:
- To characterize the kinetic properties of inhibitory postsynaptic currents (IPSCs) in cat motoneurons.
- To determine the reversal potential and ionic basis of these IPSCs.
- To investigate factors influencing the decay time course of IPSCs.
Main Methods:
- Recording of population and unitary IPSCs in voltage-clamped cat motoneurons.
- Stimulation of quadriceps muscle nerve and spike-triggered averaging from inhibitory interneurons.
- Measurement of IPSC time-to-peak, decay time constant, amplitude, and reversal potential.
Main Results:
- Population IPSCs peaked at 0.51 ms and decayed with a time constant of 0.99 ms.
- Unitary IPSCs showed faster kinetics (peak 0.40 ms, time constant 0.82 ms) and amplitudes of 120-220 pA.
- Reversal potential was -80.7 mV, suggesting a chloride ion (Cl-) mediated current with an estimated intracellular [Cl-] of 6.5 mM.
- IPSC decay was voltage-dependent, increasing with depolarization, indicative of voltage-gated glycine channel kinetics.
Conclusions:
- IPSCs in cat motoneurons exhibit distinct population and unitary properties.
- The inhibitory current is primarily mediated by chloride ions, with a low estimated intracellular concentration.
- Voltage-dependent gating of glycine channels significantly influences the decay kinetics of these inhibitory synaptic currents.
Abstract:
1. Inhibitory postsynaptic currents (IPSCs) were recorded in voltage clamped posterior biceps or semitendinosus motoneurones of the cat during reciprocal inhibition. 2. Population IPSCs, recorded following stimulation of the whole quadriceps muscle nerve, had an average time-to-peak of 0.51 +/- 0.02 ms (+/- S.E.M., n = 22) and decayed exponentially, with an average time constant of 0.99 +/- 0.04 ms (at 37 degrees C) at resting membrane potentials. 3. Unitary IPSCs, recorded following spike-triggered averaging from an identified reciprocal inhibitory interneurone, had amplitudes of 120-220 pA with an average time-to-peak of 0.40 +/- 0.06 ms (n = 5). The decay of these unitary currents was exponential, with an average time constant of 0.82 +/- 0.07 ms (at 37 degrees C) at resting membrane potentials. 4. The time course of IPSCs was unaffected by either alpha-chloralose or pentobarbitone at concentrations necessary for deep anaesthesia. 5. The peak synaptic current varied linearly with the membrane potential over the range -90 to -30 mV, and had an average reversal potential of -80.7 +/- 1.5 mV (+/- S.E.M., n = 6) when measured using KCH3SO4-filled electrodes. 6. The reversal potential for the IPSC was used to calculate [Cl-]i. This was estimated to be 6.5 mM assuming that the inhibitory synaptic current was mediated purely by Cl- ions. 7. The rate at which synaptic currents decayed was exponentially dependent on the postsynaptic membrane potential, the decay time constant increasing e-fold for a 91 mV depolarization. This result was independent of [Cl-]i or of the magnitude of the synaptic conductance and was interpreted as a voltage dependence of the glycine channel open time. 8. The average unitary peak conductance was 9.1 +/- 1.7 nS (+/- S.E.M., n = 5), corresponding to the opening of approximately 200 glycine-activated postsynaptic channels following neurotransmitter release from a single Ia reciprocal interneurone.
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