Voltage dependence of Ia reciprocal inhibitory currents in cat spinal motoneurones

G J Stuart1, S J Redman

  • 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.

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