Glutamate current noise: post-synaptic channel kinetics investigated under voltage clamp

1. Analysis of voltage-clamped noise has been used to investigate the operation of glutamate receptors and associated channels at the locust nerve-muscle junction. Channels opened by glutamate and an agonist have been compared. 2. Glutamate-induced current fluctuations have a power spectrum with a single (1/frequency2) component which fits a simple model for the operation of channels. The form of the spectra for glutamate voltage noise and for 'background' noise has been determined. 3. The single channel conductance was estimated from the spectra, gamma glutamate = 122 +/- 0.4 (S.E.) pS. This estimate is independent of membrane potential and of the amplitude of membrane current change produced by glutamate. 4. The rate constant, alpha, for the closing of glutamate-operated channels depends exponentially on membrane potential, conforming to the equation alpha = approximately alphaeetaVm (approximately alpha = 0.26 +/- 0.014 msec-1, eta = 0.0054 +/- 0.001 msec-1); the duration of the channel lifetime (tau) decreases with hyperpolarization. Membrane potential dependence of alpha reduces as temperature is lowered. 5. For glutamate-operated channels, the temperature dependence of alpha and gamma fits the Arrhenius equation; alpha and gamma decrease exponentially as a function of T-1 (degrees K) with a descrete change in slope at about 6 degrees C, indicating a change in the activaiton energies of the respective rate processes. 6. Spectra of quisqualate-induced current fluctuations have the same form as spectra for glutamate noise. The single channel conductance was estimated from the spectra, gamma quisqualate = 120 +/- 3.9 (S.E.) pS. 7. The rate constnt, alpha, for the closing of quisqualate-induced channels depends exponentially on membrane potential. The duration of the open state for quisqualate channels was 2.2 times longer than for glutamate channels. 8. For glutamate receptors the voltage-sensitivity of the channel life-time is in the opposite direction to that of ACh receptors in vertebrate muscle. Possible explanations for the sharp change in the activation energy of the rate processes associated with the channel are discussed.