Single glutamate-activated channels in locust muscle.
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Biomedical subjects
Publications and source records attributed to K A Gration.
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1 The responses of excitatory junctions on locust skeletal muscle fibres to iontophoretically applied L-glutamic acid and DL-ibotenic acid, a rigidly extended analogue of glutamate, were recorded by means of intracellular microelectrodes.2 Iontophoresis of L-glutamate to junctional sites produced transient depolarizations. Ibotenate applied iontophoretically to these sites usually evoked small hyperpolarizations which probably resulted from the activation of glutamate H-receptors on the extrajunctional membrane surrounding the junctions. However, at a minority ( approximately 20%) of junctions, ibotenate iontophoresis evoked transient depolarizations.3 Iontophoretically applied glutamate desensitized the ibotenate receptors, and vice versa. In experiments performed at junctional sites at which ibotenate depolarizations were absent, ibotenate had no effect on the responses to glutamate.4 Glutamate and ibotenate junctional currents had similar reversal potentials, measured under voltage-clamp, suggesting that the ionic bases for these currents are identical.5 It is proposed that the excitation caused by ibotenate results from the activation of receptors for extended L-glutamate and that these receptors co-exist on the post-junctional membranes of locust excitatory nerve-muscle synapses with ibotenate-insensitive glutamate receptors activated by glutamate in partially folded conformation.
Depolarizations to L-glutamate, applied locally by microinophoresis to the extrajunctional membrane of locust extensor tibiae muscle fibres and measured either in current clamp or voltage clamp, increased in amplitude for equivalent doses of glutamate following chronic denervation of the muscle. 2. A two-pulse method was used to examine recovery from desentization of junctional and extrajunctional receptors. A 'response ratio', i.e. the amplitude of response to the second (test) of a pair of glutamate pulses over to the pulses. The 'response ratio' for extrajunctional depolarizations of innervated fibres increased exponentially with pulse interval, with a time constant of 15.6 +/- 4.7 sec (n = 11). Recovery of extrajunctional receptor populations from desensitization was accelerated after denervation. The recovery kinetics for responses from fibres 6-22 days after denervation were generally described by two exponential terms, with time constants in the range 0.5-10 sec which were inversely related to the glutamate sensitivity of the extrajunctional membrane. For junctional receptors on both innervated and denervated fibres the recovery kinetics were described by a single exponential with a time constant of 0.2-1 sec. 3. The results suggest that the increased extrajunctional glutamate sensitivity which occurs after denervation results from the 'appearance' of glutamate receptors with properties similar to those found at the post-junctional membrane on locust muscle fibres.
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