Abstract
Application of ketamine (10-4-10-3mol l-1) to locust retractor unguis muscle produced a reversible, dose-dependent reduction in neurally evoked twitches, and blocked agonist-induced contractions. With increasing ketamine concentration (5 x 10-5-10-3 mol l-1), the amplitude of glutamate potentials was reduced and dose-response curves for ionophoresis of L-glutamate were shifted to the right, particularly after concanavalin A treatment. Ketamine (10-4 mol l-1) enhanced the rate of desensitization to consecutive pulses of L-glutamate and this action was eliminated by concanavalin A. The amplitude of the excitatory postsynaptic current (EPSC) was reduced by ketamine (10-5-5 x 10-4 mol l-1) in a dose-dependent manner but without a concomitant reduction in EPSC rise time. The decay phase of the EPSC was usually biphasic in the presence of ketamine (>5 x 10-5 mol l-1) but did not exhibit any voltage dependence. It is concluded that ketamine enhances desensitization and blocks the channel, particularly the closed form.
Original language | English |
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Pages (from-to) | 73-86 |
Number of pages | 14 |
Journal | Journal of Experimental Biology |
Volume | 141 |
Publication status | Published - 1 Jan 1989 |
Keywords
- Animals
- Quisqualic Acid
- Neuromuscular Junction
- Oxadiazoles
- Dose-Response Relationship, Drug
- Glutamic Acid
- Receptors, Glutamate
- Ion Channels
- Muscles
- Action Potentials
- Grasshoppers
- Concanavalin A
- Kinetics
- Receptors, Neurotransmitter
- Ketamine
- Membrane Potentials
- Glutamates
- Muscle Contraction