Enhancement of desensitization of quisqualate-type glutamate receptor by the dissociative anaesthetic ketamine

M. L. J. Ashford, P. Boden, R. L. Ramsey, P. N. R. Usherwood

    Research output: Contribution to journalArticle

    11 Citations (Scopus)

    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 languageEnglish
    Pages (from-to)73-86
    Number of pages14
    JournalJournal of Experimental Biology
    Volume141
    Publication statusPublished - 1 Jan 1989

    Fingerprint

    Dissociative Anesthetics
    anesthetic
    AMPA Receptors
    Glutamate Receptors
    Ketamine
    ketamine
    anesthetics
    Excitatory Postsynaptic Potentials
    glutamates
    Glutamic Acid
    locust
    concanavalin A
    Concanavalin A
    contraction
    muscle
    Grasshoppers
    locusts
    dosage
    agonists
    dose response

    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

    Cite this

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    title = "Enhancement of desensitization of quisqualate-type glutamate receptor by the dissociative anaesthetic ketamine",
    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.",
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    author = "Ashford, {M. L. J.} and P. Boden and Ramsey, {R. L.} and Usherwood, {P. N. R.}",
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    Enhancement of desensitization of quisqualate-type glutamate receptor by the dissociative anaesthetic ketamine. / Ashford, M. L. J.; Boden, P.; Ramsey, R. L.; Usherwood, P. N. R.

    In: Journal of Experimental Biology, Vol. 141, 01.01.1989, p. 73-86.

    Research output: Contribution to journalArticle

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    T1 - Enhancement of desensitization of quisqualate-type glutamate receptor by the dissociative anaesthetic ketamine

    AU - Ashford, M. L. J.

    AU - Boden, P.

    AU - Ramsey, R. L.

    AU - Usherwood, P. N. R.

    PY - 1989/1/1

    Y1 - 1989/1/1

    N2 - 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.

    AB - 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.

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    KW - Oxadiazoles

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