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Phencyclidine (PCP) blocks glutamate-activated postsynaptic currents.

M Idriss, E X Albuquerque

    FEBS Letters
    |September 9, 1985
    PubMed
    Summary
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    Phencyclidine (PCP) depresses excitatory postsynaptic currents in locust muscles by shortening glutamate-activated channel open times. This suggests PCP interacts with open ion channels, affecting neurotransmission.

    Area of Science:

    • Neuroscience
    • Pharmacology
    • Insect Physiology

    Background:

    • Phencyclidine (PCP) is a dissociative anesthetic with known neurological effects.
    • Glutamate receptors are crucial for excitatory neurotransmission in many organisms.
    • Understanding PCP's mechanism of action at the channel level is important for its pharmacological profile.

    Purpose of the Study:

    • To investigate the effects of Phencyclidine (PCP) on excitatory postsynaptic currents (EPSCs) in Locusta migratoria.
    • To determine how PCP influences the kinetics and voltage dependence of glutamate-activated ion channels.
    • To elucidate the interaction site of PCP with glutamate receptors.

    Main Methods:

    • Electrophysiological recordings of excitatory postsynaptic currents (EPSCs) in locust metathoracic tibialis muscles.

    Related Experiment Videos

  • Voltage clamp analysis to study current-voltage relationships and decay time constants.
  • Fluctuation analysis to assess changes in ion channel kinetics.

    • Main Results:

    • PCP (5-40 microM) reduced EPSC peak amplitude and decay time constant (tau EPSC) in a concentration-dependent manner.
    • PCP shortened the open-channel lifetime of glutamate-activated channels by approximately 25.7%.
    • PCP did not induce desensitization of glutamate receptors and primarily affected the open channel conformation.

    Conclusions:

    • PCP acts by interacting with the open conformation of glutamate-activated ion channels.
    • The drug's effects on EPSC kinetics suggest a direct modulation of channel gating.
    • These findings provide insights into the molecular mechanisms underlying PCP's neuropharmacological actions.