Idriss_1985_FEBS.Lett_189_150

Reference

Title : Phencyclidine (PCP) blocks glutamate-activated postsynaptic currents - Idriss_1985_FEBS.Lett_189_150
Author(s) : Idriss M , Albuquerque EX
Ref : FEBS Letters , 189 :150 , 1985
Abstract :

Phencyclidine (PCP) was tested on the metathoracic tibialis muscles of Locusta migratoria. In physiological solution, the peak amplitude of the excitatory postsynaptic currents (EPSCs) evoked by nerve stimulation was linearly related to membrane potential between -50 and -150 mV. The decay time constant of the EPSC (tau EPSC) was exponentially dependent on voltage and decreased with hyperpolarization. The membrane potential change required to produce an e-fold change in tau EPSC was 315 mV. PCP (5-40 microM) produced a concentration-dependent depression of both EPSC peak amplitude and tau EPSC. A slight nonlinearity in the current-voltage relationship could be discerned at high concentrations of PCP. The shortening of the decay time constant of EPSC (tau EPSC) occurred without significant change in the voltage sensitivity observed under control conditions. Under all experimental conditions, the decay of the EPSCs remained a single exponential of time. Fluctuation analysis indicated that 5 microM PCP shortens the lifetime of the glutamate-activated channels by 25.7 +/- 3%. PCP (10-80 microM) did not induced desensitization of the glutamate receptors. These results suggest that PCP interacts with the open conformation of ion channels activated by the glutamate receptor.

PubMedSearch : Idriss_1985_FEBS.Lett_189_150
PubMedID: 2863172

Related information

Citations formats

Idriss M, Albuquerque EX (1985)
Phencyclidine (PCP) blocks glutamate-activated postsynaptic currents
FEBS Letters 189 :150

Idriss M, Albuquerque EX (1985)
FEBS Letters 189 :150