Abstract

Opioid peptides exert a variety of cellular effects in the central nervous system including increase of K + conductance, modulation of Ca 2+ currents and a decrease of excitatory postsynaptic potentials (EPSPs; for review see 1). In the neocortex EPSPs evoked at low stimulus intensities are attenuated by the μ receptor selective opioid peptide agonist D-Ala 2 -NMe-Phe 4 -Gly 5 ol (DAMGO). At higher stimulus intensities, however, EPSPs are augmented by DAMGO (1). This differential effect of the opioid agonist may be due to an attenuation of inhibition (2), which is recruited preferentially at higher stimulus intensities. Additionally, selective effects on NMDA vs. non-NMDA receptor-mediated components contributing to the EPSP (3) may participate

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