Sustained potentiation of NMDA receptor-mediated glutamate responses through activation of protein kinase C by a μ opioid

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μ opioids, such as morphine and certain enkephalin analogs, are known to modulate glutamate-evoked activity in dorsal horn neurons in the spinal cord and caudal brain stem. Yet the molecular mechanism by which this modulation occurs is not understood. We examined the interactions between glutamate and a selective μ opioid receptor agonist, d-Ala2-MePhe4-Gly-ol5-enkephalin (DAGO), in spinal trigeminal neurons in thin medullary slices of rats. DAGO caused a sustained increase in glutamate-activated currents that are mediated by N-methyl-d-aspartate receptors. Intracellularly applied protein kinase C (PKC) mimics the effect of DAGO, and a specific PKC inhibitor interrupts the sustained potentiation produced by DAGO. Thus, PKC plays a key role in mediating the action of μ opioid peptides.

Original languageEnglish (US)
Pages (from-to)319-326
Number of pages8
Issue number2
StatePublished - Aug 1991
Externally publishedYes


ASJC Scopus subject areas

  • Neuroscience(all)

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