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

Li Chen, Li-Yen Huang

Research output: Contribution to journalArticle

416 Citations (Scopus)

Abstract

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
JournalNeuron
Volume7
Issue number2
DOIs
StatePublished - 1991
Externally publishedYes

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Enkephalins
N-Methyl-D-Aspartate Receptors
Protein Kinase C
Opioid Analgesics
Glutamic Acid
Posterior Horn Cells
Opioid Peptides
Protein C Inhibitor
Opioid Receptors
Protein Kinase Inhibitors
Morphine
Brain Stem
Spinal Cord
Neurons

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Sustained potentiation of NMDA receptor-mediated glutamate responses through activation of protein kinase C by a μ opioid. / Chen, Li; Huang, Li-Yen.

In: Neuron, Vol. 7, No. 2, 1991, p. 319-326.

Research output: Contribution to journalArticle

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