TY - JOUR
T1 - Sustained potentiation of NMDA receptor-mediated glutamate responses through activation of protein kinase C by a μ opioid
AU - Chen, Li
AU - Huang Marine, Li Yen Mae
N1 - Funding Information:
We thank Drs. R. Leonard, R. Puzdrowski, and W. Willis for their comments on the manuscript, K. Forni and S. Y. Wong fortechni-cal assistance, and L. Simmons and M. Watson for preparing the manuscript. This work was supported by National Institutes of Health grants NS23061 and NS01050 (Research Career Development Award, L.-Y. M. H) and the John Scaly Endowment Fund.
PY - 1991/8
Y1 - 1991/8
N2 - 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.
AB - 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.
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U2 - 10.1016/0896-6273(91)90270-A
DO - 10.1016/0896-6273(91)90270-A
M3 - Article
C2 - 1678615
AN - SCOPUS:0025895334
SN - 0896-6273
VL - 7
SP - 319
EP - 326
JO - Neuron
JF - Neuron
IS - 2
ER -