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K Nomura, E Reuveny and T Narahashi
Department of Pharmacology, Northwestern University Medical School, Chicago, Illinois.
The mu-opioid [D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin (DAMGO) inhibited the high voltage-activated calcium channel currents of neonatal rat dorsal root ganglion neurons in a voltage-dependent manner. The low voltage-activated currents were not affected by DAMGO. The inhibitory effect was eliminated by pretreatment of the cell with pertussis toxin, indicating that the receptor was coupled with the pertussis toxin- sensitive G protein. Although the DAMGO inhibition occurred quickly, it was relieved gradually during the 5-min application of DAMGO. The recovery from desensitization after washout of DAMGO was very slow. Pretreatment of the cell with 1 microM DAMGO for 18 hr induced almost complete tolerance to the agonist. GTP-gamma-S also inhibited the high voltage-activated calcium channel currents mimicking DAMGO inhibition and the inhibition diminished during continuous application, suggesting that desensitization could occur without receptor stimulation by the agonist. Baclofen caused a similar inhibition and desensitization to those by DAMGO, and the inhibition by the subsequently applied DAMGO was attenuated. Thus, desensitization by these distinct receptor agonists is heterologous. Modulation of G proteins which are coupled with these agonists may be involved in the desensitization process.
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