PubMed · 9750634
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M Pinaud. 1997. [Remifentanyl].. https://doi.org/10.1016/s0750-7658(97)89859-0
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Arginine vasotocin (AVT), an avian neurohypophysial hormone, is released during osmotic stimulation and oviposition. In the present study, the role of opioid peptides on AVT release was studied by examining the effects of an opioid agonist and antagonist on osmotic- and oviposition-induced secretion of AVT. The administration of hypertonic saline (1.5 M NaCl) induced an increase in the plasma levels of AVT. The simultaneous administration of morphine, an opioid receptor agonist, inhibited the osmotically induced increase in plasma levels of AVT in a dose-dependent manner. On the other hand, the co-administration of morphine with naloxone, an opioid receptor antagonist, attenuated the inhibitory effect of morphine. Moreover, injection of naloxone alone enhanced the osmotically induced increase in plasma levels of AVT. However, the administration of morphine did not inhibit the oviposition-induced increase in plasma levels of AVT. These results suggest that osmotic-induced release of AVT may be under opioid regulation, while oviposition-induced release of AVT may be controlled by a different mechanism. J. Exp. Zool. 286:481-486, 2000.
Chronic activation of adenylate cyclase-cAMP-cAMP-dependent protein kinase (PKA) systems by administration of opioid receptor agonists has been considered as one of the mechanisms of opioid tolerance and dependence. Although analysis of the micro opioid receptor (MOR) gene suggests that cAMP-related signal transduction systems regulate the expression of this gene, which transcription factors affect the MOR gene expression in brain and neural cells has not been clarified. This study deals with the effects of fentanyl on MOR mRNA levels in the rat pheochromocytoma cell line (PC12 cells). PC12 cells were cultured in medium with clinically relevant concentrations of fentanyl. The quantitative reverse transcription and polymerase chain reaction (RT-PCR) method was used for determination of MOR mRNA. Treatment of PC12 cells with fentanyl induced the MOR mRNA up-regulation in a concentration- and time-dependent manner. A cAMP analogue also up-regulated MOR mRNA. The intracellular cAMP level increased after fentanyl treatment. A PKA inhibitor blocked the MOR mRNA up-regulation by fentanyl and the cAMP analogue. Expression of a dominant inhibitory Ras also inhibited the MOR mRNA up-regulation. Fentanyl-induced up-regulation of MOR mRNA via activation of cAMP signaling may be important in compensating for the MOR reduction during long-term treatment of PC12 cells with fentanyl. The present study could be relevant to understanding the molecular mechanisms of opioids in a state of drug tolerance or dependence, and in patients under anesthesia or being treated for pain.