Rationale: Despite the critical role attributed to phosphorylated extracellular signal regulated kinase (pERK) in the nucleus accumbens (Acb) in the actions of addictive drugs, the effects of morphine on ERK phosphorylation in this area are still controversial. Objectives: In order to investigate further this issue, we studied (1) the ability of morphine to affect ERK phosphorylation in the shell (AcbSh) and core (AcbC) of Sprague-Dawley and Wistar rats and of CD-1 and C57BL/6J mice and (2) the role of dopamine D and ?-opioid receptors in Sprague-Dawley rats and CD-1 mice. Methods: The pERK expression was assessed by immunohistochemistry. Results: In rats, morphine decreased AcbSh and AcbC pERK expression, whereas in mice, increased it preferentially in the AcbSh compared with the AcbC. Systemic SCH 39166 decreased pERK expression on its own in the AcbSh and AcbC of Sprague-Dawley rats and CD-1 mice; furthermore, in rats, SCH 39166 disclosed the ability of morphine to stimulate pERK expression. Systemic (rats and mice) and intra-Acb (rats) naltrexone prevented both decreases, in rats, and increases, in mice. Conclusions: These findings confirm the differential effects of morphine in rats and mice Acb and that D receptors exert a facilitatory role on ERK phosphorylation; furthermore, they indicate that, in rats, removal of the D-dependent pERK expression discloses the stimulatory influence of morphine on ERK phosphorylation and that the morphine's ability to decrease pERK expression is mediated by Acb ?-opioid receptors. Future experiments may disentangle the psychopharmacological significance of the effects of morphine on pERK in the Acb.
Role of nucleus accumbens ? opioid receptors in the effects of morphine on ERK1/2 phosphorylation
Ruiu S;
2016
Abstract
Rationale: Despite the critical role attributed to phosphorylated extracellular signal regulated kinase (pERK) in the nucleus accumbens (Acb) in the actions of addictive drugs, the effects of morphine on ERK phosphorylation in this area are still controversial. Objectives: In order to investigate further this issue, we studied (1) the ability of morphine to affect ERK phosphorylation in the shell (AcbSh) and core (AcbC) of Sprague-Dawley and Wistar rats and of CD-1 and C57BL/6J mice and (2) the role of dopamine D and ?-opioid receptors in Sprague-Dawley rats and CD-1 mice. Methods: The pERK expression was assessed by immunohistochemistry. Results: In rats, morphine decreased AcbSh and AcbC pERK expression, whereas in mice, increased it preferentially in the AcbSh compared with the AcbC. Systemic SCH 39166 decreased pERK expression on its own in the AcbSh and AcbC of Sprague-Dawley rats and CD-1 mice; furthermore, in rats, SCH 39166 disclosed the ability of morphine to stimulate pERK expression. Systemic (rats and mice) and intra-Acb (rats) naltrexone prevented both decreases, in rats, and increases, in mice. Conclusions: These findings confirm the differential effects of morphine in rats and mice Acb and that D receptors exert a facilitatory role on ERK phosphorylation; furthermore, they indicate that, in rats, removal of the D-dependent pERK expression discloses the stimulatory influence of morphine on ERK phosphorylation and that the morphine's ability to decrease pERK expression is mediated by Acb ?-opioid receptors. Future experiments may disentangle the psychopharmacological significance of the effects of morphine on pERK in the Acb.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
