μ opioid receptor signaling in morphine sensitization

Viganò, Daniela; Rubino, Tiziana; Chiara, G. Di; Ascari, I. J.; Massi, Paola; Parolaro, Daniela

doi:10.1016/s0306-4522(02)00825-4

Cited by 68 publications

(50 citation statements)

References 32 publications

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“…Repeated administration of morphine or repeated activation of μ-opioid receptors was found to initiate behavioral sensitization to AMPH [8,50]. A significant increase in μ-opioid receptor autoradiography in some brain regions was also found in morphine-sensitized animals [52]. The findings described above raise the possibility that μ-opioid receptors are susceptible to repeated AMPH or METH treatment, and provide a possible hypothesis to explain our observation that the up-regulation of μ-opioid receptors by chronic NAT treatment potentiates the expression of behavioral sensitization.…”

Section: Discussionmentioning

confidence: 91%

Attenuation of methamphetamine-induced behavioral sensitization in mice by systemic administration of naltrexone

Chiu

2005

Brain Research Bulletin

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Repeated intermittent exposure to psychostimulants was found to produce behavioral sensitization. The present study was designed to establish a mouse model and by which to investigate whether opioidergic system plays a role in methamphetamine-induced behavioral sensitization. Mice injected with 2.5 mg/kg of methamphetamine once a day for 7 consecutive days showed behavioral sensitization after challenge with 0.3125 mg/kg of the drug on day 11, whereas mice injected with a lower daily dose (1.25 mg/kg) did not. Mice received daily injections with either 1.25 or 2.5 mg/kg of methamphetamine showed behavioral sensitization after challenge with 1.25 mg/kg of the drug on days 11, 21, and 28. To investigate the role of opioidergic system in the induction and expression of behavioral sensitization, long-acting but non-selective opioid antagonist naltrexone was administrated prior to the daily injections of and challenge with methamphetamine, respectively. Our results show that the expressions of behavioral sensitization were attenuated by pretreatment with 10 or 20 mg/kg of naltrexone either during the induction period or before methamphetamine challenge when they were tested on days 11 and 21. These results indicate that repeated injection with methamphetamine dose-dependently induced behavioral sensitization in mice, and suggest the involvement of opioid receptors in the induction and expression of methamphetamine-induced behavioral sensitization.

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Section: Discussionmentioning

confidence: 91%

Attenuation of methamphetamine-induced behavioral sensitization in mice by systemic administration of naltrexone

Chiu

2005

Brain Research Bulletin

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“…Acute activation of the μ-opioid receptor decreases cAMP activity (Wang and Gintzler, 1994) leading to a decrease in presynaptic GABAergic transmission (Bonci and Williams, 1997). μ-Opioid receptor-induced decreases in cAMP are attenuated in the striatum in morphine-sensitized rats (Vigano et al, 2003). A similar 'blunting effect' may occur in the VP.…”

Section: Discussionmentioning

confidence: 99%

Changes in Accumbal and Pallidal pCREB and ΔFosB in Morphine-Sensitized Rats: Correlations with Receptor-Evoked Electrophysiological Measures in the Ventral Pallidum

McDaid

Dallimore

Mackie

et al. 2005

Neuropsychopharmacol

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Activation of μ-opioid receptors in the ventral pallidum (VP) is important for the induction of behavioral sensitization to morphine in rats. The present study was designed to ascertain if neurons within the VP demonstrate sensitization at a time when morphine-induced behavioral sensitization occurred (ie 3 or 14 days after five once-daily injections of 10 mg/kg i.p. morphine) in rats. Western blotting was used to evaluate transcription factors altered by opiates, CREB and ΔFosB. CREB levels did not change in the VP, but there was a significant decrease in levels of its active, phosphorylated form (pCREB) at both 3-and 14-days withdrawal. ΔFosB levels were elevated following a 3-day withdrawal, but returned to normal by 14 days. This profile also was obtained from nucleus accumbens tissue. In a separate group of similarly treated rats, in vivo electrophysiological recordings of VP neuronal responses to microiontophoretically applied ligands were carried out after 14-days withdrawal. The firing rate effects of local applications of morphine were diminished in rats withdrawn from i.p. morphine. Repeated i.p. morphine did not alter GABA-mediated suppression of firing, or the rate enhancing effects of the D1 dopamine receptor agonist SKF82958 or glutamate. However, VP neurons from rats withdrawn from repeated i.p. morphine showed a higher propensity to enter a state of depolarization inactivation to locally applied glutamate. Overall, these findings reveal that decreased pCREB in brain regions such as the VP accompanies persistent behavioral sensitization to morphine and that this biochemical alteration may influence the excitability of neurons in this brain region.

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“…The effects of chronic morphine administration on MOP binding site density have also been investigated in animal brain and brain regions. These studies produced all possible changes in MOP density, namely, up-regulation (Besse et al, 1992;Brady et al, 1989;Fabian et al, 2002;Fabian et al, 2003;Holaday et al, 1982;Ray et al, 2004;Rothman et al, 1991;Schmidt et al, 2003;Vigano et al, 2003), down-regulation (Bhargava and Gulati, 1990;Meuser et al, 2003;Werling et al, 1989) or no change (Polastron et al, 1994;Stafford et al, 2001;Turchan et al, 1999). Some of these results appear to be regional differences, but others, performed on whole brain or the same regions of the same animal, appear to be discrepancies between different laboratories.…”

Section: Discussionmentioning

confidence: 99%

Chronic morphine treatment up-regulates mu opioid receptor binding in cells lacking filamin A

Onoprishvili

Simon

2007

Brain Research

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We investigated the effects of morphine and other agonists on the human mu opioid receptor (MOP) expressed in M2 melanoma cells, lacking the actin cytoskeleton protein filamin A and in A7, a sub clone of the M2 melanoma cells, stably transfected with filamin A cDNA. The results of binding experiments showed, that after chronic morphine treatment (24 hr) of A7 cells, MOP binding sites were down-regulated to 63% of control, whereas, unexpectedly, in M2 cells, MOP binding was upregulated to 188% of control naïve cells. Similar up-regulation was observed with the agonists methadone and levorphanol. The presence of antagonists (naloxone or CTAP) during chronic morphine treatment inhibited MOP down-regulation in A7 cells. In contrast, morphine-induced upregulation of MOP in M2 cells was further increased by these antagonists. Chronic morphine desensitized MOP in A7 cells, i.e. it decreased DAMGO-induced stimulation of GTPγS binding. In M2 cells DAMGO stimulation of GTPγS binding was significantly greater than in A7 cells and was not desensitized by chronic morphine. Pertussis toxin treatment abolished morphine-induced receptor up-regulation in M2 cells, whereas it had no effect on morphine-induced down-regulation in A7 cells. These results indicate that, in the absence of filamin A, chronic treatment with morphine, methadone or levorphanol leads to up-regulation of MOP, to our knowledge, the first instance of opioid receptor up-regulation by agonists in cell culture.

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μ opioid receptor signaling in morphine sensitization

Cited by 68 publications

References 32 publications

Attenuation of methamphetamine-induced behavioral sensitization in mice by systemic administration of naltrexone

Attenuation of methamphetamine-induced behavioral sensitization in mice by systemic administration of naltrexone

Changes in Accumbal and Pallidal pCREB and ΔFosB in Morphine-Sensitized Rats: Correlations with Receptor-Evoked Electrophysiological Measures in the Ventral Pallidum

Chronic morphine treatment up-regulates mu opioid receptor binding in cells lacking filamin A

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