Involvement of μ‐Opioid Receptor in the Salsolinol‐Associated Place Preference in Rats Exposed to Conditioned Fear Stress

Matsuzawa, Shigeki; Suzuki, Tsutomu; Misawa, Miwa

doi:10.1111/j.1530-0277.2000.tb04624.x

Cited by 34 publications

(38 citation statements)

References 37 publications

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“…According to this hypothesis, the blockade of the formation of these compounds (for example, through the inhibition of the ethanol metabolism in the brain) or their interaction with their targets, probably the opioid receptors (Critcher et al 1983;Myers et al 1986;Myers and Robinson 1999;Matsuzawa et al 2000), could suppress some of the behavioral consequences produced by ethanol administration. In that sense, local microinjections of ethanol or ACH into a DA-rich environment (such as the VTA) could lead to an increase in the local levels of THIQs.…”

Section: Discussionmentioning

confidence: 98%

Motor stimulant effects of ethanol and acetaldehyde injected into the posterior ventral tegmental area of rats: role of opioid receptors

et al. 2009

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The posterior VTA is another brain region involved in the locomotor activation after the intracerebroventricular administration of ethanol or acetaldehyde. Our data indicate that opioid receptors, particularly the micro-opioid receptors, could be the target of the actions of these compounds in the VTA. These results are consistent with the hypothesis that acetaldehyde could be a mediator of some ethanol effects.

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Section: Discussionmentioning

confidence: 98%

Motor stimulant effects of ethanol and acetaldehyde injected into the posterior ventral tegmental area of rats: role of opioid receptors

et al. 2009

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“…Other authors also suggest this possibility. So, Matsuzawa et al (2000) showed that the blockade of the μ-opioid receptors significantly attenuated the place preference for Sal. Thus, one possible scenario is that Sal is responsible for some of the effects of ACH and ethanol through interactions with the μ-opioid receptors.…”

Section: Introductionmentioning

confidence: 98%

“…Systemic administration of Sal induces a slight place preference that can be potentiated under fear stress conditioning (Matsuzawa et al 2000). Rats learn to selfadminister this compound directly into the shell of the NAc (Rodd et al 2003) and directly into the ventral tegmental area (VTA; Rodd et al 2008).…”

Section: Introductionmentioning

confidence: 99%

Locomotor stimulant effects of acute and repeated intrategmental injections of salsolinol in rats: role of μ-opioid receptors

et al. 2010

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“…All drugs were dissolved in saline and administered in a volume of 10 ml/kg. The pretreatment times and doses of naloxone, naloxone methiodide, and naloxonazine were based on our previous reports (Suzuki et al, 1995;Matsuzawa et al, 2000).…”

Section: Methodsmentioning

confidence: 99%

Mechanisms That Underlie μ-Opioid Receptor Agonist–Induced Constipation: Differential Involvement of μ-Opioid Receptor Sites and Responsible Regions

Mori

Shibasaki

Matsumoto

et al. 2013

J Pharmacol Exp Ther

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Reducing the side effects of pain treatment is one of the most important strategies for improving the quality of life of cancer patients. However, little is known about the mechanisms that underlie these side effects, especially constipation induced by opioid receptor agonists; i.e., do they involve naloxonazinesensitive versus -insensitive sites or central-versus-peripheral m-opioid receptors? The present study was designed to investigate the mechanisms of m-opioid receptor agonist-induced constipation (i.e., the inhibition of gastrointestinal transit and colonic expulsion) that are antagonized by the peripherally restricted opioid receptor antagonist naloxone methiodide and naloxonazine in mice. Naloxonazine attenuated the fentanylinduced inhibition of gastrointestinal transit more potently than the inhibition induced by morphine or oxycodone. Naloxone methiodide suppressed the oxycodone-induced inhibition of gastrointestinal transit more potently than the inhibition induced by morphine, indicating that m-opioid receptor agonists induce the inhibition of gastrointestinal transit through different mechanisms. Furthermore, we found that the route of administration (intracerebroventricular, intrathecally, and/or intraperitoneally) of naloxone methiodide differentially influenced the suppressive effect on the inhibition of colorectal transit induced by morphine, oxycodone, and fentanyl. These results suggest that morphine, oxycodone, and fentanyl induce constipation through different mechanisms (naloxonazine-sensitive versus naloxonazine-insensitive sites and central versus peripheral opioid receptors), and these findings may help us to understand the characteristics of the constipation induced by each m-opioid receptor agonist and improve the quality of life by reducing constipation in patients being treated for pain.

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Involvement of μ‐Opioid Receptor in the Salsolinol‐Associated Place Preference in Rats Exposed to Conditioned Fear Stress

Abstract: Salsolinol may have some rewarding effect, and its rewarding effect may be potentiated by psychological stress. In addition, the rewarding effect of salsolinol especially under psychological stress may involve the endogenous central opioid system, i.e., mu-opioid receptor.

Cited by 34 publications

References 37 publications

Motor stimulant effects of ethanol and acetaldehyde injected into the posterior ventral tegmental area of rats: role of opioid receptors

Motor stimulant effects of ethanol and acetaldehyde injected into the posterior ventral tegmental area of rats: role of opioid receptors

Locomotor stimulant effects of acute and repeated intrategmental injections of salsolinol in rats: role of μ-opioid receptors

Mechanisms That Underlie μ-Opioid Receptor Agonist–Induced Constipation: Differential Involvement of μ-Opioid Receptor Sites and Responsible Regions

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