Effect of repeated administration of morphine on the activity of extracellular signal regulated kinase in the mouse brain
Section snippets
Acknowledgements
This work was supported by the Ministry of Education, Culture, Sports, Science and Technology of Japan. The authors wish to thank Ms Mizuho Yamada for her expert technical assistance.
References (19)
- et al.
Specific G protein activation and μ-opioid receptor internalization caused by morphine, DAMGO and endomorphin I
Eur. J. Pharmacol.
(1998) - et al.
New insights into the control of MAP kinase pathways
Exp. Cell Res.
(1999) MAP kinase pathways in yeast: for mating and more
Cell
(1995)- et al.
Morphine activates opioid receptors without causing their rapid internalization
J. Biol. Chem.
(1996) Protein phosphatases and the regulation of mitogen-activated protein kinase signalling
Curr. Opin. Cell Biol.
(2000)Specificity of receptor tyrosine kinase signaling: transient versus sustained extracellular signal-regulated kinase activation
Cell
(1995)- et al.
Influence of chronic morphine treatment on protein kinase C activity: comparison with butorphanol and implication for opioid tolerance
Brain Res.
(1994) - et al.
Agonist-induced desensitization of the μ opioid receptor is determined by threonine 394 preceded by acidic amino acids in the COOH-terminal tail
J. Biol. Chem.
(1997) - et al.
Truncated, desensitization-defective neurokinin receptors mediate sustained MAP kinase activation, cell growth and transformation by a Ras-independent mechanism
EMBO J.
(1996)
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2015, ToxiconCitation Excerpt :Therefore, lt14a likely prevents drug-seeking behavior by suppressing the ERK pathway. The transcription factor CREB is related to the development of opioid dependence (Narita et al., 2002). Our results (Fig. 4D) showed that the expression of CREB1 was up-regulated in the morphine withdrawal group.
Rosuvastatin attenuated the existing morphine tolerance in rats with L5 spinal nerve transection through inhibiting activation of astrocytes and phosphorylation of ERK<inf>42/44</inf>
2015, Neuroscience LettersCitation Excerpt :Proinflammatory cytokines such as TNFα and IL-1β have been implicated in the development of morphine tolerance [27]. Both TNFα and IL-1β could regulate synaptic and neural activity directly [28], act with glia reciprocally and eventually lead to decrease of morphine antinociceptive efficacy [25]. Pharmacological blockade of TNFα and IL-1β could attenuate morphine tolerance [10,29].
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2014, European Journal of PharmacologyChanges in phosphorylation of CREB, ERK, and c-fos induction in rat ventral tegmental area, hippocampus and prefrontal cortex after conditioned place preference induced by chemical stimulation of lateral hypothalamus
2011, Behavioural Brain ResearchCitation Excerpt :It seems that in reward processing, there are crucial intracellular signaling changes in brain areas associated with addiction such as the aforementioned regions. The persistent neuroadaptations to addictive drugs induce changes in the number and efficiency of receptors, signal transduction pathways, gene expression and subsequent component of proteins [17,42,50]. At the molecular level, several lines of evidence have suggested that phosphorylation of cyclic AMP-response element binding protein (CREB) [5,46,59], extracellular signal-regulated kinase (ERK) [16,36,55], and c-fos induction [37,46] are highly involved in many forms of experience-dependent plasticity, such as long-term potentiation (LTP), and play an important role in the rewarding effects of many drugs of abuse, such as nicotine [68], morphine [36], cocaine [28], and alcohol [45].