Abstract
Several studies using selective opioid agonists or mice with a deletion of the μ-opioid receptor, have shown that morphine dependence is essentially due to chronic stimulation of μ- but not δ-opioid receptors. Because dependence is assumed to be related to persistent intracellular modifications, we have investigated modifications putatively induced by chronic activation of μ receptors with morphine or selective agonists in vitro in SH-SY5Y cells and in vivo in different strains of mice, including mice lacking the μ-opioid receptor gene. The results show a similar down- regulation and desensitization of μ and δ binding sites, whereas an overexpression of dynamin occurred only with μ agonists, strongly suggesting the relevance of this upregulation with the opiate dependence. Moreover, translocation of overexpressed dynamin from intracellular pools to plasma membranes was observed in chronic morphine-treated rats. This recruitment could be critically involved in long-lasting changes such as alterations of axonal transport observed in opioid dependence.
| Original language | English |
|---|---|
| Pages (from-to) | 159-166 |
| Number of pages | 8 |
| Journal | Molecular Pharmacology |
| Volume | 58 |
| Issue number | 1 |
| Publication status | Published - 2000 |
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ASJC Scopus subject areas
- Pharmacology
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Overexpression of dynamin is induced by chronic stimulation of μ but not δ-opioid receptors : Relationships with μ-related morphine dependence. / Noble, Florence; Szücs, M.; Kieffer, Brigitte; Roques, Bernard P.
In: Molecular Pharmacology, Vol. 58, No. 1, 2000, p. 159-166.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Overexpression of dynamin is induced by chronic stimulation of μ but not δ-opioid receptors
T2 - Relationships with μ-related morphine dependence
AU - Noble, Florence
AU - Szücs, M.
AU - Kieffer, Brigitte
AU - Roques, Bernard P.
PY - 2000
Y1 - 2000
N2 - Several studies using selective opioid agonists or mice with a deletion of the μ-opioid receptor, have shown that morphine dependence is essentially due to chronic stimulation of μ- but not δ-opioid receptors. Because dependence is assumed to be related to persistent intracellular modifications, we have investigated modifications putatively induced by chronic activation of μ receptors with morphine or selective agonists in vitro in SH-SY5Y cells and in vivo in different strains of mice, including mice lacking the μ-opioid receptor gene. The results show a similar down- regulation and desensitization of μ and δ binding sites, whereas an overexpression of dynamin occurred only with μ agonists, strongly suggesting the relevance of this upregulation with the opiate dependence. Moreover, translocation of overexpressed dynamin from intracellular pools to plasma membranes was observed in chronic morphine-treated rats. This recruitment could be critically involved in long-lasting changes such as alterations of axonal transport observed in opioid dependence.
AB - Several studies using selective opioid agonists or mice with a deletion of the μ-opioid receptor, have shown that morphine dependence is essentially due to chronic stimulation of μ- but not δ-opioid receptors. Because dependence is assumed to be related to persistent intracellular modifications, we have investigated modifications putatively induced by chronic activation of μ receptors with morphine or selective agonists in vitro in SH-SY5Y cells and in vivo in different strains of mice, including mice lacking the μ-opioid receptor gene. The results show a similar down- regulation and desensitization of μ and δ binding sites, whereas an overexpression of dynamin occurred only with μ agonists, strongly suggesting the relevance of this upregulation with the opiate dependence. Moreover, translocation of overexpressed dynamin from intracellular pools to plasma membranes was observed in chronic morphine-treated rats. This recruitment could be critically involved in long-lasting changes such as alterations of axonal transport observed in opioid dependence.
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M3 - Article
C2 - 10860938
AN - SCOPUS:0343953039
VL - 58
SP - 159
EP - 166
JO - Molecular Pharmacology
JF - Molecular Pharmacology
SN - 0026-895X
IS - 1
ER -