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Mu-Opioid Receptors Modulate the Stability of Dendritic Spines
Dezhi Liao, Hang Lin, Ping Yee Law, Horace H. Loh and Richard L. Huganir
Proceedings of the National Academy of Sciences of the United States of America
Vol. 102, No. 5 (Feb. 1, 2005), pp. 1725-1730
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/3374498
Page Count: 6
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Opioids classically regulate the excitability of neurons by suppressing synaptic GABA release from inhibitory neurons. Here, we report a role for opioids in modulating excitatory synaptic transmission. By activating ubiquitously clustered μ-opioid receptor (MOR) in excitatory synapses, morphine caused collapse of preexisting dendritic spines and decreased synaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors. Meanwhile, the opioid antagonist naloxone increased the density of spines. Chronic treatment with morphine decreased the density of dendritic spines even in the presence of Tetrodotoxin, a sodium channel blocker, indicating that the morphine's effect was not caused by altered activity in neural network through suppression of GABA release. The effect of morphine on dendritic spines was absent in transgenic mice lacking MORs and was blocked by CTOP ( D- Phe- Cys- Tyr- D- Trp- Orn- Thr- Pen- ThrNH2), a μ-receptor antagonist. These data together with others suggest that endogenous opioids and/or constitutive activity of MORs participate in maintaining normal morphology and function of spines, challenging the classical model of opioids. Abnormal alteration of spines may occur in drug addiction when opioid receptors are overactivated by exogenous opiates.
Proceedings of the National Academy of Sciences of the United States of America © 2005 National Academy of Sciences