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Science 21 June 1985:
Vol. 228. no. 4706, pp. 1451 - 1453
DOI: 10.1126/science.2990029

Articles

Science, Vol 228, Issue 4706, 1451-1453
Copyright © 1985 by American Association for the Advancement of Science


articles

Morphine-induced delay of normal cell death in the avian ciliary ganglion

SD Meriney, DB Gray, and G Pilar

Repeated administration of morphine in increasing doses delayed normal cell death in the ciliary ganglion of the chick embryo; the effect was completely blocked by naloxone. Survival of spinal motoneurons was not affected. Morphine also inhibited potassium-stimulated synthesis of acetylcholine in ganglion cells cultured with muscle, suggesting that morphine can influence neurotransmission. Morphine's effect on cell death may be due to an inhibition of transmission at the neuromuscular junction, but opiates may also directly affect cell death. Although it is now known whether the endogenous opiates in the ciliary ganglion influence neuronal survival during embryogenesis, exogenous opiates can affect normal cell death in the autonomic nervous system.


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G Protein-independent G1 Cell Cycle Block and Apoptosis with Morphine in Adenocarcinoma Cells: Involvement of p53 Phosphorylation.
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{micro}-Opioid receptor inhibits N-type Ca2+ channels in the calyx presynaptic terminal of the embryonic chick ciliary ganglion.
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µ-Opioid Receptor Activates Signaling Pathways Implicated in Cell Survival and Translational Control.
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Developmental Expression of the µ, kappa , and delta  Opioid Receptor mRNAs in Mouse.
Y. Zhu, M.-S. Hsu, and J. E. Pintar (1998)
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Control of embryonic motoneuron survival in vivo by ciliary neurotrophic factor.
R. Oppenheim, D Prevette, Q. Yin, F Collins, and J MacDonald (1991)
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