The rescue of developing avian motoneurons from programmed cell death by a selective inhibitor of the fetal muscle-specific nicotinic acetylcholine receptor

Developmental Neurobiology
Ronald W OppenheimRussell W Teichert

Abstract

In an attempt to determine whether the rescue of developing motoneurons (MNS) from programmed cell death (PCD) in the chick embryo following reductions in neuromuscular function involves muscle or neuronal nicotinic acetylcholine receptors (nAChRs), we have employed a novel cone snail toxin alphaA-OIVA that acts selectively to antagonize the embryonic/fetal form of muscle nAChRs. The results demonstrate that alphaA-OIVA is nearly as effective as curare or alpha-bungarotoxin (alpha-BTX) in reducing neuromuscular function and is equally effective in increasing MN survival and intramuscular axon branching. Together with previous reports, we also provide evidence consistent with a transition between the embryonic/fetal form to the adult form of muscle nAChRs in chicken that involves the loss of the gamma subunit in the adult receptor. We conclude that selective inhibition of the embryonic/fetal form of the chicken muscle nAChR is sufficient to rescue MNs from PCD without any involvement of neuronal nAChRs.

References

Oct 1, 1979·Experimental Neurology·T L Creazzo, G S Sohal
Dec 1, 1990·Journal of Neurobiology·L J HouenouF Rieger
Jul 1, 1989·Trends in Neurosciences·R W Oppenheim
Jan 1, 1989·Toxicon : Official Journal of the International Society on Toxinology·N H Tan, C S Tan
Mar 1, 1988·Proceedings of the National Academy of Sciences of the United States of America·D A HarrisG D Fischbach
Dec 1, 1983·Journal of Neurocytology·R DingH Tønnesen
Jan 1, 1995·Toxicon : Official Journal of the International Society on Toxinology·W W LinC Y Lee
Jan 1, 1997·Annual Review of Neuroscience·G D Fischbach, K M Rosen
Sep 5, 1997·The Journal of Biological Chemistry·R JacobsenJ M McIntosh
May 15, 1998·Neuron·B Pettmann, C E Henderson
Nov 22, 2000·The Journal of Comparative Neurology·G B BanksP G Noakes
Sep 3, 2002·The Journal of Comparative Neurology·Gillian L Bunker, Rae Nishi
Nov 28, 2002·The Journal of Comparative Neurology·C Jane H KeigerRonald W Oppenheim
Jul 13, 2004·Toxicon : Official Journal of the International Society on Toxinology·Russell W TeichertBaldomero M Olivera
Jan 22, 2005·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Russell W TeichertBaldomero M Olivera
May 11, 2005·Biochemical and Biophysical Research Communications·Norihiro YumotoAtsuko Sehara-Fujisawa
Oct 26, 2007·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Martin Hruska, Rae Nishi
Jan 1, 1951·Journal of Morphology·V HAMBURGER, H L HAMILTON

❮ Previous
Next ❯

Citations

May 26, 2010·Proceedings of the National Academy of Sciences of the United States of America·Mahru C AnKuo-Fen Lee
Nov 13, 2013·The Journal of Cell Biology·Martijn P J DekkersYves-Alain Barde
Jul 29, 2009·Molecular and Cellular Biology·Braulio M de CastroVania F Prado
Mar 2, 2016·Proceedings of the National Academy of Sciences of the United States of America·Eleonora PalmaMaurizio Inghilleri
Feb 13, 2010·The European Journal of Neuroscience·Pessah YampolskyVeit Witzemann
Sep 2, 2011·Journal of Neurophysiology·Andrew A Sharp, Sylvia Fromherz

❮ Previous
Next ❯

Related Concepts

Related Feeds

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis