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Activation of α 7 nicotinic acetylcholine receptor promotes survival of spinal cord motoneurons
Author(s) -
Messi M.L,
Renganathan M,
Grigorenko E,
Delbono O
Publication year - 1997
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(97)00600-5
Subject(s) - spinal cord , programmed cell death , amyotrophic lateral sclerosis , nicotinic agonist , microbiology and biotechnology , nicotinic acetylcholine receptor , intracellular , acetylcholine receptor , receptor , embryonic stem cell , biology , acetylcholine , neuroscience , chemistry , pharmacology , medicine , biochemistry , apoptosis , disease , gene
Spinal cord motoneurons (MNs) undergo a process of cell death during embryonic development [1]and are the target of lethal acquired or inherited disorders, such as the amyotrophic lateral sclerosis. Therefore, the identification of mechanisms leading to MN survival is of crucial importance. Elevations in intracellular Ca 2+ promote chicken MN survival during the embryonic period of naturally occurring cell death [2, 3]. We have recently demonstrated that the α 7 nicotinic acetylcholine receptor (nAChR) mediates significant increases in free Ca 2+ concentration at membrane potentials at which other pathways for Ca 2+ influx are inactive [4, 5]. Although it is possible that Ca 2+ influx through α 7 nAChR promotes cell survival, the relation between α 7 nAChR activation, cytosolic free Ca 2+ and mammalian spinal cord MN survival has not been established. In the present study we have now demonstrated that Ca 2+ influx through the α 7 ‐subunit is sufficient to rescue a significant number of cultured spinal cord MNs from programmed cell death induced by trophic factor deprivation. This is the first demonstration that neuronal nAChRs are involved in the regulation of MN survival.