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Development of a neural phenotype in differentiating ganglion cell‐derived human neuroblastoma cells
Author(s) -
Scott Ian G.,
Åkerman Karl E. O.,
Heikkilä Jari E.,
Kaila Kai,
Andersson Leif C.
Publication year - 1986
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041280221
Subject(s) - acetylcholine , muscarine , muscarinic acetylcholine receptor , chemistry , endocrinology , medicine , quinuclidinyl benzilate , atropine , agonist , muscarinic agonist , acetylcholine receptor , neuroblastoma , ionophore , receptor , biophysics , microbiology and biotechnology , biology , cell culture , biochemistry , membrane , genetics
Human neuroblastoma cells (clone SHSY‐5Y) induced to differentiate by 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) are shown to possess properties characteristic of mature ganglion cells. Elevation of the external K + concentration, exposure to Ca 2+ ionophore A23187, and acetylcholine all stimulate the release of preloaded 3 H‐noradrenaline in the presence but not in the absence of added Ca 2+ . Acetylcholine causes a fall in the 86 Rb + or 14 C‐TPMP equilibrium potential across the plasma membrane and stimulates 86 Rb + efflux. These responses are prevented by atropine. Acetylcholine and muscarine but not nicotine stimulate an increase in 45 Ca 2+ influx, an effect blocked by atropine. None of these responses have been observed in nondifferentiating cells. Muscarinic receptors, however, as measured by the binding of tritiated quinuclidinyl benzilate ( 3 H‐QNB), were present to a similar extent in control and differentiated cells. Both cell types also exhibit an accelerated release of Ca 2+ in response to acetylcholine, but the control cells were at least 1 order of magnitude more sensitive to the agonist.