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Potassium‐ and Carbachol‐Evoked Release of [ 3 H]Noradrenaline from Human Neuroblastoma Cells, SH‐SY5Y
Author(s) -
Murphy Nuala P.,
Ball Stephen G.,
Vaughan Peter F. T.
Publication year - 1991
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1991.tb02085.x
Subject(s) - carbachol , pirenzepine , endocrinology , chemistry , medicine , potassium , calcium , cholinergic , antagonist , sh sy5y , receptor antagonist , receptor , neuroblastoma , biology , cell culture , biochemistry , genetics , organic chemistry
The human neuroblastoma clone SH‐SY5Y expresses potassium‐, carbachol‐, and calcium ionophore A23187‐evoked, calcium‐dependent release of [ 3 H]noradrenaline. Release in response to carbachol and potassium was greater than additive. Atropine ( K i = 0.33 n M ), hexahydrosiladifenidol ( K i = 18 n M ), and pirenzepine ( K i = 1,183 n M ) completely inhibited the carbachol‐evoked noradrenaline release, an order of potency suggesting that an M 3 receptor was linked to release. In contrast, noradrenaline release was only partially inhibited by the M 2 ‐selective antagonists meth‐octramine (10 ‐4 M ) and AFDX‐116 (10 ‐4 M ), by ∼14 and 46%, respectively. The nicotinic antagonist d ‐tubocurarine (10 ‐4 M ) resulted in a partial inhibition of release, a finding suggesting that a nicotinic receptor may also be involved. SH‐SY5Y provides a suitable cell line in which to study the biochemical mechanisms underlying the cholinergic receptor regulation of noradrenaline release.