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Nicotinic acetylcholine receptor subtypes in human frontal cortex: Changes in Alzheimer's disease
Author(s) -
Sugaya K.,
Giacobini E.,
Chiappinelli V. A.
Publication year - 1990
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490270314
Subject(s) - nicotinic agonist , acetylcholine receptor , nicotine , bungarotoxin , acetylcholine , cerebral cortex , neuroscience , receptor , alpha 4 beta 2 nicotinic receptor , alzheimer's disease , cortex (anatomy) , nicotinic acetylcholine receptor , medicine , biology , endocrinology , chemistry , disease
Molecular genetic and pharmacological studies have suggested that several subtypes of nicotinic acetylcholine receptors exist in the mammalian and avian brain. Combining 3 H‐(−)‐nicotine, 125 I‐α‐bungarotoxin, and 125 I‐κ‐bungarotoxin as ligands, we report here the first evidence for the existence in human frontal cortex of at least three different subtypes of nicotinic receptors. Autoradiographic analysis shows that specific 125 I‐κ‐bungarotoxin binding sites are concentrated mainly in several cortical layers. We also show that κ‐bungarotoxin, but not κ‐bungarotoxin decreases the evoked release of 3 H‐acetylcholine in rat cortical slices, indicating a likely presynaptic localization for some of the α‐bungarotoxin‐insensitive κ‐bungarotoxin sites in mammalian brain. The brains of patients with Alzheimer's disease show marked decreases in B max values for low‐affinity 125I‐κ‐bungarotoxin sites and both high‐ and low‐affinity 3 H‐nicotine sites, whereas 125 I‐κ‐bungarotoxin sites are not significantly different in number from age‐matched control brains. We conclude that Alzheimer's disease does not affect all subtypes of nicotinic receptors in the frontal cortex to the same extent.