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Selective changes in expression of different nicotinic receptor subtypes in brain and adrenal glands of mice carrying human mutated gene for APP or over‐expressing human acetylcholinestrase
Author(s) -
Mousavi Malahat,
Bednar Ivan,
Nordberg Agneta
Publication year - 2004
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2004.07.005
Subject(s) - endocrinology , medicine , epibatidine , nicotinic agonist , cholinergic , acetylcholine receptor , receptor , biology , cortex (anatomy) , genetically modified mouse , nicotinic acetylcholine receptor , human brain , transgene , neuroscience , gene , biochemistry
In this study, we investigated regulatory mechanisms and plasticity of the nicotinic acetylcholine receptors (nAChRs) in the brain and adrenal glands of two transgenic mice models over‐expressing human β‐amyloid precursor protein (APP SWE Tg) and human AChE enzyme (hAChE‐Tg), respectively. All animals were studied at 3 months of age. Binding studies showed higher 125 I‐α‐bungarotoxin (α7 nAChRs) and 3 H‐epibatidine (α3 and α4 nAChRs) binding in the brain cortex and adrenal glands of hAChE‐Tg mice compared to control mice. The APP SWE Tg mice showed a significantly lower relative level for the α4 mRNA in the brain cortex as well as a lower level of α3 mRNA, and higher level of α7 mRNA in the adrenal glands compared to control mice. A higher relative mRNA level of α3 and α4 nAChRs was observed in the brain as well as of α3 and α7 nAChRs in the adrenal glands of hAChE‐Tg mice compared to control mice. Different nicotinic receptor plasticity is revealed in the brain cortex and adrenal glands in two transgenic mice models with different underlying pathophysiological mechanisms. Deposition of β‐amyloid (Aβ) may impair neurotransmitter activity in brain as well as in the adrenal gland.