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Beta‐amyloid peptide is toxic to cholinoceptive neurones in vivo via indirect mechanisms
Author(s) -
Gonzalez I.,
Gonzalo P.,
GonzaloRuiz A.
Publication year - 2003
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 - 10.1046/j.1471-4159.85.s2.16_1.x
Subject(s) - hippocampus , parvalbumin , neuroscience , cerebral cortex , gabaergic , cortex (anatomy) , chemistry , in vivo , somatostatin , biology , inhibitory postsynaptic potential , microbiology and biotechnology
The effects of amyloid‐beta (Aβ) protein on the expression of m1, m2 subunits of mAChR and on α7nAChR were analyzed in the cerebral cortex and in the hippocampus of rats following injections of Aβ (1–40) (BACHEM, 2 μg in 1 μL of PBS) into the left retroesplenial cortex (RSg) and injections of 1 μL of PBS into the right RSg. Sections were immunoreacted for the localization of α7, m1, m2, GABA, somatostatin and parvalbumin. Injections of Aβ resulted in loss of neurones expressing α7‐ and m1‐like immunoreactivity (IR) in frontal, RSg cortices, hippocampus and subicular complex. A decrease of α7, m1‐ and m2‐like‐IR fibers and structures‐like terminals was also seen in hippocampus, subicular and cerebral cortex. α7nAChR and m1, m2 subuntis of mAChRs were most commonly identified on GABAergic interneurones. These results point to an effect of Aβ on the synthesis of α7nAChR and mAChRs and suggest an important role of cholinoceptive interneurones in the dysfunction of hippocampus and cerebral cortex seen in AD.