Beta-amyloid peptide-induced modifications in α7 nicotinic acetylcholine receptor immunoreactivity in the hippocampus of the rat:: Relationship with GABAergic and calcium-binding proteins perikarya

The effects of the injected beta-amyloid (AP) protein on the alpha 7 subtype of nicotinic acetylcholine receptor protein (alpha 7nAChR) in the hippocampus were studied in rats. Injections of AP into the retrosplenial cortex resulted in a decrease in alpha 7nAChR-immunoreactivity in the hippocampus. Quantitative analysis revealed a significant reduction in (alpha 7nAChR-immunoreactivity in the dorsal part of the CA1 ipsilateral to the A beta-injected side as compared to the corresponding hemisphere of non-treated control animals and with that seen in the contralateral hemisphere, which corresponds to the control (PBS)-injected side. A significant decrease in alpha 7nAChR-immunoreactivity was also found in the dorsal part of the ipsilateral CA1 as compared with that in the ventral part of the CA1, in CA2, and in CA3 ipsilateral to the A beta-injected side. The analysis also revealed a significant decrease in (alpha 7nAChR-immunoreactivity in the dentate gyrus ipsilateral to the A beta-injected side as compared to the corresponding hemisphere of non-treated control animals and with that in the PBS-injected side co-localization studies showed that the alpha 7nAChR protein is highly localized in GABA- and Parv-immunoreactive cells, while only few Calb-positive cells expressed immunoreactivity for alpha 7nAChR. In addition, injections of AP protein resulted in a significant reduction in the number of GABA- and Parv-immunoreactive cells in the dorsal part of the ipsilateral CA1 as compared to the corresponding region of non-treated control animals and with that in the corresponding region of the PBS-injected side. Our findings suggest that AP induces a reduction in alpha 7nAChR-containing cells, which may contribute to impairment of GABAergic synaptic transmission in the hippocampus. (C) 2007 Elsevier Inc. All rights reserved.