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. 2005 Feb 10;102(8):3046–3051. doi: 10.1073/pnas.0408500102

Fig. 2.

Fig. 2.

Age-dependent reduction in α7nAChRs levels in the hippocampus of 3xTg-AD mice. (A) Quantitative analysis of α-bungarotoxin binding reveals an age-related decrease in α7nAChR steady-state levels in the hippocampus of 3xTg-AD mice beginning at 6 months of age (P < 0.001). At 2 and 4 months of age, no difference in the α7nAChRs steady-state levels is apparent between 3xTg-AD and NonTg mice, indicating that the 3xTg-AD mice are not born with this deficit (P = 0.208 and 0.087 for 2 and 4 month olds, respectively). The reduction in α7nAChRs correlates with intraneuronal Aβ accumulation because 2- and 4-month-old 3xTg-AD mice do not show any immunoreactivity with an anti-Aβ antibody. (B) A representative microphotograph of the hippocampus of a 4-month-old hemizygous 3xTg-AD mouse stained with an Aβ42 specific-antibody. Note the lack of immunostaining in the CA1 pyramidal neurons defined by the arrows. (C) By 6 months of age, hemizygous 3xTg-AD mice show prominent intraneuronal Aβ42 buildup in CA1 pyramidal neurons after staining with an anti-Aβ specific antibody.