The effect of β-Amyloid (1-40), Rat was studied in long-term potentiation of glutamatergic excitatory field potentials recorded postsynaptic molecular in the inner layer in the dentate gyrus in rats in vitro. In the presence of 200 nM β-amyloid (1-40) there was an increase in long-term potentiation of 51%. Basal synaptic transmission was not affected. These results provide direct evidence that the relatively low concentration of β-Amyloid (1-40), Rat increases synaptic plasticity.
We examined the histological changes produced by injections of beta-amyloid [β (1-40)], and control peptides in rat and monkey cerebral cortex. ß (25-35) injections were also studied in the rat cortex. Immunoperoxidase procedures standards were used to detect the distribution of tau, MAP2, β (1-40) and ALZ 50 immunoreactivity. All injections of localized necrosis at the injection site surrounded by a zone of neuronal loss and gliosis. In rat cortex, the lesions produced by solubilized β-Amyloid (1-40), Rat and β (25-35) in water were generally larger than those produced by control peptides. Tau and ALZ 50 antibodies labeled neurites and diffuse positive perikarya around β-Amyloid (1-40), Ratinjections, whereas MAP2 staining was reduced in parallel with the distribution of neuronal loss and gliosis. In the cortex of aged primates, lesion size β (1-40) was dose dependent. Hyalinized, ALZ 50 positive neurons, and abnormal neurites were prominent around the injection site. Although β-amyloid is strongly neurotoxic in the rat and monkey cerebral cortex, neuronal degeneration in primates is more similar to that found in AD.
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