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fEPSPs were recorded on a computerised stimulating and recording unit (PowerLab, ADI instruments) in which the trigger threshold was adjustable. Recordings of field excitatory postsynaptic potentials (fEPSPs) were made from the stratum radiatum in the CA1 region of the right hippocampal hemisphere in response to stimulation of the Schaffer collateral/commissural pathway. 1.2 mm) until the appearance of a negative deflecting excitatory postsynaptic potential (EPSP) that had a latency of ca. The electrodes were slowly lowered through the cortex and the upper layers of the hippocampus and into the CA1 region (approx. The earth electrode location was at 3.0 mm posterior to bregma and 2.5 mm lateral to the midline, contralateral to the electrode sites. Electrodes (tungsten with Teflon coating, Bilaney, Kent, UK) were implanted in the following coordinates: 1.5 mm posterior and 1.0 mm lateral to the midline for the recording electrode, and the stimulating electrode 2.0 mm posterior to bregma and 1.5 mm lateral to the midline. The skull was exposed and 3 holes with 0.8 mm diameter were drilled. Mice were anaesthetised with urethane (ethyl carbamate, 1.8 g/kg, i.p.) for the duration of all experiments. Surgery and LTP recording in the hippocampus area CA1 We therefore set out to investigate if short-term potentiation (paired-pulse facilitation) or long-term potentiation of synaptic transmission in area CA1 in vivo is affected in the APPPS1-21 mice and correlated that with beta-amyloid plaque load in the hippocampus. These findings underscore the differences between different transgenic constructs, and show that the formation of β-amyloid plaques is no guarantee that synaptic impairments develop in the brains of tg mice. In a mouse model that expresses the Swedish APP and the PS1 delta E9 transgenes, in vitro LTP in area CA1 was hardly affected at all. Another mouse model carrying the Swedish mutated human APP and the PS1 (A246E) transgenes showed that LTP in vitro in area CA1 was unaffected, and in vivo LTP the dentate gyrus was only slightly effected in 18 months old mice. In contrast, a mouse model that expresses the Swedish APP K595N, M596L double mutation showed impaired LTP in the dentate gyrus and the area CA1 in 15–17 months old mice. A mouse model that expresses the KM670/671NL human mutated APP showed no impairment in LTP in area CA1 up to 24 months of age. However, studies of mouse models of AD that also overexpress human mutated APP show mixed results. The accumulation of plaques, the development of the inflammation response, and the impairment in memory formation would suggest that synaptic activity will be affected. Synaptic plasticity is a form of rapid upregulation of neurotransmission after repetitive stimulation of axonal projections that is considered to be related to the cellular changes that underlie memory formation. In this study, we have investigated synaptic plasticity in APPPS1-21 mice.
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#MICE HIPPOCAMPUS ANATOMY SERIES#
These findings suggest that the overproduction of β-amyloid, the formation of plaques and the subsequent inflammation response is sufficient to produce a series of symptoms that are consistent with those observed in patients with AD.
#MICE HIPPOCAMPUS ANATOMY PLUS#
Furthermore, spatial memory deficits in a plus maze task is apparent at the age of 8 months. Global neocortical neuron loss is not apparent in this mouse model, but local neuronal loss in the dentate gyrus is observed at 17 months of age (Rupp et al., 2009). Amyloid-associated pathologies include dystrophic synaptic boutons, hyperphosphorylated tau-positive neuritic structures and robust gliosis and microglia numbers. Consistent with this ratio, extensive congophilic parenchymal amyloid but minimal amyloid angiopathy is observed. Plaque formation starts after 2 months in the neocortex and 4 months in the hippocampus, and the ratio of β-amyloid42 to β-amyloid40 is 1.5 in young and 5 in amyloid-depositing older mice, respectively. APPPS1-21 mice are a recently generated transgenic mouse model on a C57BL/6J genetic background that co-expresses the KM670/671NL mutated human amyloid precursor protein and the L166P mutated human presenilin 1 (APPPS1-21 mice) and model aspects of cerebral amyloidosis. Two of the hallmarks are the accumulation of β-amyloid plaques and of tau tangles. Alzheimer disease (AD) is a neurodegenerative disorder for which there is no cure.