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. Author manuscript; available in PMC: 2012 Apr 4.
Published in final edited form as: Neuromolecular Med. 2009 Oct 17;12(1):48–55. doi: 10.1007/s12017-009-8097-7

Figure 2. High Levels of Aβ Lead to Synapse-Specific Electrophysiological Deficits and Increased Network Synchronization in Animal Models.

Figure 2

A) hAPPJ20 mice with high levels of Aβ had different synaptic impairments in CA1 (top) and the dentate gyrus (DG) (bottom). At the Schaffer collateral to CA1 pyramidal cell synapse, long-term potentiation (LTP) (left) and paired-pulse facilitation (middle) were normal, whereas synaptic transmission strength (right) was impaired. At the perforant path to granule cell synapse in the DG, LTP (left) and paired-pulse modification (middle) were impaired, whereas synaptic transmission strength (right) was normal, as compared with NTG controls. B) Cortical and hippocampal EEG recordings demonstrating epileptiform spike discharges (left) and generalized non-convulsive seizures (right) in hAPPJ20 mice. fEPSP, field excitatory postsynaptic potentials; HFS, high frequency stimulation; TBS, theta-burst stimulation. L, left; R, right; F, frontal; T, temporal; P, parietal; O, posterior-parietal; and H, hippocampal. Adapted from (Palop et al., 2007).