Figure 1. EFFECT OF ALZHEIMER'S Ab1-40 ON SYNAPTIC PLASTICITY IN CA1 AREA OF ADULT RAT HIPPOCAMPUS. A, Field excitatory postsynaptic potentials (fEPSPs) recorded from a single site in stratum radiatum of CA1 (C) under the condition of the prolonged incubation of slices without the peptide Ab1-40 (Control) or in the presence of the peptide (Ab) are presented as normalized slopes versus time to yield LTP charts. Ab peptide reversed the impairment of the LTP, a characteristic of synaptic plasticity, in slices subjected to 21+ hrs of in vitro maintenance, and made it statistically not different from the slices maintained for 6-8 hrs only (see text). Inset (I/O maximum) illustrates the maximum values of the input-stimulus/output-response (I/O) curves (indicative of basic synaptic physiology) that show no statistical differences (n=6, Pb or without the peptide. D, Representative fEPSPs at the bottom right show that statin mevinolin, a cholesterol synthesis inhibitor (see Scheme 1 for details) abolishes LTP restored by Ab (see text below for discussion details). The presented waveforms are recorded during the baseline stimulation (1), immediately after the tetanic stimulus (2), as well as three (3) and twenty (4) minutes thereafter. Panel B illustrates amino acid sequence differences between rat and used in the study human Ab1-40. Dots on the schematic hippocampal slice (Panel C) illustrate positioning of electrodes.
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