conferenceObject
Acute amyloid ? (25–35 and 1–40) effects on oscillatory activity and synaptic plasticity in the CA3–CA1 circuit of the hippocampus
Autor
Nava-Mesa, Mauricio O.
Gauthier-Umaña, Cecile
Muñoz-Cabrera, Jonhatan
Valderrama, Mario
Munera, Alejandro
Institución
Resumen
Recent evidence suggests that soluble amyloid ? (A?) species induce glutamatergic, cholinergic and GABAergic systems imbalance resulting in neural network functional impairment during early stages of Alzheimer's disease (AD). Given the critical relevance of finely-tuned oscillatory activity via fimbria/fornix complex for hippocampal-dependent learning and memory processes, such A? induced dysfunction results particularly deleterious. Acute intrahippocampal A? injection in anesthetized rats was used to evaluate soluble A? variants (25–35 and 1–40) effects on synaptic plasticity and oscillatory activity in the commissural CA3 to CA1 circuit of the hippocampus. Impaired long- term potentiation (LTP) was found after soluble A? injection in CA1. Contralateral CA3 stimulation-induced CA1 oscillatory activity spectral power distribution significantly changed 60 min after high frequency stimulation (HFS) due to theta and gamma band changes in power spectral density (PSD). Moreover, HFS-induced delta to gamma phase-amplitude coupling enhancement was significantly impaired after either A? 25–35 or A? 1–40. Therefore, this work shows evidence that soluble A? species-induced neural network activity impairment is associated with changes on oscillatory activity and synaptic plasticity in the hippocampal CA3–CA1 circuit. In addition the ad hoc developed analytic procedures set up for this study are a useful model approach not only to characterize oscillatory activity organization and dynamics, but also for understanding AD pathophysiology, suggesting that oscillatory dysfunction as a useful early A? pathology biomarker.