In fact, A ОІ-induced synaptic dysfunction precedes selective neuronal degeneration and may explain memory impairment during early AD stages and mild cognitive impairment, a prodromal stage of AD. Recent evidence indicates that soluble forms of A ОІ induce glutamatergic, cholinergic, and GABAergic imbalance, resulting in functional impairment of neural networks during early AD stages. IntroductionДЄlzheimerвЂ™s disease (AD), the most common type of dementia and progressive neurodegenerative disorder worldwide, is characterized by selective neuronal loss, and two histopathological features in postmortem tissue are extracellular amyloid plaques composed of amyloid beta peptide (A ОІ) and intracellular neurofibrillary tangles composed of hyperphosphorylated tau protein. These results provide further evidence that soluble A ОІ species induce synaptic dysfunction causing abnormal synaptic variability, impaired long-term plasticity, and deviant oscillatory activity, leading to network activity derailment in the hippocampus. Although soluble A ОІ microinjection significantly increased the relative power of Оі-band and ripple oscillations and significantly shifted the average vector of Оё-to- Оі phase-amplitude coupling (PAC) in CA1, it prevented Оё-to- Оі PAC shift induced by high-frequency CA3 stimulation, opposite to what was observed in vehicle-injected animals. High-frequency CA3 stimulation was rendered inefficient by soluble A ОІ intrahippocampal injection to induce long-term potentiation and to enhance synaptic variability in CA1, contrasting with what was observed in vehicle-injected subjects. Soluble A ОІ microinjection increased cCA3-to-CA1 synaptic variability without significant changes in synaptic efficiency. To evaluate the in vivo effects of two soluble A ОІ species (A ОІ 25-35 and A ОІ 1-40) on commissural CA3-to-CA1 (cCA3-to-CA1) synaptic transmission and plasticity, and CA1 oscillatory activity, we used acute intrahippocampal microinjections in adult anaesthetized male Wistar rats. Recent evidence indicates that soluble amyloid- ОІ (A ОІ) species induce imbalances in excitatory and inhibitory transmission, resulting in neural network functional impairment and cognitive deficits during early stages of AlzheimerвЂ™s disease (AD).

Hippocampus anatomy diagram ca1 ca2 ca3