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Rhynchophylline Protects Against the Amyloid β-Induced Increase of Spontaneous Discharges in the Hippocampal CA1 Region of Rats
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Rhynchophylline Protects Against the Amyloid β-Induced Increase of Spontaneous Discharges in the Hippocampal CA1 Region of Rats
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Rhynchophylline Protects Against the Amyloid β-Induced Increase of Spontaneous Discharges in the Hippocampal CA1 Region of Rats
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Journal Article
Rhynchophylline Protects Against the Amyloid β-Induced Increase of Spontaneous Discharges in the Hippocampal CA1 Region of Rats
2015
Overview
Accumulated soluble amyloid β (Aβ)-induced aberrant neuronal network activity has been recognized as a key causative factor leading to cognitive deficits which are the most outstanding characteristic of Alzheimer’s disease (AD). As an important structure associated with learning and memory, the hippocampus is one of the brain regions that are impaired very early in AD, and the hippocampal CA1 region is selectively vulnerable to soluble Aβ oligomers. Our recent study showed that soluble Aβ
1–42
oligomers induced hyperactivity and perturbed the firing patterns in hippocampal neurons. Rhynchophylline (RIN) is an important active tetracyclic oxindole alkaloid isolated from
Uncaria rhynchophylla
which is a traditional Chinese medicine and often used to treat central nervous system illnesses such as hypertension, convulsions, tremor, stroke etc. Previous evidence showed that RIN possessed neuroprotective effects of improving the cognitive function of mice with Alzheimer-like symptoms. In the present study, we aimed to investigate the protective effect of RIN against soluble Aβ
1–42
oligomers-induced hippocampal hyperactivity. The results showed that (1) the mean frequency of spontaneous discharge was increased by the local application of 3 μM soluble Aβ
1–42
oligomers; (2) 30 μM RIN did not exert any obvious effects on basal physiological discharges; and (3) treatment with RIN effectively inhibited the soluble Aβ
1–42
oligomers-induced enhancement of spontaneous discharge, in a concentration-dependent manner with an IC
50
= 9.0 μM. These in vivo electrophysiological results indicate that RIN can remold the spontaneous discharges disturbed by Aβ and counteract the deleterious effect of Aβ
1–42
on neural circuit. The experimental findings provide further evidence to affirm the potential of RIN as a worthy candidate for further development into a therapeutic agent for AD.
Publisher
Springer US
Subject
Amyloid beta-Peptides - antagonists & inhibitors
/ Amyloid beta-Peptides - toxicity
/ Amyloid Neuropathies - physiopathology
/ Amyloid Neuropathies - prevention & control
/ Amyloid Neuropathies - psychology
/ Animals
/ Biomedical and Life Sciences
/ CA1 Region, Hippocampal - drug effects
/ CA1 Region, Hippocampal - physiopathology
/ Cognition Disorders - chemically induced
/ Cognition Disorders - psychology
/ Dose-Response Relationship, Drug
/ Indole Alkaloids - pharmacology
/ Male
/ Neuroprotective Agents - pharmacology
/ Peptide Fragments - antagonists & inhibitors
/ Peptide Fragments - toxicity
/ Rats
