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Cindy Chu

Researcher at University of Sydney

Publications -  6
Citations -  278

Cindy Chu is an academic researcher from University of Sydney. The author has contributed to research in topics: Nicotinic agonist & Acetylcholine receptor. The author has an hindex of 4, co-authored 6 publications receiving 250 citations.

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The Flavonoid Glycosides, Myricitrin, Gossypin and Naringin Exert Anxiolytic Action in Mice

TL;DR: The results suggest that flavonoid glycosides have the potential to exert a range of CNS-mediated biological activities, including anxiolytic and sedative effects.
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The β‐amyloid protein of Alzheimer’s disease binds to membrane lipids but does not bind to the α7 nicotinic acetylcholine receptor

TL;DR: The effects of Aβ are unlikely to be mediated by direct binding to the α7nAChR, and it is speculated that Aβ may exert its effects by altering the packing of lipids within the plasma membrane, which could, in turn, influence the function of a variety of receptors and channels on the cell surface.
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Methyllycaconitine analogues have mixed antagonist effects at nicotinic acetylcholine receptors

TL;DR: This study more clearly defines the biological effects of MLA analogues at nA ChRs and demonstrates that these analogues are not selective ligands for the alpha7 nAChR subtype.
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Presence of multiple binding sites on α9α10 nAChR receptors alludes to stoichiometric-dependent action of the α-conotoxin, Vc1.1.

TL;DR: Using 2-electrode voltage clamp methods and maintaining a constant intracellular Ca(2+) concentration, this study observed a biphasic activation curve for ACh that is dependent on receptor stoichiometry and infer that there is an additional binding site for A Ch and Vc1.1 at the α9-α9 interface on the hypothesized (α9)₃(α10)⁂ nAChR.
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Role of Aβ and the α7 nicotinic acetylcholine receptor in regulating synaptic plasticity in Alzheimer's disease

TL;DR: In cell culture experiments, the binding of Aβ to the α7 nAChR has been found to cause an increase in the level of acetylcholinesterase, which is also increased around amyloid plaques in the AD brain.