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Jingjing Cheng

Researcher at Zhejiang University

Publications -  5
Citations -  174

Jingjing Cheng is an academic researcher from Zhejiang University. The author has contributed to research in topics: Nucleus accumbens & Internal medicine. The author has an hindex of 4, co-authored 4 publications receiving 118 citations.

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Amyloid β oligomers suppress excitatory transmitter release via presynaptic depletion of phosphatidylinositol-4,5-bisphosphate.

TL;DR: The results first reveal the presynaptic mGluR5-PIP2 pathway whereby oligomeric Aβ induces early synaptic deficits in AD and rescues synaptic and spatial learning and memory deficits in APP/PS1 mice.
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Anterior Paraventricular Thalamus to Nucleus Accumbens Projection Is Involved in Feeding Behavior in a Novel Environment.

TL;DR: This work reveals that activation of the aPVT-NAc pathway in mice generates a motivation to consume food in a novel environment.
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Toll-Like Receptor 4 Deficiency Causes Reduced Exploratory Behavior in Mice Under Approach-Avoidance Conflict

TL;DR: The reduced exploratory behaviors under approach-avoidance conflict were not due to a high anxiety level or an enhanced fear response in the TLR4−/− mice, as these mice showed normal anxiety and fear responses in the open field and passive avoidance tests, respectively.
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Postnatal feeding with high-fat diet induces obesity and precocious puberty in C57BL/6J mouse pups: a novel model of obesity and puberty

TL;DR: High-fat diet is provided to dams during lactation and to pups after weaning and a novel model of C57BL/6J mouse pups with HFD-induced postnatal obesity suggests good construction validity of obesity and precocious puberty.
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Diet-induced inflammation in the anterior paraventricular thalamus induces compulsive sucrose-seeking

TL;DR: It is reported that high-fat diet consumption impedes threat-cue-induced suppression of sucrose-seeking in mice and compulsive food-seeking was due to enhanced cue-triggered neuronal activity in the anterior paraventricular thalamus resulting from HFD-induced microglia activation.