Publications by authors named "Hui-Feng Jiao"

Mutations in some cell adhesion molecules (CAMs) cause abnormal synapse formation and maturation, and serve as one of the potential mechanisms of autism spectrum disorders (ASDs). Recently, (Down syndrome cell adhesion molecule) was found to be a high-risk gene for autism. However, it is still unclear how DSCAM contributes to ASD.

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Neurotransmission in dentate gyrus (DG) is critical for spatial coding, learning memory, and emotion processing. Although DG dysfunction is implicated in psychiatric disorders, including schizophrenia, underlying pathological mechanisms remain unclear. Here we report that transmembrane protein 108 (Tmem108), a novel schizophrenia susceptibility gene, is highly enriched in DG granule neurons and its expression increased at the postnatal period critical for DG development.

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A series of all-conjugated polythiophene diblock copolymers containing hydrophobic (hexyl) and hydrophilic (triethylene glycol) side chains were synthesized via a nickel-catalyzed quasi-living polymerization. The correlations between block ratios and the self-assembled nanostructures of the block copolymers in thin films and in various solutions were examined. The copolymers dispersed in water via a slow dialysis method produced molecular-level self-assembled core-shell nanospheres with a crystallized hydrophobic core and a hydrophilic amorphous shell, which was proved by TEM images.

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Neurotransmission requires precise control of neurotransmitter release from axon terminals. This process is regulated by glial cells; however, the underlying mechanisms are not fully understood. We found that glutamate release in the brain was impaired in mice lacking low-density lipoprotein receptor-related protein 4 (Lrp4), a protein that is critical for neuromuscular junction formation.

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Article Synopsis
  • - The study explores how inhibitory neurotransmission in the amygdala is vital for fear learning and memory, focusing on the role of neuregulin 1 (NRG1) and its receptor ErbB4 in controlling GABAergic activity.
  • - It was found that disabling NRG1 or removing ErbB4 led to reduced GABA transmission and impaired fear conditioning, particularly when ErbB4 was absent in specific neurons.
  • - The research suggests that NRG1 signaling is crucial for maintaining GABA activity in the amygdala, linking these findings to potential mechanisms for schizophrenia since both NRG1 and ErbB4 are implicated in this disorder.
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