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Elevated NEGR1 in brain induces anxiety or depression-like phenotypes and synaptic dysfunction.

Ya-Qi Zhang1,2,3, Qing Zhang4,5, Yi Yang1,2,3

  • 1State Key Laboratory of Genetic Evolution & Animal Models, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, China.

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A specific gene variant (rs3101339) linked to depression increases NEGR1 expression. This gene overexpression in mice brains causes anxiety, depression, and impaired synaptic function, suggesting a role in mental health disorders.

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Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Single nucleotide polymorphisms (SNPs) in the 1p31.1 region are associated with depression.
  • A specific regulatory variant, rs3101339, was previously identified but its role in depression pathogenesis was unclear.

Purpose of the Study:

  • To elucidate the precise role of the rs3101339 variant in depression.
  • To investigate the functional consequences of NEGR1 gene upregulation in the brain.

Main Methods:

  • Regulatory element annotation, brain expression quantitative trait loci (eQTL) analysis.
  • Reporter gene assays, electrophoretic mobility shift assay (EMSA), and genome editing.
  • Stereotaxic injection for NEGR1 overexpression in mouse brain regions (mPFC, vHIP), behavioral tests, neuronal labeling, electron microscopy, immunoprecipitation-mass spectrometry (IP-MS), and transcriptomic profiling.

Main Results:

  • The rs3101339 risk allele C upregulates NEGR1 expression, confirming it as a causal variant.
  • NEGR1 overexpression in the mouse ventral hippocampus (vHIP) induced anxiety, depression-like behaviors, and working memory deficits.
  • NEGR1 overexpression led to dendritic spine loss, synaptic abnormalities, and altered protein interactions, impacting neurotransmitter exocytosis and vesicle endocytosis.
  • Transcriptomic analysis revealed enrichment of myelination-related pathways in NEGR1-overexpressing mice.

Conclusions:

  • NEGR1 upregulation in the brain is implicated as a driver of anxiety and depression-like phenotypes.
  • Impaired synaptic function and myelination are potential mechanisms underlying these behaviors.
  • The rs3101339 variant's role in NEGR1 regulation offers a potential target for understanding and treating depression.