Glutamatergic CYLD deletion leads to aberrant excitatory activity in the basolateral amygdala: association with enhanced cued fear expression DOI Creative Commons
H. N. Li, F. Li,

Zhaoyi Chen

et al.

Neural Regeneration Research, Journal Year: 2024, Volume and Issue: 20(11), P. 3259 - 3272

Published: June 3, 2024

JOURNAL/nrgr/04.03/01300535-202511000-00029/figure1/v/2024-12-20T164640Z/r/image-tiff Neuronal activity, synaptic transmission, and molecular changes in the basolateral amygdala play critical roles fear memory. Cylindromatosis (CYLD) is a deubiquitinase that negatively regulates nuclear factor kappa-B pathway. CYLD well studied non-neuronal cells, yet under-investigated brain, where it highly expressed. Emerging studies have shown involvement of remodeling glutamatergic synapses, neuroinflammation, memory, anxiety- autism-like behaviors. However, precise role neurons largely unknown. Here, we first proposed cued expression. We next constructed transgenic model mice with specific deletion Cyld from neurons. Our results show deficiency exaggerated expression only male mice. Further, loss resulted enhanced neuronal activation, impaired excitatory altered levels glutamate receptors accompanied by over-activation microglia Altogether, our study suggests maintaining normal neuronal, synaptic, microglial activation. This may contribute, at least part, to

Language: Английский

Glutamatergic CYLD deletion leads to aberrant excitatory activity in the basolateral amygdala: association with enhanced cued fear expression DOI Creative Commons
H. N. Li, F. Li,

Zhaoyi Chen

et al.

Neural Regeneration Research, Journal Year: 2024, Volume and Issue: 20(11), P. 3259 - 3272

Published: June 3, 2024

JOURNAL/nrgr/04.03/01300535-202511000-00029/figure1/v/2024-12-20T164640Z/r/image-tiff Neuronal activity, synaptic transmission, and molecular changes in the basolateral amygdala play critical roles fear memory. Cylindromatosis (CYLD) is a deubiquitinase that negatively regulates nuclear factor kappa-B pathway. CYLD well studied non-neuronal cells, yet under-investigated brain, where it highly expressed. Emerging studies have shown involvement of remodeling glutamatergic synapses, neuroinflammation, memory, anxiety- autism-like behaviors. However, precise role neurons largely unknown. Here, we first proposed cued expression. We next constructed transgenic model mice with specific deletion Cyld from neurons. Our results show deficiency exaggerated expression only male mice. Further, loss resulted enhanced neuronal activation, impaired excitatory altered levels glutamate receptors accompanied by over-activation microglia Altogether, our study suggests maintaining normal neuronal, synaptic, microglial activation. This may contribute, at least part, to

Language: Английский

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