Toward Antifragility: Social Defeat Stress Enhances Learning and Memory in Young Mice Via Hippocampal Synaptosome Associated Protein 25

Yang, Ligong; Shi, Lijun; Shen, S. C.; Yang, Jianmin; Lv, Su‐Su; Wang, Zhe‐Chen; Huang, Qian; Xu, Wendong; Yu, Jin; Zhang, Yu‐Qiu

doi:10.1177/09567976231160098

Cited by 2 publications

(1 citation statement)

References 45 publications

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“…It is known that environmental factors can influence LTP. For example, poor maternal care (low grooming by mothers) inhibits the induction of LTP in the offspring [86,87], and social defeat stress has been found to enhance LTP [88]. The majority of studies in other brain HET and KO KO mice.…”

Section: (A) Cage Effects On Long-term Potentiationmentioning

confidence: 99%

Cage effects on synaptic plasticity and its modulation in a mouse model of fragile X syndrome

Volianskis,

Lundbye,

Petroff

et al. 2024

Phil. Trans. R. Soc. B

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Fragile X syndrome (FXS) is characterized by impairments in executive function including different types of learning and memory. Long-term potentiation (LTP), thought to underlie the formation of memories, has been studied in the Fmr1 mouse model of FXS. However, there have been many discrepancies in the literature with inconsistent use of littermate and non-littermate Fmr1 knockout (KO) and wild-type (WT) control mice. Here, the influence of the breeding strategy (cage effect) on short-term potentiation (STP), LTP, contextual fear conditioning (CFC), expression of N -methyl- d -aspartate receptor (NMDAR) subunits and the modulation of NMDARs, were examined. The largest deficits in STP, LTP and CFC were found in KO mice compared with non-littermate WT. However, the expression of NMDAR subunits was unchanged in this comparison. Rather, NMDAR subunit (GluN1, 2A, 2B) expression was sensitive to the cage effect, with decreased expression in both WT and KO littermates compared with non-littermates. Interestingly, an NMDAR-positive allosteric modulator, UBP714, was only effective in potentiating the induction of LTP in non-littermate KO mice and not the littermate KO mice. These results suggest that commonly studied phenotypes in Fmr1 KOs are sensitive to the cage effect and therefore the breeding strategy may contribute to discrepancies in the literature. This article is part of a discussion meeting issue ‘Long-term potentiation: 50 years on’.

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Section: (A) Cage Effects On Long-term Potentiationmentioning

confidence: 99%

Cage effects on synaptic plasticity and its modulation in a mouse model of fragile X syndrome

Volianskis,

Lundbye,

Petroff

et al. 2024

Phil. Trans. R. Soc. B

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Neuronal-specific TNFAIP1 ablation attenuates postoperative cognitive dysfunction via targeting SNAP25 for K48-linked ubiquitination

Wang,

Gao,

Gong

et al. 2023

Cell Commun Signal

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Background Synaptosomal-associated protein 25 (SNAP25) exerts protective effects against postoperative cognitive dysfunction (POCD) by promoting PTEN-induced kinase 1 (PINK1)/Parkin-mediated mitophagy and repressing caspase-3/gasdermin E (GSDME)-mediated pyroptosis. However, the regulatory mechanisms of SNAP25 protein remain unclear. Methods We employed recombinant adeno-associated virus 9 (AAV9)-hSyn to knockdown tumor necrosis factor α-induced protein 1 (TNFAIP1) or SNAP25 and investigate the role of TNFAIP1 in POCD. Cognitive performance, hippocampal injury, mitophagy, and pyroptosis were assessed. Co-immunoprecipitation (co-IP) and ubiquitination assays were conducted to elucidate the mechanisms by which TNFAIP1 stabilizes SNAP25. Results Our results demonstrated that the ubiquitin ligase TNFAIP1 was upregulated in the hippocampus of mice following isoflurane (Iso) anesthesia and laparotomy. The N-terminal region (residues 1–96) of TNFAIP1 formed a conjugate with SNAP25, leading to lysine (K) 48-linked polyubiquitination of SNAP25 at K69. Silencing TNFAIP1 enhanced SH-SY5Y cell viability and conferred antioxidant, pro-mitophagy, and anti-pyroptosis properties in response to Iso and lipopolysaccharide (LPS) challenges. Conversely, TNFAIP1 overexpression reduced HT22 cell viability, increased reactive oxygen species (ROS) accumulation, impaired PINK1/Parkin-dependent mitophagy, and induced caspase-3/GSDME-dependent pyroptosis by suppressing SNAP25 expression. Neuron-specific knockdown of TNFAIP1 ameliorated POCD, restored mitophagy, and reduced pyroptosis, which was reversed by SNAP25 depletion. Conclusions In summary, our findings demonstrated that inhibiting TNFAIP1-mediated degradation of SNAP25 might be a promising therapeutic approach for mitigating postoperative cognitive decline.

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Toward Antifragility: Social Defeat Stress Enhances Learning and Memory in Young Mice Via Hippocampal Synaptosome Associated Protein 25

Cited by 2 publications

References 45 publications

Cage effects on synaptic plasticity and its modulation in a mouse model of fragile X syndrome

Cage effects on synaptic plasticity and its modulation in a mouse model of fragile X syndrome

Neuronal-specific TNFAIP1 ablation attenuates postoperative cognitive dysfunction via targeting SNAP25 for K48-linked ubiquitination

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