Polysialylation of NCAM is upregulated by hyperthermia and participates in heat shock preconditioning-induced neuroprotection

Neurobiology of Disease

G. Le Gal La Salle¹  A. Rougier²  V. Duveau²  S. Arthaud² 

[1] Corresponding author.;Université Bordeaux 2, CNRS UMR 5227–Mouvement, Adaptation, Cognition, 146, rue Léo Saignat, 33076 Bordeaux Cedex, France;

关键词: Brain tolerance;    Plasticity;    Neuroprotection;    PSA-NCAM;    Polysialic acid;    Hippocampus;   

DOI  :  

来源: DOAJ

【 摘 要 】

“Brain tolerance” – a phenomenon in which a subtoxic challenge confers resistance to subsequent brain injuries – provides an ideal opportunity for investigating endogenous neuroprotective mechanisms. We investigated the potential role of the polysialylated (PSA) form of neural cell adhesion molecule (NCAM), which is thought to play a key role in plasticity. In a model where prior exposure to heat shock protects against kainate-induced cell damage in the hippocampus, we show that hyperthermia upregulates PSA-NCAM expression for at least 1 week, without affecting neurogenesis. Pharmacological manipulation of heat shock protein (HSP) expression demonstrates a tight positive link between HSP70 and PSA-NCAM. Finally, the presence of PSA was functionally linked to brain tolerance, as protection against kainate-induced cell death by heat shock pre-exposure was abolished in the absence of NCAM polysialylation. The upregulation of PSA-NCAM by hyperthermia may have a significant impact on hippocampal plasticity, permitting induction of the complex molecular cascade responsible for neuroprotection.

【 授权许可】

Unknown