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  • N-3-oxo-dodecanoyl-L-Homoserine lactone It is reported that

    2024-02-23

    It is reported that calpain-2 plays a critical role in BDNF-induced signaling and memory formation, and knockdown of calpain-2, but not calpain-1, completely suppresses BDNF-induced pathway activation and protein translation (Briz et al., 2013). BDNF prevents neuronal apoptosis or death (Ferrer et al., 1998; Huang et al., 2017; Li et al., 2017), regulates neuronal survival, differentiation, and synaptic plasticity and recognition via binding to its receptors, tyrosine kinase receptor B (TrkB), and activating the downstream signaling pathways (Huang et al., 2017; Leal et al., 2017). Calpain activation impairs BDNF function via mediating cleavage on the BDNF’s high-affinity full-length TrkB receptor in brain of rats, and which can be reverted by a calpain inhibitor (MDL28170) (Jeronimo-Santos et al., 2015). GDNF has an important role in neuronal survival through binding to the GDNF family receptor alpha-1 (GFRα1) and the receptor tyrosine kinase Ret activation. The induced Ret down-regulation is dependent on calpain activation in cultured hippocampal neurons (Curcio et al., 2015). The cholinergic system, in its developing stage, can be a target for PBDEs. The cholinergic enzyme plays a critical role in the cholinergic innervation of cortical mantle, synaptic plasticity and learning memory in brain via the neurotransmitter N-3-oxo-dodecanoyl-L-Homoserine lactone (Ach). Hippocampal ChaT activity is positively correlated with spatial learning skills in rats (Gokcek-Sarac et al., 2013). The inhibition of ChaT and AchE activities in adult rat’s cerebral cortex and primary neurons following the BDE-153 treatment in this study is consistent with the decrement in nicotinic cholinergic receptor (nAchR) density in hippocampus of adult mice following neonatal BDE-99 or BDE-153 administration (Viberg et al., 2003, Viberg et al., 2004), and consistent with the dose-dependent reduction in cholinergic system susceptibility in mice following neonatal BDE-209 administration (Johansson et al., 2008). However, all above results are inconsistent with the elevated cortical gene transcriptions of AchE, nAchR and mAchR in adult mice treated by BDE-99 at neonatal stage (Hallgren et al., 2015), which may be resulted from differences of gene and protein or enzymatic activity levels. Moreover, calpain-2 activation is indicated to regulate the cholinergic enzymes in this study, and the AchE and ChaT enzyme activities can be reverted by the calpain-2 inhibition. Calpain is demonstrated to participate in Ach-induced dispersion of AchR clusters at the neuromuscular junction (Chen et al., 2007), and calpain-2 activation reduces the accounts of nAchR in primary hippocampal neurons and in rat brains (Yin et al., 2016). In addition, neurotrophins promote cholinergic neurons maturation and maintain the cholinergic neuron function. Neurotrophins and its receptors p75 (NTR), TrkA, and TrkB are required for the cholinergic neuronal survival, can enhance the ChaT activity and Ach release in the basal forebrain (Auld et al., 2001; Burgess and Aubert, 2006; Mufson et al., 2007; Nonner et al., 2000). Neurotrophins can also rescue basal forebrain cholinergic neurons and improve learning and memory performance in rats (Lee et al., 2013). BDNF deficiency disturbs expression of mAchR and nAchR (Sakata and Overacre, 2017). NGF modulated the ChaT and AchE activities in the basal forebrain neurons (Isaev et al., 2017; Skaper, 2017), and the pre-synaptic function in cholinergic neurons (Latina et al., 2017). NT-3 promoted neural stem cells differentiating into cholinergic neurons, and elevated the acetylcholine (ACh) levels via the notch signaling pathway (Yan et al., 2016). NT-4 maintained the phenotype of basal forebrain cholinergic neurons (Alderson et al., 1996).
    Funds This work received the financial support from the National Natural Science Foundation of China (81001258, 31000481), Science and Technology Innovation Project of Shanxi Province (2016155), Research Project Supported by Shanxi Scholarship Council of China (2017-059), Shanxi Provincial Foundation for Leaders of Disciplines in Science, China (2011), Natural Science Foundation of Shanxi Province, China (2013021033-3, 2011011040-2) and 131 Leading Talent Project of Shanxi Province, China (2013).