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  • The association between mental disorders and smoking was fir


    The association between mental disorders and smoking was firmly established, and their inter-relationship was due to the reciprocal causal effects (Tjora et al., 2014). Previous research found that negative affect and the urge to smoke as well as the urge to smoke and nicotine dependence had significantly linear relationships (Lechner et al., 2018). This suggests that higher degree of nicotine addiction was often accompanied with more severe negative affect and even with mental disorders. In the present study, depression status increased significantly in heavy smokers, a finding that agrees with those of other studies (Lawrence et al., 2009, Lechner et al., 2018). Glutamate, a dominant excitatory neurotransmitter, was not only associated with nicotine addiction (Alasmari et al., 2016, Janes et al., 2016), but also with major mental disorders (Bruno et al., 2017). Glutamate is not allowed to enter into the Hoechst 34580 because of the blood-brain barrier (BBB) under normal conditions (Hawkins, 2009). Nevertheless, BBB function may change when exposed to some genetic and environmental risk factors, including smoking (Spencer et al., 2018). In this study, partial correlation was performed to evaluate the association between CSF glutamate and mental status with age and education years as covariates. Interestingly, the result showed that CSF glutamate negatively correlated with BID scores in heavy smokers, but not with SAS scores. In the NS-group, no correlation was found. These significant alterations and negative correlations possibly indicated that nicotine disturbed the balance of BBB in heavy smokers. Depression disorder was associated with many factors, including older age, female gender, lower education, poor economic status and others (Brown et al., 2017). In the general populations, about 4% of older persons suffer from major depression disorder (Rosenvinge and Rosenvinge, 2003). Two studies from Haiti found higher depression scores with increasing age than with decreasing age, and higher depression scores among those with more education than with less (Martsolf, 2004, Wagenaar et al., 2012), suggesting that age and education year both affect depression scores. Thus, in the present study, we performed partial correlations after adjusting for age and education year as covariates to minimize the impact of age and education year on the correlation between BDI scores and CSF glutamate levels.
    Funding This work was supported by Technology Support Project of Xinjiang (2017E0267, 2018E02061), Natural Science Foundation of Xinjiang (2017D01C245), Wenling Foundation of Science and Technology (2015C312055), Projects of Medical and Health Technology Program in Zhejiang Province (2017KY720), Basic and public research project of Zhejiang province (LGF18H020001) and the Opening Project of Zhejiang Provincial Top Key Discipline of Pharmaceutical Sciences.
    Conflict of interest
    Ethical approval
    Introduction Synapses are the fundamental elements of neuronal networks that enable the processing, encoding, and retrieval of information in the brain, and pathological disruptions in synapse structure are broadly held to underlie the development of neurological disorders such as autism and schizophrenia (Volk et al., 2015). To maintain and adjust the efficiency of synaptic signaling, synapses are built from a broad array of components that assemble into large macromolecular machineries. At the presynaptic terminal, action potentials trigger the fast release of synaptic vesicles. Synaptic vesicles are docked at the active zone and primed for exocytosis by protein complexes containing e.g. Rab3-interacting molecules (RIM) and soluble N-ethylmaleimide-sensitive factor activating protein receptors (SNARE) (Sudhof, 2012). The release of glutamate is closely aligned with the postsynaptic receptors that are stably anchored in the opposing postsynaptic density (PSD), a complex molecular machine containing a plethora of scaffolding proteins and signaling molecules (Okabe, 2007; Sheng and Hoogenraad, 2007). How are these molecular complexes organized and precisely positioned to sustain synaptic transmission? In this review we will focus particularly on the functional distribution of glutamate receptors at the postsynaptic membrane.