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  • AZD0530 A previous study reported that the serotonergic mech

    2022-11-09

    A previous study reported that the serotonergic mechanism was involved in the psychological stress-induced alteration in synaptic plasticity in the rat hippocampal CA1 field (Matsumoto et al., 2004). Sumitaka Inoue et al. (Inoue et al., 2014) reported that pretreatment with a 5-HT1A receptor partial agonist, suppressed LTP, and this inhibition was reversed by a 5-HT1A receptor selective antagonist in the males. These results indicate that stimulation of 5-HT1A receptors lead to suppression of LTP, the median raphe nucleus (MRN)-hippocampus 5-HT pathway via 5-HT1A receptors could certainly influence the synaptic plasticity. Therefore, the 5-HTergic neural system affects cognition and emotional states by modulating synaptic plasticity (Jabeen, 2011). Although previous studies have shown that the 5-HT receptor is associated with a depression of excitatory transmission, it was still unclear what type of 5-HT receptor was responsible for this effect (Lippiello et al., 2016). By using EA treatment on WKY depression model rats, we found that 5-HTT and 5-HT1A receptors may be associated with synaptic plasticity in the hippocampal CA1 region. 5-HT is an important neuromodulatory transmitter with distinctive neuroplastic capabilities (Kraus et al., 2017). Consequently, these data suggest that unbalanced 5-HT receptor levels coupled with altered synaptic plasticity is a key pathophysiological mechanism in depression. Assuming 5-HT can modulate neuroplasticity (Batsikadze et al., 2013), our study illustrates that EA treatment may decrease the AZD0530 of 5-HTT and 5-HT1A proteins, thereby promoting synaptic plasticity and alleviating depression-like behavior. Traditional Chinese acupuncture treatment has been shown to have an effect on nervous system diseases for thousands of years (Lu et al., 2016). Therapeutic effects of EA at Baihui (GV20) and Yintang (EX-HN3) points on depression have been confirmed by our previous studies (Yin et al., 2016). The present study demonstrates that EA at Baihui (GV20) and Yintang (EX-HN3) exhibits antidepressant-like effects by decreasing the expression of 5-HTT and 5-HT1A in the CA1, attenuating impaired synaptic plasticity. It is reported that P11 has emerged as a key for the study of the pathophysiology of depression in the lateral habenula (LHb) (Seo et al., 2017). While P11 is present in various neuronal circuits in distinct neuronal types, it has different molecular mechanisms in different brain regions. Although P11 modulates 5-HT1B functioning, and several 5-HT receptor subtypes are associated with depression, these receptor differences vary across different brain regions (Anisman et al., 2008). Therefore, further studies will focus on the expression of P11 and 5-HT receptor signal pathways in other brain regions after EA, which may explore new mechanisms of EA for depression.
    Conclusions
    Conflict of interest
    Acknowledgements This study was partly supported by a grant awarded by the National Natural Science Foundation of China (No 81704145), and supported by Shanghai Hospital Development Center (No SHDC12016124). We would like to thank Dr. Andrew Zeng from the International Education College, Shanghai University of Traditional Chinese Medicine, for his editorial support.
    Introduction Until now, significant progress was achieved in understanding the mechanisms of long-term memory formation and stabilization. However, processes of the reverse amnestic direction, such as memory loss, forgetting, amnesia, despite their undoubted theoretical, social, and medical significance, are far less understood. Discovery of memory reconsolidation phenomena provided a significant contribution to elucidation about amnesia mechanisms. It was demonstrated that reactivation of long-term memory, induced in particular by retrieval, leads to destabilization of memory trace and its transition into a labile phase [[1], [2], [3], [4], [5], [6], [7], [8], [9]]. The labile memory phase takes a few hours (called a "time window"), and then memory trace stabilizes again (reconsolidates). Impairment of memory reconsolidation induced by different amnesic agents, including inhibitors of the translation or transcription processes, neurotransmitter receptors antagonists and others, caused development of amnesia [1,2,5,[9], [10], [11], [12], [13], [14]].