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  • Calphostin C The overall adjustment the non toxicity

    2024-11-12

    The overall adjustment, the non-toxicity and the addiction-free treatment methods are the advantages of EA. EA treatment for depression has achieved great clinical effect in recent years (Dong et al., 2017). The clinical practice guideline of the American college of physicians (ACP) have pointed out that EA therapy for depression has significant efficacy and low side effects (Qaseem et al., 2016). However, the precise contributing factors and mechanisms of EA for depression are still unknown. In this study, we investigated the effect of EA on synaptic plasticity and 5-HT receptors in WKY transgenic rat models.
    Materials and methods
    Results
    Discussion The present study aimed to determine the effect of EA on neuronal synaptic plasticity and 5-HT receptor Calphostin C in depressive model rats. The WKY rat is characterized as a genetic model of depression. WKY rats showed a series of depressive symptoms that mimic those in humans such as exaggerated immobility in the FST and low levels of social activity (DaSilva et al., 2011). This strain also showed resistance to the antidepressant efficacy of selective serotonin Calphostin C reuptake inhibitors, suggesting that it may provide insight into mechanisms that confer resistance to antidepressant treatment (Xu et al., 2011). The behavioral tests were used to evaluate the rat's ability to adapt to new environments, the sensitivity to reward stimulation and pleasure, and the state of anhedonia (Jiang et al., 2017). Our findings indicated that the WKY rats’ (Model group) immobility time was significantly increased in the FST; the center time, total move time, center distance, total distance, rearing and grooming incidents were all decreased in the OFT; the sucrose consumption was significantly decreased in the SPT. The data of the present study is consistent with a current study that shows chronic unpredictable mild stress (CUMS) could induce depressive-like behaviors, illustrating that WKY rats could effectively imitate the symptoms of depression in patients (Xu et al., 2015). Importantly, the results showed that EA intervention significantly decreased the immobility time in FST when compared to the Sham EA group. The center time, total move time and sucrose intake were significantly increased in the EA group when compared to the Model group. The above experimental results showed that EA has a strong effect on ameliorating depression-related behaviors. Hippocampal LTP, as a model of synaptic plasticity, plays a critical role in learning and memory (Li et al., 2015; Li et al., 2010). The study found that HFS-induced LTP at CA3–CA1 synapses significantly decreased in CUMS depressive rats, indicating that the depression resulted in LTP impairment and cognitive decline (Zhang et al., 2016). Related research reported that LTP-like plasticity in depression patients is significantly impaired in comparison to that of healthy people; this synaptic plasticity attenuation recovers after depressive state remission (Kuhn et al., 2016). This study showed that EA improved the learning impairment and hippocampal synaptic plasticity of depressed rats. In our study, high-frequency stimulation failed to induce LTP in the Model group, suggesting that the synaptic plasticity of WKY depression model rats was impaired. Compared to that of the Model group, the fEPSP slope of the EA group increased significantly; also, the LTP induction was successful, which indicates that the damaged synaptic plasticity of depression rats was restored after the EA treatment. This further identifies impaired LTP-like plasticity as a potential pathomechanism and treatment target of the disorder. Many studies have reported that 5-HT plays an important role in shaping synaptic plasticity of the developing and mature nervous system and that alterations in 5-HT receptors and other components of serotonergic can result in neurodevelopmental and psychiatry disorders (Lesch and Waider, 2012). An important study found that brain serotonin turnover was significantly increased in depression patients who are influenced by the 5-HTT genotype; after receiving 12 weeks of treatment with an SSRI, the serotonin turnover decreased (Barton et al., 2008). 5-HTT plays a critical role in autoregulation of serotonergic neurotransmission and emotional regulation. Alterations in 5-HTT activity are associated with increased risk for depression (Hagan et al., 2012). Another study reported that mice with higher 5-HT1A autoreceptor levels had decreased resilience to stress, increased behavioral despair and a depressive phenotype (Richardson-Jones et al., 2010). Quantification of 5-HT1A receptor levels in humans from post mortem and positron emission tomography imaging studies reveals an increased level of 5-HT1A receptors in depression patients (Nautiyal and Hen, 2017). Our findings are consistent with current evidence that excessive 5-HTT and 5-HT1A expression can lead to depression. The western blot results revealed that EA can significantly reduce 5-HTT and 5-HT1A protein expression in the hippocampus CA1 region of depression model rats.