Zheng Zhihua, Zeng Yingtong, Yang Wei, Wu Junyan
Guangdong Province Pharmaceutical Association, Guangzhou, China.
Guangdong General Hospital, Guangdong Academy of Medical Science, Guangzhou, China.
Neuro Endocrinol Lett. 2014;35(8):655-65.
Neuroplasticity is the nervous system's ability to respond to intrinsic or extrinsic stimuli by reorganizing its structure, function and connections. And the nervous system monitors and coordinates internal organ function. Thus neuroplasticity may also be associated with the pathogenesis of other diseases besides neuropsychiatric diseases, such as cardiovascular disease. The digestive system is controlled by the nervous system, mainly by the autonomic nervous system. Stress may lead to depression/anxiety and irritable bowel syndrome (IBS). IBS is commonly comorbid with depression/anxiety, which are disorders of decreased neuroplasticity. And the mechanisms of depression/anxiety and IBS are related. The hypothalamo-pituitary-adrenal axis, hippocampus, amygdala and stress-related factors and hormones, such as corticotropin-releasing factor, glucocorticoids and brain-derived neurotrophic factor are involved in both neuroplasticity and the pathogenesis of depression/anxiety and IBS. So we conclude that decreased neuroplasticity causes the comorbidity of depression/anxiety and IBS, and increased neuroplasticity may be beneficial against the development of IBS. This theory provides another angle that can explain some of the reported phenomena related to IBS and neuropsychiatry, and provide a potential treatment to protect against IBS.
神经可塑性是神经系统通过重组其结构、功能和连接来响应内在或外在刺激的能力。并且神经系统监测和协调内脏器官功能。因此，神经可塑性可能也与除神经精神疾病之外的其他疾病的发病机制相关，比如心血管疾病。消化系统受神经系统控制，主要是自主神经系统。压力可能导致抑郁/焦虑和肠易激综合征（IBS）。IBS常与抑郁/焦虑共病，而抑郁/焦虑是神经可塑性降低的病症。并且抑郁/焦虑和IBS的机制相关。下丘脑 - 垂体 - 肾上腺轴、海马体、杏仁核以及与压力相关的因子和激素，如促肾上腺皮质激素释放因子、糖皮质激素和脑源性神经营养因子，都参与神经可塑性以及抑郁/焦虑和IBS的发病机制。所以我们得出结论，神经可塑性降低导致抑郁/焦虑和IBS共病，而神经可塑性增加可能对IBS的发展有益。这一理论提供了另一个角度来解释一些与IBS和神经精神病学相关的已报道现象，并为预防IBS提供了一种潜在的治疗方法。
