胶质细胞连接蛋白的下调和上调可能导致突触失衡，从而导致双相情感障碍的病理生理学变化。
Downregulation and upregulation of glial connexins may cause synaptic imbalances responsible for the pathophysiology of bipolar disorder.
机构信息
Volitronics-Institute for Basic Research, Psychopathology and Brain Philosophy, Wals (Salzburg), Austria.
出版信息
CNS Neurosci Ther. 2011 Oct;17(5):281-93. doi: 10.1111/j.1755-5949.2010.00178.x. Epub 2010 Jul 8.
Abstract
The model of the pathophysiology of bipolar disorder proposed is based on imbalances in tripartite synapses caused by dysregulations of connexin expression in the astrocytic syncytium. If the expression of connexins is downregulated, a compensatory upregulation of astrocytic receptors may occur and be responsible for the pathophysiology of depression. Conversely, if the expression of connexins is upregulated, the expression of the astrocytic receptors may be downregulated and be responsible for the pathophysiology of mania. In depression, a relative lack of neurotransmitters exerts a protracted synaptic information processing, whereas in mania a relative increase of neurotransmitters may accelerate synaptic information processing. In addition, the modulatory role of gliotransmitters may be affected in bipolar disorder. Since the dysregulations of connexins impair the astrocytic syncytium, these disorders could be explanatory for cognitive impairment both in depression and in mania. Finally, the testability of this model is discussed.
摘要
所提出的双相情感障碍病理生理学模型基于三突触连接体的不平衡，这是由星形胶质细胞合胞体中连接蛋白表达失调引起的。如果连接蛋白的表达下调，星形胶质细胞受体可能会发生代偿性上调，并负责抑郁症的病理生理学。相反，如果连接蛋白的表达上调，星形胶质细胞受体的表达可能下调，并负责躁狂症的病理生理学。在抑郁症中，相对缺乏神经递质会对突触信息处理产生持久影响，而在躁狂症中，相对增加的神经递质可能会加速突触信息处理。此外，双相情感障碍中神经胶质递质的调节作用可能受到影响。由于连接蛋白的失调会损害星形胶质细胞合胞体，因此这些紊乱可能可以解释抑郁症和躁狂症中的认知障碍。最后，讨论了该模型的可检验性。
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