Potential synergistic action of 19 schizophrenia risk genes in the thalamus.
Potential synergistic action of 19 schizophrenia risk genes in the thalamus.
复制标题
丘脑中19个精神分裂症风险基因的潜在协同作用。
DOI：
10.1016/j.schres.2016.09.008
复制
发表时间：
2017-02
影响因子：
4.5
通讯作者：
Lisman JE
中科院分区：
文献类型：
--
作者：
Richard EA;Khlestova E;Nanu R;Lisman JE
当前精神分裂症（SZ）研究的一个目标是了解多种风险基因如何与环境因素共同作用以产生这种疾病。在精神分裂症患者中，在清醒状态下，脑电图的δ频率功率升高，这种升高可以通过丘脑中的n -甲基- d -天冬氨酸受体（NMDAR）拮抗剂作用来模仿。这种丘脑三角洲可以被多巴胺D2受体拮抗剂阻断，这些药物已知对SZ有治疗作用。实验表明，这些振荡可以干扰大脑功能，因此可能是产生精神病的原因。在这里，我们评估了一个问题，即确定的精神分裂症风险基因是否可能相互作用以影响delta生成过程。我们确定了19个风险基因，它们可能以协同方式产生delta振荡。
A goal of current schizophrenia (SZ) research is to understand how multiple risk genes work together with environmental factors to produce the disease. In schizophrenia, there is elevated delta frequency EEG power in the awake state, an elevation that can be mimicked in rodents by N-methyl-D-aspartate receptor (NMDAR) antagonist action in the thalamus. This thalamic delta can be blocked by dopamine D2 receptor antagonists, agents known to be therapeutic in SZ. Experiments suggest that these oscillations can interfere with brain function and may thus be causal in producing psychosis. Here we evaluate the question of whether well-established schizophrenia risk genes may interact to affect the delta generation process. We identify 19 risk genes that can plausibly work in a synergistic fashion to generate delta oscillations.