Increased glutamine in patients undergoing long-term treatment for schizophrenia: a proton magnetic resonance spectroscopy study at 3 T.
Increased glutamine in patients undergoing long-term treatment for schizophrenia: a proton magnetic resonance spectroscopy study at 3 T.
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DOI：
10.1001/jamapsychiatry.2013.3939
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发表时间：
2014-03
期刊：
影响因子：
25.8
通讯作者：
Gasparovic C
中科院分区：
文献类型：
--
作者：
Bustillo JR;Chen H;Jones T;Lemke N;Abbott C;Qualls C;Canive J;Gasparovic C
精神分裂症的n -甲基-d-天冬氨酸受体功能减退模型预测突触谷氨酸释放的矛盾增加。体内测量人类谷氨酸能神经传递具有挑战性，但谷氨酰胺是突触谷氨酸的主要代谢物，可以用质子磁共振波谱（1H-MRS）进行量化。虽然有一些研究测量了谷氨酸、谷氨酰胺和谷氨酰胺与谷氨酸的比值，但尚不清楚在精神分裂症中哪些h - mrs指标的谷氨酸能神经传递发生了改变。目的探讨前扣带背侧谷氨酰胺、谷氨酸、谷氨酰胺与谷氨酸比值及其与精神分裂症患者症状和认知的关系。横断面设计采用3-T - 1H-MRS对在附属研究机构接受神经成像的大学精神科门诊招募的参与者进行研究。参与者是84名DSM-IV-TR诊断为精神分裂症的患者和81名精神健康的志愿者，在年龄、性别、种族和职业水平上与原籍家庭的户主相匹配。谷氨酰胺，谷氨酸，谷氨酰胺和谷氨酸的比例。还有症状和认知。精神分裂症组谷氨酰胺升高（P = 0.01），谷氨酰胺与谷氨酸比值升高（P = 0.007），谷氨酸无升高（P = 0.89）。谷氨酰胺水平与精神病症状严重程度呈正相关（P = 0.02）。精神分裂症患者胆碱含量也升高（P = 0.002）。正如n -甲基-d-天冬氨酸受体功能减退模型所预测的那样，与精神病症状直接相关的谷氨酰胺升高与精神分裂症中谷氨酸能突触释放增加一致。进一步了解精神分裂症中谷氨酸能功能障碍的潜在机制可能会导致新的治疗精神病的药物策略。
The N-methyl-d-aspartic acid receptor hypofunction model of schizophrenia predicts a paradoxical increase in synaptic glutamate release. In vivo measurement of glutamatergic neurotransmission in humans is challenging, but glutamine, the principal metabolite of synaptic glutamate, can be quantified with proton magnetic resonance spectroscopy (1H-MRS). Although a few studies have measured glutamate, glutamine, and glutamine to glutamate ratio, it is not clear which of these 1H-MRS indices of glutamatergic neurotransmission is altered in schizophrenia. To examine glutamine, glutamate, and glutamine to glutamate ratio in the dorsal anterior cingulate, as well as their relationships with symptoms and cognition in schizophrenia. Cross-sectional design using 3-T 1H-MRS in participants recruited from university-based psychiatric outpatient clinics who underwent neuroimaging at an affiliated research facility. Participants were 84 patients with a DSM-IV-TR diagnosis of schizophrenia and 81 psychiatrically healthy volunteers, matched in age, sex, ethnicity, and occupational level to the head of household of family of origin. Glutamine, glutamate, and glutamine to glutamate ratio. Also symptoms and cognition. Glutamine was increased in the schizophrenia group (P = .01) as well as the glutamine to glutamate ratio (P = .007) but not glutamate (P = .89). Glutamine levels were positively correlated with severity of psychotic symptoms (P = .02). Choline was also increased in schizophrenia (P = .002). Elevated glutamine, which was directly related to psychotic symptoms, is consistent with increased glutamatergic synaptic release in schizophrenia, as predicted by the N-methyl-d-aspartic acid receptor hypofunction model. Further understanding the underlying mechanism of glutamatergic dysfunction in schizophrenia may lead to new pharmacological strategies to treat psychosis.
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