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谷氨酸受体
谷氨酰胺
病理生理学
γ-氨基丁酸
焦虑
谷氨酸的
精神科
扣带皮质
前额叶皮质
内科学
临床心理学
神经科学
谷氨酸脱羧酶
心理学
功能磁共振成像
医学
加巴能
纹状体
后扣带
化学
神经递质
中枢神经系统
生物
受体
认知
氨基酸
生物化学
作者
Yan Li,Chencheng Zhang,Kathrin Weidacker,Yingying Zhang,Naying He,Jin Hu,Weibo Chen,Valerie Voon,Richard A.E. Edden,Fuhua Yan
标识
DOI:10.1186/s12888-019-2160-1
摘要
Obsessive-compulsive disorder (OCD) is a relatively common and disabling psychiatric disorder whose pathophysiology is incompletely understood. In this study, we utilized magnetic resonance spectroscopy (MRS) in an effort to provide a better understanding of the role of brain gamma-aminobutyric acid (GABA) and glutamate in the pathophysiology of OCD. We hypothesized that beyond the separate effects of these neurotransmitter systems, a disruption in the balance between GABA and glutamate could be particularly relevant to OCD. We obtained MRS measures of GABA and glutamate concentrations in the anterior cingulate cortex from 23 adult patients with OCD and 20 sex- and age-matched healthy community volunteers. Established clinical rating scales were used to assess the severities of OCD, anxiety, and depression symptoms. Statistical analysis involved the assessment of patient-control group differences in the individual measures of GABA and glutamate, as well as in the ratio of the GABA to glutamate measures. Additionally, we explored whether differences in the MRS measures existed between two subgroups of patients formed according to the severity of their OCD symptoms. Finally, we assessed the relations of demographic and clinical variables to the MRS measures. Patients with OCD displayed a higher estimated GABA level and a higher GABA to glutamate ratio than healthy participants, but no significant group differences were observed in the measure of glutamate. The MRS measures did not vary by subgroup and showed no correlations with demographic and clinical variables. These results indicate that GABA abnormalities within the anterior cingulate cortex contribute to the pathophysiology of OCD. The results fail to provide evidence that glutamate abnormalities alone are involved in adult OCD. Yet, it seems that a disruption in the balance between glutamate and GABA neurotransmission may have a particularly important role to play in OCD pathophysiology.
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