Lepeta Katarzyna, Kaczmarek Leszek
Department of Molecular and Cellular Neurobiology, Nencki Institute, Warsaw, Poland.
Department of Molecular and Cellular Neurobiology, Nencki Institute, Warsaw, Poland
Schizophr Bull. 2015 Sep;41(5):1003-9. doi: 10.1093/schbul/sbv036. Epub 2015 Apr 2.
Recent findings implicate alterations in glutamate signaling, leading to aberrant synaptic plasticity, in schizophrenia. Matrix metalloproteinase-9 (MMP-9) has been shown to regulate glutamate receptors, be regulated by glutamate at excitatory synapses, and modulate physiological and morphological synaptic plasticity. By means of functional gene polymorphism, gene responsiveness to antipsychotics and blood plasma levels MMP-9 has recently been implicated in schizophrenia. This commentary critically reviews these findings based on the hypothesis that MMP-9 contributes to pathological synaptic plasticity in schizophrenia.
近期研究结果表明,精神分裂症患者存在谷氨酸信号传导改变,进而导致异常的突触可塑性。基质金属蛋白酶-9(MMP-9)已被证明可调节谷氨酸受体,在兴奋性突触处受谷氨酸调节,并调节生理和形态学突触可塑性。通过功能基因多态性、基因对抗精神病药物的反应性以及血浆中MMP-9水平,近期研究已将其与精神分裂症联系起来。本述评基于MMP-9导致精神分裂症患者病理性突触可塑性这一假说,对这些研究结果进行了批判性综述。