Perspect Psychiatr Care. 2012 Jul;48(3):125-8. doi: 10.1111/j.1744-6163.2012.00333.x. Epub 2012 Apr 17.
Schizophrenia is a heartbreaking, debilitating, youth-stealing, lifetime disorder for most individuals afflicted with it. While the serendipitous discovery of chlorpromazine 60 plus years ago and the subsequent “discoveries” since have significantly reduced positive symptoms, the devastation of negative/cognitive symptoms continues to ruin lives. Given the cost in lives and dollars that schizophrenia drains out of our society, neuroscientists will continue to explore better approaches to fighting this disorder. The hypoglutamate model appears promising, yet there are miles to go before we sleep. As Nestler et al. (2009, p. 398) deftly acknowledge, “. . . it is important to point out that postulating a role for abnormal glutamatergic neurotransmission in schizophrenia is akin to proposing that the brain is involved in schizophrenia since every single neuron in the brain receives thousands of excitatory synapses that utilize glutamate as their neurotransmitter.”
精神分裂症是一种令人心碎、使人虚弱、偷走青春、伴随终生的疾病,大多数患者深受其害。虽然 60 多年前氯丙嗪的偶然发现以及此后的“发现”极大地减轻了阳性症状,但阴性/认知症状的破坏仍在继续摧毁人们的生活。鉴于精神分裂症给我们的社会带来的生命和金钱损失,神经科学家将继续探索更好的方法来对抗这种疾病。谷氨酸不足模型似乎很有前景,但在我们入睡之前还有很长的路要走。正如 Nestler 等人(2009 年,第 398 页)巧妙地承认的那样,“……重要的是要指出,推测异常谷氨酸能神经传递在精神分裂症中的作用类似于提出大脑参与精神分裂症,因为大脑中的每个神经元都接收数千个兴奋性突触,这些突触利用谷氨酸作为其神经递质。”