Ceftriaxone is a beta-lactam antibiotic that increases the expression of the major glutamate transporter, GLT-1. As such, ceftriaxone ameliorates symptoms across multiple rodent models of neurological diseases and substance use disorders. However, the mechanism behind GLT-1 upregulation is unknown. The present review synthesizes this literature in order to identify commonalities in molecular changes. We find that ceftriaxone (200 mg/kg for at least two days) consistently restores GLT-1 expression in multiple rodent models of neurological disease, especially when GLT-1 is decreased in the disease model. The same dose given to healthy/drug-naive rodents does not reliably upregulate GLT-1 in any brain region except the hippocampus. Increased GLT-1 expression does not consistently arise from transcriptional regulation, and is likely to be due to trafficking changes. In addition to altered transporter expression, ceftriaxone ameliorates neuropathologies (e.g. tau, amyloid beta, cell death) and aberrant protein expression associated with a number of neurological disease models. Taken together, these results indicate that ceftriaxone remains a strong candidate for treatment of multiple disorders in the clinic.

头孢曲松是一种 β-内酰胺抗生素，可增加主要谷氨酸转运蛋白 GLT-1 的表达。因此，头孢曲松可改善神经系统疾病和物质使用障碍的多种啮齿动物模型的症状。然而，GLT-1 上调背后的机制尚不清楚。本综述综合这些文献以确定分子变化的共性。我们发现头孢曲松（200 mg/kg 至少两天）在多种啮齿动物神经疾病模型中始终如一地恢复 GLT-1 表达，尤其是当 GLT-1 在疾病模型中降低时。给予健康/未接受药物治疗的啮齿动物相同剂量并不能可靠地上调除海马体以外的任何大脑区域的 GLT-1。GLT-1 表达的增加并非始终由转录调控引起，并且很可能是由于广告投放的变化。除了改变的转运蛋白表达外，头孢曲松还可改善神经病理学（例如 tau、β 淀粉样蛋白、细胞死亡）和与许多神经疾病模型相关的异常蛋白质表达。总之，这些结果表明头孢曲松仍然是临床治疗多种疾病的有力候选者。