作者: N. Li , B. Lee , R.-J. Liu , M. Banasr , J. M. Dwyer
关键词: Hydroxynorketamine 、 Biology 、 Esketamine 、 Endocrinology 、 Rapastinel 、 NMDA receptor 、 Synaptic signaling 、 Synaptogenesis 、 Neuroscience 、 Internal medicine 、 Ketamine 、 PI3K/AKT/mTOR pathway
摘要: The rapid antidepressant response after ketamine administration in treatment-resistant depressed patients suggests a possible new approach for treating mood disorders compared to the weeks or months required standard medications. However, mechanisms underlying this action of [a glutamate N-methyl-D-aspartic acid (NMDA) receptor antagonist] have not been identified. We observed that rapidly activated mammalian target rapamycin (mTOR) pathway, leading increased synaptic signaling proteins and number function spine synapses prefrontal cortex rats. Moreover, blockade mTOR completely blocked induction synaptogenesis behavioral responses models depression. Our results demonstrate these effects are opposite deficits result from exposure stress could contribute fast actions ketamine.