Deutschenbaur, LorenzLorenzDeutschenbaurBeck, JohannesJohannesBeckKiyhankhadiv, AnnaAnnaKiyhankhadivMühlhauser, MarkusMarkusMühlhauserBorgwardt, StefanStefanBorgwardtWalter, MarcMarcWalterHasler, GregorGregorHasler0000-0002-8311-0138Sollberger, DanielDanielSollbergerLang, Undine EUndine ELang2024-10-232024-10-232016-01-04https://boris-portal.unibe.ch/handle/20.500.12422/136928Major depression is a common, recurrent mental illness that affects millions of people worldwide. Recently, a unique fast neuroprotective and antidepressant treatment effect has been observed by ketamine, which acts via the glutamatergic system. Hence, a steady accumulation of evidence supporting a role for the excitatory amino acid neurotransmitter (EAA) glutamate in the treatment of depression has been observed in the last years. Emerging evidence indicates that N-methyl-D-aspartate (NMDA), group 1 metabotropic glutamate receptor antagonists and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) agonists have antidepressant properties. Indeed, treatment with NMDA receptor antagonists has shown the ability to sprout new synaptic connections and reverse stress-induced neuronal changes. Based on glutamatergic signaling, a number of therapeutic drugs might gain interest in the future. Several compounds such as ketamine, memantine, amantadine, tianeptine, pioglitazone, riluzole, lamotrigine, AZD6765, magnesium, zinc, guanosine, adenosine aniracetam, traxoprodil (CP-101,606), MK-0657, GLYX-13, NRX-1047, Ro25-6981, LY392098, LY341495, D-cycloserine, D-serine, dextromethorphan, sarcosine, scopolamine, pomaglumetad methionil, LY2140023, LY404039, MGS0039, MPEP, 1-aminocyclopropanecarboxylic acid, all of which target this system, have already been brought up, some of them recently. Drugs targeting the glutamatergic system might open up a promising new territory for the development of drugs to meet the needs of patients with major depression.enNMDAdepressioncalciumketamineBDNFGSK3PI3KmTOR600 - Technology::610 - Medicine & healtharticle10.7892/boris.744372574780110.1016/j.pnpbp.2015.02.015