Gunduz, O.Topuz, R. D.Todurga, Z. G.Duvan, K.Karadag, C. H.Ulugol, A.2024-06-122024-06-1220150090-29771573-9007https://doi.org/10.1007/s11062-015-9494-1https://hdl.handle.net/20.500.14551/19627Glutamate is believed to be the predominant excitatory neurotransmitter in the networks responsible for itch-related behavior. Beta-lactam antibiotics were shown to exert neuroprotective effects by increasing expression of the glutamate transporter GLT-1. We observed whether repeated administration of the beta-lactam antibiotic ceftriaxone suppresses serotonin-induced itch-related behavior (similarly to the effect of this agent on pain transmission) in mice. Chronic, but not acute, ceftriaxone introductions reduced the number of serotonin-induced scratches; dihydrokainic acid, a selective GLT-1 transporter inhibitor, partly but significantly abolished this effect of ceftriaxone. Our findings suggest that GLT-1 activation by beta-lactam antibiotics looks promising for the treatment of chronic itch.en10.1007/s11062-015-9494-1info:eu-repo/semantics/openAccessCeftriaxoneGlutamate Transporter GLT-1ItchSerotoninSpinal-CordItchPainNeurotransmitterTransmissionCeftriaxoneExpressionToleranceInsightsNeuronsArticle4713639Q4WOS:0003540545000072-s2.0-84953363041Q4