İş, MerihTanrıverdi, TanerAkyüz, FevzullahUlu, Mustafa OnurÜstündağ, NilGezen, FerruhYavuz, Özlem2021-06-232021-06-2320051050-64381534-4916https://doi.org/10.1097/01.wnq.0000152407.39871.c7https://hdl.handle.net/20.500.12491/5754Although the deleterious effects of acute alcohol intoxication on traumatic brain injury (TBI) are well known, neuroprotective features of lower doses of ethanol (EtOH) before head trauma have been reported during recent years. Inhibition of N-methyl-D-aspartate receptor (NMDA)-mediated excitotoxicity by lower doses of EtOH has been believed to be responsible for this protection. The aim of this study was to show the neuroprotective effects of low and moderate doses of EtOH and to compare their efficacy in each group. Acute EtOH intoxication at low and moderate doses was induced 40 minutes before trauma. Severe TBI was administered in Sprague-Dawley rats using an impact acceleration model. At 24 hours after trauma, all the rats were decapitated and hippocampi were evaluated under light microscopy. According to our results, red neuron formation and vacuolar degeneration in the CA1 and CA3 sectors of the hippocampi were less prominent in the lowdose and moderate-dose EtOH plus trauma groups than in the trauma only group. In addition, edema formation was less prominent in the EtOH plus trauma group. When comparing the low-dose EtOH Plus trauma and moderate-dose EtOH Plus trauma groups, an almost normal appearance of the hippocampus was noted in the moderate-dose EtOH plus trauma group. EtOH may have a neuroprotective effect when administered at a lower dose, particularly a moderate dose, and this protection may be a result of the inhibition of NMDA receptor-mediated excitotoxicity.eninfo:eu-repo/semantics/closedAccessEthanolHead InjuryTraumatic Brain InjuryArticle10.1097/01.wnq.0000152407.39871.c715160642-s2.0-14144249162N/AWOS:000227291400009Q4