Acute ethanol intoxication in a model of traumatic brain injury: The protective role of moderate doses demonstrated by immunoreactivity of synaptophysin in hippocampal neurons

Abstract

Although ethanol intoxication is reported to be a complicating factor in traumatic brain injury, some recent studies are indicating its possible protective role especially at lower doses. Ethanol inhibition of NMDA-mediated excitotoxicity which predominates at lower doses is believed to be responsible for this protection. The aim of this study was to demonstrate this neuroprotective role of alcohol using immunoreactivity for synaptophysin as an indirect marker for severity of injury. Acute ethanol intoxication at moderate doses was performed 2 h prior to trauma. Severe traumatic brain injury was administrated using an impact acceleration model in Sprague-Dawley rats. At post-traumatic 48th hour, immunorectivity for synapthophysin in the rat hippocampi was evaluated under light microscopy. According to our results there were slight increases in immunoreactivity for synaptophysin in the stratum oriens and striatum radiatum of CA1 subfield of hippocampus when ethanol was administered prior to trauma comparing to moderate increase in the trauma-only group. On the other hand vacuolar degeneration and red neuron formation was more prominent in the pyramidal cell layer of CA1 and CA3 when ethanol was not administered. Ethanol may have a neuroprotective role when administered at moderate doses prior to traumatic brain injury. This effect of ethanol may primarily be due to inhibition of NMDA receptors.

Association Between Alcohol and Mortality in Patients With Severe Traumatic Head Injury

“…At high doses (Ͼ240 mg/ dL), alcohol was shown in animal studies to be deleterious to neurologic outcomes. [10][11][12][13] In our study, a BAC of 230 mg/dL or greater was shown to be associated with higher mortality than a BAC of 0. Also, there was a trend in both our study group and in our tracer group to suggest that patients with a high BAC were more likely to die earlier after trauma compared with patients with no BAC.…”

Ethanol and isolated traumatic brain injury

“…Low dose ethanol inhibition of N-methyl-D-aspartate (NMDA) receptors could be neuroprotective as potassium and calcium influx through NMDA receptor channels following TBI leads to neuronal excitotoxicity [9][10][11][12][13]. The systemic catecholamine surge following TBI which is associated with worse outcomes has been shown to be moderated by ethanol [14][15][16].…”

Alcohol Use at Time of Injury and Survival Following Traumatic Brain Injury: Results From the National Trauma Data Bank

“…have suggested that alcohol might have a neuroprotective effect on the brain following traumatic brain injury (TBI) through such mechanisms as inhibiting N-methyl-Daspartate (NMDA) receptor-mediated excitotoxicity (Cebere and Liljequist, 2003;Chandler et al, 1993;Is et al, 2005;Türeci et al, 2004), decreasing the degree of uncoupling between glucose metabolism and cerebral blood fl ow (Kelly et al, 2000), inhibiting the production of pro-infl ammatory cytokines (Gottesfeld et al, 2002), attenuating TBI-induced hyperthermia (Taylor et al, 2002), and blunting the sympathoadrenal response in TBI (Opreanu et al, 2010). Premised on the evidence from animal research, one recent study confi rmed that patients who were intoxicated at the time of injury had better acute neuropsychological outcomes when recovering from TBI than did nonintoxicated patients (Lange et al, 2008).…”