Abstract
Background
Alcohol has been shown to have both neuroprotective and deleterious effects after traumatic brain injury. Alcohol acts on numerous receptors within the brain (including GABAergic receptors). Non-chronic alcohol consumption works by keeping GABAergic receptors open longer, and thus increasing neural inhibition. During blast-exposure, we have observed micro-tears centered on GABAergic neurons. We hypothesize that single-use alcohol may increasing the efficacy of intact or slightly damaged GABAergic neurons and thus help re-stabilize circuitry that has sustained damage to GABAergic neurons.
Methods
To test this hypothesis, animals were orally gavaged ethanol either immediately prior or 2 days post blast exposure. They were monitored for motor ability with RotoRod and Versimax. They were also monitored for tinnitus with acoustic startle tests. To allow statistical comparisons of behaviors pre/post blast- exposure in each animal, all tests were performed both prior and post blastexposure.
Results
Thirty minutes after alcohol administration all animals had a significant motor impairment. Analysis of behavioral measures pre/post blast-exposure indicated that the alcohol groups performed better in motor tests and had decreased incidences of tinnitus after blast-exposure.
Conclusion
We conclude that single-dose alcohol has protective effects on behavioral measures of injury after blast-induced traumatic brain injury.
| Original language | American English |
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| DOIs | |
| State | Published - 2013 |
| Event | Association for Research in Otolaryngology MidWinter Meeting - Baltimore, MD Duration: Feb 1 2019 → … |
Conference
| Conference | Association for Research in Otolaryngology MidWinter Meeting |
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| Period | 2/1/19 → … |
Disciplines
- Medicine and Health Sciences