Brain injury and recovery following binge ethanol: evidence from in vivo magnetic resonance spectroscopy.
BACKGROUND
The binge-drinking model in rodents using intragastric injections of ethanol (EtOH) for 4 days results in argyrophilic corticolimbic tissue classically interpreted as indicating irreversible neuronal degeneration. However, recent findings suggest that acquired argyrophilia can also identify injured neurons that have the potential to recover. The current in vivo magnetic resonance (MR) imaging and spectroscopy study was conducted to test the hypothesis that binge EtOH exposure would injure but not cause the death of neurons as previously ascertained postmortem.


METHODS
After baseline MR scanning, 11 of 19 rats received a loading dose of 5 g/kg EtOH via oral gavage, then a maximum of 3 g/kg every 8 hours for 4 days, for a total average cumulative EtOH dose of 43 +/- 1.2 g/kg and average blood alcohol levels of 258 +/- 12 mg/dL. All animals were scanned after 4 days of gavage (post-gavage scan) with EtOH (EtOH group) or dextrose (control [Con] group) and again after 7 days of abstinence from EtOH (recovery scan).


RESULTS
Tissue shrinkage at the post-gavage scan was reflected by significantly increased lateral ventricular volume in the EtOH group compared with the Con group. At the post-gavage scan, the EtOH group had lower dorsal hippocampal N-acetylaspartate and total creatine and higher choline-containing compounds than the Con group. At the recovery scan, neither ventricular volume nor metabolite levels differentiated the groups.


CONCLUSIONS
Rapid recovery of ventricular volume and metabolite levels with removal of the causative agent argues for transient rather than permanent effects of a single EtOH binge episode in rats.
Zahr
Natalie M
NM
Psychiatry & Behavioral Sciences, Stanford University School of Medicine, Stanford, California 94305, USA.
Mayer
Dirk
D
Rohlfing
Torsten
T
Hasak
Michael P
MP
Hsu
Oliver
O
Vinco
Shara
S
Orduna
Juan
J
Luong
Richard
R
Sullivan
Edith V
EV
Pfefferbaum
Adolf
A
D000437:Alcoholism / Q000097:blood / Q000150:complications*; D000704:Analysis of Variance; D000818:Animals; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D001930:Brain Injuries / Q000097:blood / Q000209:etiology* / Q000473:pathology; D001931:Brain Mapping; D002492:Central Nervous System Depressants / Q000009:adverse effects; D002552:Cerebral Ventricles / Q000473:pathology; D002794:Choline / Q000378:metabolism; D003401:Creatine / Q000378:metabolism; D000431:Ethanol / Q000009:adverse effects; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism; D009682:Magnetic Resonance Spectroscopy / Q000379:methods*; D008297:Male; D010100:Oxygen / Q000097:blood; D051381:Rats; D017208:Rats, Wistar; D020127:Recovery of Function / Q000502:physiology*; D013223:Statistics as Topic; D013654:Taurine / Q000378:metabolism; D013997:Time Factors
D002492:Central Nervous System Depressants; D013654:Taurine; D001224:Aspartic Acid; D000431:Ethanol; C000179:N-acetylaspartate; D003401:Creatine; D002794:Choline; D010100:Oxygen