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Jacobian Mapping Reveals Converging Brain Substrates of Disruption and Repair in Response to Ethanol Exposure and Abstinence in 2 Strains of Rats
Author(s) -
Zhao Qingyu,
Pohl Kilian M.,
Sullivan Edith V.,
Pfefferbaum Adolf,
Zahr Natalie M.
Publication year - 2021
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/acer.14496
Subject(s) - stria terminalis , amygdala , inferior colliculus , neuroscience , medicine , endocrinology , corpus callosum , periaqueductal gray , midbrain , central nervous system , psychology , nucleus
Background In a previous study using Jacobian mapping to evaluate the morphological effects on the brain of binge (4‐day) intragastric ethanol (EtOH) on wild‐type Wistar rats, we reported reversible thalamic shrinkage and lateral ventricular enlargement, but persistent superior and inferior colliculi shrinkage in response to binge EtOH treatment. Methods Herein, we used similar voxel‐based comparisons of Magnetic Resonance Images collected in EtOH‐exposed relative to control animals to test the hypothesis that regardless of the intoxication protocol or the rat strain, the hippocampi, thalami, and colliculi would be affected. Results Two experiments [binge (4‐day) intragastric EtOH in Fisher 344 rats and chronic (1‐month) vaporized EtOH in Wistar rats] showed similarly affected brain regions including retrosplenial and cingulate cortices, dorsal hippocampi, central and ventroposterior thalami, superior and inferior colliculi, periaqueductal gray, and corpus callosum. While most of these regions showed significant recovery, volumes of the colliculi and periaqueductal gray continued to show response to each proximal EtOH exposure but at diminished levels with repeated cycles. Conclusions Given the high metabolic rate of these enduringly affected regions, the current findings suggest that EtOH per se may affect cellular respiration leading to brain volume deficits. Further, responsivity greatly diminished likely reflecting neuroadaptation to repeated alcohol exposure. In summary, this unbiased, in vivo‐based approach demonstrating convergent brain systems responsive to 2 EtOH exposure protocols in 2 rat strains highlights regions that warrant further investigation in both animal models of alcoholism and in humans with alcohol use disorder.