| Title |
Adolescent Binge Alcohol Exposure Affects the Brain Function Through Mitochondrial Impairment
|
|---|---|
| Published in |
Molecular Neurobiology, June 2017
|
| DOI | 10.1007/s12035-017-0613-4 |
| Pubmed ID | |
| Authors |
Cheril Tapia-Rojas, Francisco J. Carvajal, Rodrigo G. Mira, Camila Arce, José Manuel Lerma-Cabrera, Juan A. Orellana, Waldo Cerpa, Rodrigo A. Quintanilla |
| Abstract |
In the young population, binge drinking is a pattern of problematic alcohol consumption, characterized by a short period of heavy drinking followed by abstinence which is frequently repeated over time. This drinking pattern is associated with mental problems, use of other drugs, and an increased risk of excessive alcohol intake during adulthood. However, little is known about the effects of binge drinking on brain function in adolescents and its neurobiological impact during the adulthood. In the present study, we evaluated the effects of alcohol on hippocampal memory, synaptic plasticity, and mitochondrial function in adolescent rats after a binge drinking episode in vivo. These effects were analyzed at 1, 3, or 7 weeks post alcohol exposure. Our results showed that binge-like ethanol pre-treated (BEP) rats exhibited early alterations in learning and memory tests accompanied by an impairment of synaptic plasticity that was total and partially compensated, respectively. These changes could be attributed to a rapid increase in oxidative damage and a late inflammatory response induced by post ethanol exposure. Additionally, BEP alters the regulation of mitochondrial dynamics and modifies the expression of mitochondrial permeability transition pore (mPTP) components, such as cyclophilin D (Cyp-D) and the voltage-dependent anion channel (VDAC). These mitochondrial structural changes result in the impairment of mitochondrial bioenergetics, decreasing ATP production progressively until adulthood. These results strongly suggest that teenage alcohol binge drinking impairs the function of the adult hippocampus including memory and synaptic plasticity as a consequence of the mitochondrial damage induced by alcohol and that the recovery of hippocampal function could implicate the activation of alternative pathways that fail to reestablish mitochondrial function. |
X Demographics
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Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 1 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 1 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 88 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 88 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Bachelor | 18 | 20% |
| Student > Ph. D. Student | 16 | 18% |
| Student > Master | 7 | 8% |
| Professor | 4 | 5% |
| Student > Doctoral Student | 3 | 3% |
| Other | 10 | 11% |
| Unknown | 30 | 34% |
| Readers by discipline | Count | As % |
|---|---|---|
| Neuroscience | 14 | 16% |
| Psychology | 12 | 14% |
| Medicine and Dentistry | 10 | 11% |
| Biochemistry, Genetics and Molecular Biology | 4 | 5% |
| Pharmacology, Toxicology and Pharmaceutical Science | 4 | 5% |
| Other | 12 | 14% |
| Unknown | 32 | 36% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 05 July 2017.
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#15,467,628
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Outputs from Molecular Neurobiology
#2,076
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Outputs of similar age from Molecular Neurobiology
#66
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