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Adolescent Intermittent Alcohol Exposure: Persistence of Structural and Functional Hippocampal Abnormalities into Adulthood
Author(s) -
Risher MaryLouise,
Fleming Rebekah L.,
Risher W. Christopher,
Miller K. M.,
Klein Rebecca C.,
Wills Tiffany,
Acheson Shawn K.,
Moore Scott D.,
Wilson Wilkie A.,
Eroglu Cagla,
Swartzwelder H. S.
Publication year - 2015
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.12725
Subject(s) - postsynaptic potential , synaptic plasticity , hippocampal formation , neuroscience , long term potentiation , dendritic spine , hippocampus , neuroplasticity , psychology , postsynaptic density , alcohol abuse , inhibitory postsynaptic potential , medicine , excitatory postsynaptic potential , psychiatry , receptor
Background Human adolescence is a crucial stage of neurological development during which ethanol (EtOH) consumption is often at its highest. Alcohol abuse during adolescence may render individuals at heightened risk for subsequent alcohol abuse disorders, cognitive dysfunction, or other neurological impairments by irreversibly altering long‐term brain function. To test this possibility, we modeled adolescent alcohol abuse (i.e., intermittent EtOH exposure during adolescence [AIE]) in rats to determine whether adolescent exposure to alcohol leads to long‐term structural and functional changes that are manifested in adult neuronal circuitry. Methods We specifically focused on hippocampal area CA 1, a brain region associated with learning and memory. Using electrophysiological, immunohistochemical, and neuroanatomical approaches, we measured post‐ AIE changes in synaptic plasticity, dendritic spine morphology, and synaptic structure in adulthood. Results We found that AIE ‐pretreated adult rats manifest robust long‐term potentiation, induced at stimulus intensities lower than those required in controls, suggesting a state of enhanced synaptic plasticity. Moreover, AIE resulted in an increased number of dendritic spines with characteristics typical of immaturity. Immunohistochemistry‐based analysis of synaptic structures indicated a significant decrease in the number of co‐localized pre‐ and postsynaptic puncta. This decrease is driven by an overall decrease in 2 postsynaptic density proteins, PSD ‐95 and SAP 102. Conclusions Taken together, these findings reveal that repeated alcohol exposure during adolescence results in enduring structural and functional abnormalities in the hippocampus. These synaptic changes in the hippocampal circuits may help to explain learning‐related behavioral changes in adult animals preexposed to AIE .