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Published on: November 17, 2018
Effects of ethanol exposure on spatial learning in mice during synaptogenesis
Junichi Furumiya1, Yoshiaki Hashimoto
1Department of Legal Medicine, Kochi Medical School, Kochi University Kohasu, Oko-cho, Nankoku City, Kochi 783-8505, Japan.
Nihon Arukoru Yakubutsu Igakkai Zasshi = Japanese Journal of Alcohol Studies & Drug Dependence
|June 28, 2011
Summary
Neonatal ethanol (EtOH) exposure impairs spatial learning in mice, with deficits persisting into adulthood. This suggests EtOH-induced apoptosis in brain neurons during development causes lasting cognitive impairment.
Area of Science:
- Neuroscience
- Developmental Biology
- Toxicology
Background:
- Ethanol (EtOH) exposure during synaptogenesis can impact brain development and cognitive function.
- The long-term effects of neonatal EtOH exposure on spatial learning are not fully understood.
Purpose of the Study:
- To investigate the effects of neonatal ethanol exposure on spatial learning during synaptogenesis in mice.
- To determine if spatial learning deficits persist after maturation.
Main Methods:
- Neonatal mice received subcutaneous ethanol injections.
- Brain tissue was analyzed for apoptosis using TUNEL assay and activated caspase-3 immunohistochemistry.
- Blood and brain ethanol concentrations were measured.
- Spatial learning was assessed using a water maze test at 7 and 12 weeks of age.
Main Results:
- Mice exposed to ethanol neonatally exhibited prolonged times to reach the platform in the water maze.
- These spatial learning deficits were observed at both 7 and 12 weeks of age.
- Increased apoptosis markers (TUNEL and activated caspase-3) were found in the cerebral cortex, hippocampus, and thalamus 24 hours post-ethanol exposure.
Conclusions:
- Neonatal ethanol exposure causes persistent spatial learning impairments that do not improve with age.
- Ethanol-induced apoptosis of brain neurons during the synaptogenesis period is the likely cause of long-term cognitive deficits.
