Journal
BEHAVIOURAL PHARMACOLOGY
Volume 21, Issue 7, Pages 602-614Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/FBP.0b013e32833e7e44
Keywords
acetylcholine; apolipoprotein E; cognition; hippocampus; methamphetamine; mouse
Funding
- NIH, NIDA [R01 MH77647, T32-DA007262]
- NASA [NNJ05HE63G]
- Alzheimer's Association [IIRG-05-14021]
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH077647] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [T32DA007262] Funding Source: NIH RePORTER
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Exposure to methamphetamine during brain development impairs cognition in humans and rodents. In mice, these impairments are more severe in females than males. Genetic factors, such as apolipoprotein E genotype, may modulate the cognitive effects of methamphetamine. Methamphetamine-induced alterations in the brain acetylcholine system may contribute to the cognitive effects of methamphetamine and may also be modulated by apolipoprotein E isoform. We assessed the long-term effects of methamphetamine exposure during brain development on cognitive function and muscarinic acetylcholine receptors in mice, and whether apolipoprotein E isoform modulates these effects. Mice expressing human apolipoprotein E3 or E4 were exposed to methamphetamine (5 mg/kg) or saline once a day from postnatal days 11-20 and behaviorally tested in adulthood. Muscarinic acetylcholine receptor binding was measured in the hippocampus and cortex. Methamphetamine exposure impaired novel location recognition in female, but not male, mice. Methamphetamine-exposed male and female mice
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