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Published on: February 18, 2016
Methamphetamine treatment causes delayed decrease in novelty-induced locomotor activity in mice.
Irina N Krasnova1, Amber B Hodges, Bruce Ladenheim
1Molecular Neuropsychiatry Research Branch, National Institute on Drug Abuse, NIH/DHHS, Baltimore, MD 21224, USA.
Neuroscience Research
|June 30, 2009
Summary
Methamphetamine (METH) causes brain damage but initially shows no effect on novelty-induced activity. Long-term, METH-exposed mice exhibit reduced activity, suggesting non-dopamine neuron dysfunction.
Area of Science:
- Neuroscience
- Pharmacology
- Neurotoxicology
Background:
- Methamphetamine (METH) is a neurotoxin damaging dopamine (DA) and other neurons.
- Understanding METH's long-term behavioral effects is crucial.
Purpose of the Study:
- Investigate short- and long-term effects of METH on novelty-induced locomotor activity.
- Determine if METH-induced DA neurotoxicity correlates with behavioral changes.
Main Methods:
- Mice received METH (7.5 mg/kg x 4) or saline.
- Locomotor activity, DA levels, and cell death (TUNEL) were assessed at various time points (10 days, 3, 5 months).
Main Results:
- METH decreased striatal/cortical DA levels at 10 days, with recovery by 3-5 months.
- No initial changes in locomotor activity were observed.
- Delayed deficits in locomotor activity appeared at 5 months post-METH.
- METH increased cell death in striatum/cortex at 3 days.
Conclusions:
- Delayed locomotor deficits are not solely due to DA terminal degeneration.
- METH's long-term effects may involve age-dependent dysfunction of non-DA neurons in the striatum and cortex.
