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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

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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.

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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.