Methamphetamine treatment causes delayed decrease in novelty-induced locomotor activity in mice

详细信息    查看全文

• 作者：Irina N. Krasnova ; Amber B. Hodges ; Bruce Ladenheim ; Raina Rhoades ; Crystal G. Phillip ; Angela Ceseň ; a ; Ekaterina Ivanova ; Christine F. Hohmann ; Jean Lud Cadet
• 关键词：Methamphetamine ; Dopamine ; Neurotoxicity ; Striatum ; Cortex ; Novelty-induced locomotor activity
• 刊名：Neuroscience Research
• 出版年：2009
• 出版时间：October 2009
• 年：2009
• 卷：65
• 期：2
• 页码：160-165
• 全文大小：320 K

文摘

Methamphetamine (METH) is a psychostimulant that causes damage to dopamine (DA) axons and to non-monoaminergic neurons in the brain. The aim of the present study was to investigate short- and long-term effects of neurotoxic METH treatment on novelty-induced locomotor activity in mice. Male BALB/c mice, 12–14 weeks old, were injected with saline or METH (i.p., 7.5 mg/kg × 4 times, every 2 h). Behavior and neurotoxic effects were assessed at 10 days, 3 and 5 months following drug treatment. METH administration caused marked decreases in DA levels in the mouse striatum and cortex at 10 days post-drug. However, METH did not induce any changes in novelty-induced locomotor activity. At 3 and 5 months after treatment METH-exposed mice showed significant recovery of DA levels in the striatum and cortex. In contrast, these animals demonstrated significant decreases in locomotor activity at 5 months in comparison to aged-matched control mice. Further assessment of METH toxicity using TUNEL staining showed that the drug induced increased cell death in the striatum and cortex at 3 days after administration. Taken together, these data suggest that delayed deficits in novelty-induced locomotor activity observed in METH-exposed animals are not due to neurodegeneration of DA terminals but to combined effects of METH and age-dependent dysfunction of non-DA intrinsic striatal and/or corticostriatal neurons.