Mutual enhancement of central neurotoxicity induced by ketamine followed by methamphetamine

Ke, Jing Jer; Chen, Hsiun Ing; Jen, Chauying J.; Kuo, Yu Min; Cherng, Chianfang G.; Tsai, Yen Ping N.; Ho, Ming Che; Tsai, Chia Wen; Yu, Lung

doi:10.1016/j.taap.2007.10.017

Cited by 18 publications

(8 citation statements)

References 29 publications

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“…These concentrations are consistent with the range reported using high pressure liquid chromatography (HPLC) methods (Fumagalli et al, 1998; Ke et al, 2008). …”

Section: Resultssupporting

confidence: 90%

Sigma (σ) receptor ligand, AC927 (N-phenethylpiperidine oxalate), attenuates methamphetamine-induced hyperthermia and serotonin damage in mice

Seminerio

Kaushal

Shaikh

et al. 2011

Pharmacology Biochemistry and Behavior

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Methamphetamine interacts with sigma (σ) receptors and AC927, a selective σ receptor ligand, protects against methamphetamine-induced dopaminergic neurotoxicity. In the present study, the effects of AC927 on methamphetamine-induced hyperthermia and striatal serotonergic neurotoxicity were evaluated. Male, Swiss Webster mice were injected (i.p.) every two hours, for a total of four times, with one of the following treatments: Saline + Saline; Saline + Methamphetamine (5 mg/kg); AC927 (5, 10, 20 mg/kg) + Methamphetamine (5 mg/kg); or AC927 (5, 10, 20 mg/kg) + Saline. Pretreatment with AC927 (10 mg/kg) significantly attenuated methamphetamine-induced striatal serotonin depletions, striatal serotonin transporter reductions, and hyperthermia. At the doses tested, AC927 itself had no significant effects on serotonin levels, serotonin transporter expression, or body temperature. To evaluate the effects of higher ambient temperature on methamphetamine-induced neurotoxicity, groups of mice were treated at 37°C. Overall, there was an inverse correlation between the body temperature of the animals and striatal serotonin levels. Together, the data suggest that AC927 (10 mg/kg) protects against methamphetamine-induced neurotoxicity. The reduction of methamphetamine-induced hyperthermia by AC927 may contribute to the observed neuroprotection in vivo.

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“…These concentrations are consistent with the range reported using high pressure liquid chromatography (HPLC) methods (Fumagalli et al, 1998; Ke et al, 2008). …”

Section: Resultssupporting

confidence: 90%

Sigma (σ) receptor ligand, AC927 (N-phenethylpiperidine oxalate), attenuates methamphetamine-induced hyperthermia and serotonin damage in mice

Seminerio

Kaushal

Shaikh

et al. 2011

Pharmacology Biochemistry and Behavior

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“…In fact, NMDA receptor antagonists block the long-term dopamine loss induced by METH (Fuller et al 1992; Layer et al 1993; Ohmori et al 1993; Thomas and Kuhn 2005; Ke et al 2008). AMPA and NMDA glutamate receptors have differential distribution in the striatal compartments.…”

Section: Discussionmentioning

confidence: 99%

Selective Vulnerability in Striosomes and in the Nigrostriatal Dopaminergic Pathway After Methamphetamine Administration

et al. 2009

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Methamphetamine (METH), a commonly abused psychostimulant, causes dopamine neurotoxicity in humans, rodents, and nonhuman primates. This study examined the selective neuroanatomical pattern of dopaminergic neurotoxicity induced by METH in the mouse striatum. We examined the effect of METH on tyrosine hydroxylase (TH) and dopamine transporter (DAT) immunoreactivity in the different compartments of the striatum and in the nucleus accumbens. The levels of dopamine and its metabolites, 3,4-dihidroxyphenylacetic acid and homovanillic acid, as well as serotonin (5-HT) and its metabolite, 5-hydroxyindolacetic acid, were also quantified in the striatum. Mice were given three injections of METH (4 mg/kg, i.p.) at 3 h intervals and sacrificed 7 days later. This repeated METH injection induced a hyperthermic response and a decrease in striatal concentrations of dopamine and its metabolites without affecting 5-HT concentrations. In addition, the drug caused a reduction in TH- and DAT-immunoreactivity when compared to saline-treated animals. Interestingly, there was a significantly greater loss of TH- and DAT-immunoreactivity in striosomes than in the matrix. The predominant loss of dopaminergic terminals in the striosomes occurred along the rostrocaudal axis of the striatum. In contrast, METH did not decrease TH- or DAT-immunoreactivity in the nucleus accumbens. These results provide the first evidence that compartments of the mouse striatum, striosomes and matrix, and mesolimbic and nigrostriatal pathways have different vulnerability to METH. This pattern is similar to that observed with other neurotoxins such as MPTP, the most widely used model of Parkinson’s disease, in early Huntington’s disease and hypoxic/ischemic injury, suggesting that these conditions might share mechanisms of neurotoxicity.

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“…One-way (plasmid DNA vs. vector treatment) repeated measure ANOVAs (across various tests) were employed to test group differences in cocaineinduced CPP and food-induced CPP magnitude. ANOVAs were used to analyze group differences in locomotor activity, DA, DOPAC levels [29] , and Western immunoblotting results. The levels of statistical significance were set at p !…”

Section: Discussionmentioning

confidence: 99%

Accumbal 14-3-3ζ Protein Downregulation Is Associated with Cocaine-Conditioned Memory

et al. 2011

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Cocaine-conditioned memory has been known to cause cocaine craving and relapse, while its underlying mechanisms remain unclear. We explored accumbal protein candidates responsible for a cocaine-conditioned memory, cocaine-induced conditioned place preference (CPP). Two-dimensional gel electrophoresis in conjunction with liquid chromatography mass spectrometry analysis was utilized to identify accumbal protein candidates involved in the retrieval of cocaine-induced CPP. Among the identified candidate proteins, a downregulated 14-3-3ζ protein was chosen and confirmed by Western immunoblotting. A polymer-mediated plasmid DNA delivery system was then used to overexpress 14-3-3 protein in mouse nucleus accumbens before the CPP retrieval tests. Overexpression of accumbal 14-3-3ζ protein was found to diminish conditioned cue/context-mediated cocaine-induced CPP. In contrast, another isoform of 14-3-3 protein, 14-3-3ε protein, did not affect conditioned cue/context-mediated cocaine-induced CPP. Overexpression of accumbal 14-3-3ζ protein did not produce motor activity-impairing effect or alter local dopamine metabolism. Moreover, overexpression of accumbal 14-3-3ζ protein did not affect food-induced CPP. These results, taken together, indicated that overexpressed accumbal 14-3-3ζ protein specifically decreased conditioned cue/context-mediated cocaine memory. Further understanding of the function of accumbal 14-3-3ζ protein may shed light on the treatment of cocaine craving and relapse.

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Mutual enhancement of central neurotoxicity induced by ketamine followed by methamphetamine

Cited by 18 publications

References 29 publications

Sigma (σ) receptor ligand, AC927 (N-phenethylpiperidine oxalate), attenuates methamphetamine-induced hyperthermia and serotonin damage in mice

Sigma (σ) receptor ligand, AC927 (N-phenethylpiperidine oxalate), attenuates methamphetamine-induced hyperthermia and serotonin damage in mice

Selective Vulnerability in Striosomes and in the Nigrostriatal Dopaminergic Pathway After Methamphetamine Administration

Accumbal 14-3-3ζ Protein Downregulation Is Associated with Cocaine-Conditioned Memory

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