Administration of a single high dose of methamphetamine (METH) causes a rapid and reversible decrease in the activity of the tryptophan hydroxylase (TPH), the rate-limiting enzyme in the synthesis of 5-hydroxytryptamine. This effect can be reversed completely by exposing the METH-impaired enzyme to a reducing environment, which suggests that the decrease in TPH activity is a reversible oxidativ...

Methamphetamine (Meth) is an addictive psychostimulant widely abused around the world. The chronic use of Meth produces neurotoxicity featured by dopaminergic terminal damage and microgliosis, resulting in serious neurological and behavioral consequences. Ample evidence indicate that Meth causes microglial activation and resultant secretion of pro-inflammatory molecules leading to neural injury...

Chronic or excessive (+)-methamphetamine (METH) use often leads to addiction and toxicity to critical organs like the brain. With medical treatment as a goal, a novel single-chain variable fragment (scFv) against METH was engineered from anti-METH monoclonal antibody mAb6H4 (IgG, kappa light chain, K(d) = 11 nM) and found to have similar ligand affinity (K(d) = 10 nM) and specificity as mAb6H4....

BACKGROUND Chronic methamphetamine (METH) exposure causes neuroadaptations at glutamatergic synapses. METHODS To identify the METH-induced epigenetic underpinnings of these neuroadaptations, we injected increasing METH doses to rats for 2 weeks and measured striatal glutamate receptor expression. We then quantified the effects of METH exposure on histone acetylation. We also measured METH-ind...

In recent years, abuse of amphetamine-type stimulants (ATS) has become a severe problem to the whole world, and methamphetamine (METH) has accounted for the majority percent of global ATS seizures. It has been confirmed that the changes of histone acetylation involve in the regulation of METH addiction [1]; however, the effects of METH on histone deacetylase (HDAC) are poorly understood. Behavi...

Increasing evidence implicates apoptosis as a major mechanism of cell death in methamphetamine (METH) neurotoxicity. The involvement of a neuroimmune component in apoptotic cell death after injury or chemical damage suggests that cytokines may play a role in METH effects. In the present study, we examined if the absence of IL-6 in knockout (IL-6-/-) mice could provide protection against METH-in...

I read with interest the recent Public Health piece on methamphetamine hydrochloride (crystal meth). Two subsequent articles on the same topic provided more details, but there were no comments on prevention programs or on limiting production of this drug. I had a distinct sense of déjà vu. Forty-five years ago, I reported in CMAJ the first North American case of addiction to diethylpropion. Thi...

INTRODUCTION: Methamphetamine (METH) is a major drug of abuse in the United States and in many countries throughout the world. Preclinical and clinical studies demonstrated significant neurotoxic effects and brain changes associated with the drug. However, few studies have evaluated morphometric changes associated with METH abuse [1-3]. We performed voxel based morphometry to determine whether ...

Although the stimulating and psychotropic effects of methamphetamine (METH) on the nervous system are well documented, the impact of METH abuse on biological metabolism and the turnover of peripheral transmitters are poorly understood. Metabolomics has the potential to reveal the effect of METH abuse on systemic metabolism and potential markers suggesting the underlying mechanism of toxicity. I...