Abstract
Nowadays, drug abuse and addiction are serious public health problems in the USA. Methamphetamine (METH) is one of the most abused drugs and is known to cause brain damage after repeated exposure. In this paper, we conducted a neuroproteomic study to evaluate METH-induced brain protein dynamics, following a two-week chronic regimen of an escalating dose of METH exposure. Proteins were extracted from rat brain hippocampal and olfactory bulb tissues and subjected to liquid chromatography-mass spectrometry (LC-MS/MS) analysis. Both shotgun and targeted proteomic analysis were performed. Protein quantification was initially based on comparing the spectral counts between METH exposed animals and their control counterparts. Quantitative differences were further confirmed through multiple reaction monitoring (MRM) LC-MS/MS experiments. According to the quantitative results, the expression of 18 proteins (11 in the hippocampus and 7 in the olfactory bulb) underwent a significant alteration as a result of exposing rats to METH. 13 of these proteins were up-regulated after METH exposure while 5 were down-regulated. The altered proteins belonging to different structural and functional families were involved in processes such as cell death, inflammation, oxidation, and apoptosis.
Highlights
Methamphetamine (METH) has been recognized as one of the most abused drugs in the United States
We found that proteins belonging to different structural and functional families were involved in processes such as cell death, inflammation, oxidation, and apoptosis
We expect and as our results show through the above-mentioned protein expression, up- and down-regulation of many biological pathways involved in cell death, neuronal repair, inflammation, oxidation, and apoptosis
Summary
Methamphetamine (METH) has been recognized as one of the most abused drugs in the United States. METH is an illicit drug known to cause psychiatric manifestations such as euphoria, agitation, hallucinations, misperceptions, mood disturbances and long-term cognitive and psychomotor deficits [1,2,3]. These manifestations are mainly the result of neurotoxicity leading to striatal dopaminergic terminal degeneration [4, 5] and non-dopaminergic striatal pathologies [6]. Several studies have shown that METH is a potent psychomotor stimulant that affects dopaminergic, glutamatergic and serotonergic systems in the brain [7, 8]. Findings similar to those observed in human brains have been reported in rodents treated with METH.
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