Abstract
Methamphetamine (METH) is a widely abused psychostimulant with the potential to cause a broad range of severe cognitive deficits as well as neurobehavioral abnormalities when abused chronically, particularly at high doses. Cognitive deficits are related to METH neurotoxicity in the striatum and hippocampus. The activation of transposable Long INterspersed Nuclear Element 1 (LINE-1) is associated with several neurological diseases and drug abuse, but there are very limited data regarding the effects of high-dose METH on the activity of LINE-1 in the adult brain. Using real-time quantitative PCR, the present study demonstrates that the chronic administration of neurotoxic METH doses results in the increased expression of LINE-1-encoded Open Reading Frame 1 (ORF-1) in rat striatum shortly after the last dose of the drug and decreased ORF-1 expression during METH withdrawal, with dentate gyrus potentially developing “tolerance” to these METH effects. LINE-1 activation may be a new factor mediating the neurotoxic effects of chronic METH in the striatum and, therefore, a new drug target against METH-induced psychomotor impairments in chronic METH users.
Highlights
Methamphetamine (METH) is a potent central nervous system (CNS) psychostimulant, the abuse of which remains a major public health concern worldwide
Long INterspersed Nuclear Element 1 (LINE-1) activation may be a new factor mediating the neurotoxic effects of chronic METH in the striatum and, a new drug target against METH-induced psychomotor impairments in chronic METH users
These results suggest a common pathway of Long INterspersed Elements (LINEs)-1 induction by frontal cortex of alcoholics [40], the medial prefrontal cortex of cocaine users [75] and the cell-free these substances
Summary
Methamphetamine (METH) is a potent central nervous system (CNS) psychostimulant, the abuse of which remains a major public health concern worldwide. Abuse and Mental Health Services Administration) 2018 report, there are more than 700,000 current users of METH in the United States. Deaths from METH overdose doubled between 2013 and 2017 and keep rising [1,2]. Chronic exposure to METH early in life increases the risk of developing Parkinson’s disease later on [5,6,7]. New drug targets are needed, for heavy METH users, who suffer the most from METH abuse-related neuropsychological problems [10,11,12], are less likely to seek treatment than moderate METH users [13], and are at high risk of dying from a METH overdose [14]
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