Treatment of Methamphetamine Dependence

Mendelson, John; Rawson, Rick; Newton, Thomas F.; Wit, Harriet de; Dewey, Stephen L.; Hart, Carl L.; Epstein, David H.

doi:10.4065/83.3.369-a

Cited by 4 publications

(4 citation statements)

References 2 publications

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“…METH causes short-term symptoms related to the sympathetic response of the autonomic nervous system (tachycardia, tachypnea, hypertension, dilatation of the pupils, hyperthermia, reduced fatigue), and increases euphoria, attention, energy, and libido while decreasing appetite [ 2 , 3 , 4 , 5 ]. However, repeated METH use can disrupt the central nervous system (CNS), causing neuropsychiatric changes, and in severe cases, death [ 6 , 7 , 8 , 9 ]. As drug abuse increases worldwide, deaths from METH misuse are also on the rise [ 10 , 11 , 12 ].…”

Section: Introductionmentioning

confidence: 99%

Exercise Pills for Drug Addiction: Forced Moderate Endurance Exercise Inhibits Methamphetamine-Induced Hyperactivity through the Striatal Glutamatergic Signaling Pathway in Male Sprague Dawley Rats

Jung

Kim

et al. 2021

IJMS

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Physical exercise reduces the extent, duration, and frequency of drug use in drug addicts during the drug initiation phase, as well as during prolonged addiction, withdrawal, and recurrence. However, information about exercise-induced neurobiological changes is limited. This study aimed to investigate the effects of forced moderate endurance exercise training on methamphetamine (METH)-induced behavior and the associated neurobiological changes. Male Sprague Dawley rats were subjected to the administration of METH (1 mg/kg/day, i.p.) and/or forced moderate endurance exercise (treadmill running, 21 m/min, 60 min/day) for 2 weeks. Over the two weeks, endurance exercise training significantly reduced METH-induced hyperactivity. METH and/or exercise treatment increased striatal dopamine (DA) levels, decreased p(Thr308)-Akt expression, and increased p(Tyr216)-GSK-3β expression. However, the phosphorylation levels of Ser9-GSK-3β were significantly increased in the exercise group. METH administration significantly increased the expression of NMDAr1, CaMKK2, MAPKs, and PP1 in the striatum, and exercise treatment significantly decreased the expression of these molecules. Therefore, it is apparent that endurance exercise inhibited the METH-induced hyperactivity due to the decrease in GSK-3β activation by the regulation of the striatal glutamate signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Exercise Pills for Drug Addiction: Forced Moderate Endurance Exercise Inhibits Methamphetamine-Induced Hyperactivity through the Striatal Glutamatergic Signaling Pathway in Male Sprague Dawley Rats

Jung

Kim

et al. 2021

IJMS

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“…Long-term, regular METH use can lead to severe tooth decay, infection, weight loss, malnutrition, kidney damage, liver damage, respiratory issues, paranoia, violent behaviour, psychosis, severe anxiety and depression. Even when individuals stop taking METH, the symptoms may persist for many years (9)(10)(11)(12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

Methamphetamine: Effects on the brain, gut and immune system

Prakash

Tangalakis

Antonipillai

et al. 2017

Pharmacological Research

154

103

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Methamphetamine (METH) is a powerful central nervous system stimulant which elevates mood, alertness, energy levels and concentration in the short-term. However, chronic use and/or at higher doses METH use often results in psychosis, depression, delusions and violent behavior. METH was formerly used to treat conditions such as obesity and attention deficit hyperactivity disorder, but now is primarily used recreationally. Its addictive nature has led to METH abuse becoming a global problem. At a cellular level, METH exerts a myriad of effects on the central and peripheral nervous systems, immune system and the gastrointestinal system. Here we present how these effects might be linked and their potential contribution to the pathogenesis of neuropsychiatric disorders. In the long term, this pathway could be targeted therapeutically to protect people from the ill effects of METH use. This model of METH use may also provide insight into how gut, nervous and immune systems might break down in other conditions that may also benefit from therapeutic intervention.

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“…This often leads to the continued use and can cause a negative reinforcement cycle [ 8 ], which may lead to addiction [ 8 ]. Even when individuals stop taking METH, the symptoms may persist for years [ 9 , 10 , 11 , 12 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

Methamphetamine Induces Systemic Inflammation and Anxiety: The Role of the Gut–Immune–Brain Axis

Davidson

Mayer

Habib

et al. 2022

IJMS

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Methamphetamine (METH) is a highly addictive drug abused by millions of users worldwide, thus becoming a global health concern with limited management options. The inefficiency of existing treatment methods has driven research into understanding the mechanisms underlying METH-induced disorders and finding effective treatments. This study aims to understand the complex interactions of the gastrointestinal–immune–nervous systems following an acute METH dose administration as one of the potential underlying molecular mechanisms concentrating on the impact of METH abuse on gut permeability. Findings showed a decreased expression of tight junction proteins ZO-1 and EpCAm in intestinal tissue and the presence of FABP-1 in sera of METH treated mice suggests intestinal wall disruption. The increased presence of CD45+ immune cells in the intestinal wall further confirms gut wall inflammation/disruption. In the brain, the expression of inflammatory markers Ccl2, Cxcl1, IL-1β, TMEM119, and the presence of albumin were higher in METH mice compared to shams, suggesting METH-induced blood–brain barrier disruption. In the spleen, cellular and gene changes are also noted. In addition, mice treated with an acute dose of METH showed anxious behavior in dark and light, open field, and elevated maze tests compared to sham controls. The findings on METH-induced inflammation and anxiety may provide opportunities to develop effective treatments for METH addiction in the future.

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Treatment of Methamphetamine Dependence

Cited by 4 publications

References 2 publications

Exercise Pills for Drug Addiction: Forced Moderate Endurance Exercise Inhibits Methamphetamine-Induced Hyperactivity through the Striatal Glutamatergic Signaling Pathway in Male Sprague Dawley Rats

Exercise Pills for Drug Addiction: Forced Moderate Endurance Exercise Inhibits Methamphetamine-Induced Hyperactivity through the Striatal Glutamatergic Signaling Pathway in Male Sprague Dawley Rats

Methamphetamine: Effects on the brain, gut and immune system

Methamphetamine Induces Systemic Inflammation and Anxiety: The Role of the Gut–Immune–Brain Axis

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