Selective reduction of serotonin immunoreactivity in some forebrain regions of rats induced by acute methamphetamine treatment; quantitative morphometric analysis by serotonin immunocytochemistry

Fukui, Kenji; Nakajima, Teruo; Kariyama, Hirofumi; Kashiba, Akira; Kato, Nobukatsu; Tohyama, Ikuo; Kimura, Hiroshi

doi:10.1016/0006-8993(89)90562-3

Cited by 23 publications

(15 citation statements)

References 13 publications

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“…In agreement with the findings in humans, animal studies show that METH injures presynaptic DA and 5-HT terminals [190,191], causes a decrease of tyrosine hydroxylase (TH) and tryptophan hydroxylase (TPH) [192], depletes DA and 5-HT [193], reduces DAT, 5-HTT [194,195,196] and vesicular monoamine transporter (VMAT)-2 [197]. METH also triggers neuronal cell death in cortex [198,199], striatum [198], hippocampus [200] and olfactory bulb [201].…”

Section: Neurotoxicity Of Methsupporting

confidence: 86%

Neuronal Stress and Injury Caused by HIV-1, cART and Drug Abuse: Converging Contributions to HAND

Sánchez

Kaul

2017

Brain Sciences

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Multiple mechanisms appear to contribute to neuronal stress and injury underlying HIV-associated neurocognitive disorders (HAND), which occur despite the successful introduction of combination antiretroviral therapy (cART). Evidence is accumulating that components of cART can itself be neurotoxic upon long-term exposure. In addition, abuse of psychostimulants, such as methamphetamine (METH), seems to compromise antiretroviral therapy and aggravate HAND. However, the combined effect of virus and recreational and therapeutic drugs on the brain is still incompletely understood. However, several lines of evidence suggest a shared critical role of oxidative stress, compromised neuronal energy homeostasis and autophagy in promotion and prevention of neuronal dysfunction associated with HIV-1 infection, cART and psychostimulant use. In this review, we present a synopsis of recent work related to neuronal stress and injury induced by HIV infection, antiretrovirals (ARVs) and the highly addictive psychostimulant METH.

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Section: Neurotoxicity Of Methsupporting

confidence: 86%

Neuronal Stress and Injury Caused by HIV-1, cART and Drug Abuse: Converging Contributions to HAND

Sánchez

Kaul

2017

Brain Sciences

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“…Similar METH injections have also been reported to cause decreases in vesicular monoamine transporter 2 (VMAT-2) binding (Guilarte et al, 2003; Segal et al, 2005) and immunoreactivity (Eyerman and Yamamoto, 2007) in the rat striatum. Morphological studies suggest that the reductions in the markers of DA and 5-HT system integrity are related to degeneration of DA and 5-HT axonal terminals (Axt and Molliver, 1991; Fukui et al, 1989; Lorez, 1981; Ricaurte et al, 1982, 1984). The neurotoxic damage to striatal axonal terminals is accompanied by reactive astrocytosis (Bowyer et al, 1994; Cappon et al, 2000; Fukumura et al, 1998) and microglial activation (Pubill et al, 2002).…”

Section: Animal Models Of Meth Toxicitymentioning

confidence: 99%

Methamphetamine toxicity and messengers of death

Krasnova¹,

Cadet²

2009

Brain Research Reviews

529

534

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Methamphetamine (METH) is an illicit psychostimulant that is widely abused in the world. Several lines of evidence suggest that chronic METH abuse leads to neurodegenerative changes in the human brain. These include damage to dopamine and serotonin axons, loss of gray matter accompanied by hypertrophy of the white matter and microgliosis in different brain areas. In the present review, we summarize data on the animal models of METH neurotoxicity which include degeneration of monoaminergic terminals and neuronal apoptosis. In addition, we discuss molecular and cellular bases of METH-induced neuropathologies. The accumulated evidence indicates that multiple events, including oxidative stress, excitotoxicity, hyperthermia, neuroinflammatory responses, mitochondrial dysfunction, endoplasmic reticulum stress converge to mediate METH-induced terminal degeneration and neuronal apoptosis. When taken together, these findings suggest that pharmacological strategies geared towards the prevention and treatment of the deleterious effects of this drug will need to attack the various pathways that form the substrates of METH toxicity. Keywords methamphetamine; neurotoxicity; dopamine; oxidative stress; serotonin; cell death Epidemiology of Methamphetamine AbuseAbuse of the illegal psychostimulant, methamphetamine (METH), has become an international public health problem with an estimated 15-16 million users worldwide, a total which exceeds the number of people who abuse heroin and cocaine and makes METH the second most widely abused drug after cannabis (United Nations Office on Drugs and Crime, 2007). The inexpensive production of METH, its low cost, and long duration of action have made it a very desirable commodity. Indeed, METH is a popular drug of abuse in Australia (Australian Institure for Health and Welfare, 2005), Canada (Canadian Centre on Substance Abuse, 2005), Czech Republic and Slovakia (European Monitoring Center for Drugs and Drug Addiction, 2007). During the last decade, Southeast Asia and East Asia have become global hubs for METH production and trafficking, with a coincident epidemic of psychostimulant abuse in these regions (United Nations Office on Drugs and Crime, 2007). It is estimated that over half of the world's METH consumers reside in Southeast Asia and East Asia (United Nations Office on Drugs and Crime, 2007). Japan, in particular, has experienced several epidemics of crystal METH abuse, including a peak in 1999-2000. Since the late 1990s, METH use rose to epidemic Correspondence: Jean Lud Cadet M.D., Chief, Molecular Neuropsychiatry Reasearch Branch, Intramural Research Program, NIDA/NIH/ DHHS, 251 Bayview Boulevard, Baltimore, MD 21224, USA, jcadet@intra.nida.nih.gov, Tel: 443-740-2656, Fax: 443-740-2856. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before...

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“…Several studies suggest that repeated amphetamine treatment, especially in its methylated form, produces enduring changes in 5-HT, as well DA transmission (Seiden et al 1975;Preston et al 1985;Fukui et al 1989;Woolverton et al 1989;Axt and Molliver 1991). Indeed, it has been suggested that those limbic regions innervated by 5-HT projections are especially sensitive to the effects of repeated amphetamine administration Seiden and Ricaurte 1987), suggesting that one mechanism for altered decision making associated with chronic amphetamine abuse in humans might be altered serotonergic modulation of the ventral PFC and its interconnected structures (Groenewegen et al 1997).…”

Section: Decision Making and Monoamine Neurotransmitter Systemsmentioning

confidence: 99%

Dissociable Deficits in the Decision-Making Cognition of Chronic Amphetamine Abusers, Opiate Abusers, Patients with Focal Damage to Prefrontal Cortex, and Tryptophan-Depleted Normal Volunteers Evidence for Monoaminergic Mechanisms

Rogers

Everitt

Baldacchino³

et al. 1999

Neuropsychopharmacology

1,004

758

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Selective reduction of serotonin immunoreactivity in some forebrain regions of rats induced by acute methamphetamine treatment; quantitative morphometric analysis by serotonin immunocytochemistry

Cited by 23 publications

References 13 publications

Neuronal Stress and Injury Caused by HIV-1, cART and Drug Abuse: Converging Contributions to HAND

Neuronal Stress and Injury Caused by HIV-1, cART and Drug Abuse: Converging Contributions to HAND

Methamphetamine toxicity and messengers of death

Dissociable Deficits in the Decision-Making Cognition of Chronic Amphetamine Abusers, Opiate Abusers, Patients with Focal Damage to Prefrontal Cortex, and Tryptophan-Depleted Normal Volunteers Evidence for Monoaminergic Mechanisms

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