Acute neuropathological changes in the caudate nucleus caused by MPTP and methamphetamine: Immunohistochemical studies

Hess, Arthur; Desiderio, Carla; McAuliffe, W. Geoffrey

doi:10.1007/bf01188403

Cited by 70 publications

(39 citation statements)

References 9 publications

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“…Immunohistochemical examination reveals that MA reduces TH-IR in the striatum and other dopaminergic terminal fields in the forebrain (Hess et al, 1990;Pu and Vorhees, 1993;Pu et al, 1994;Trulson et al, 1985). Furthermore, astrogliosis and argyrophilia, indices of neuronal damage, are present in areas corresponding to the loss of TH-IR after MA treatment, thereby supporting the conclusion that MA injures dopaminergic terminals (Bowyer et al, 1994;Hess et al, 1990;Miller and O'Callaghan, 1994;O'Callaghan and Miller, 1994;Pu and Vorhees, 1993;Pu et al, 1994;Ricaurte et al, 1982).…”

Section: Introductionmentioning

confidence: 84%

“…Administration of this compound to experimental animals results in a reproducible profile of neurotoxicity that consists of persistent reductions in striatal dopamine content, loss of TH activity, and diminished numbers of dopamine reuptake sites (Bowyer et al, 1994;Hotchkiss and Gibb, 1980;O'Callaghan and Miller, 1994;Ricaurte et al, 1980;Seiden et al, 1976;Wagner et al, 1980). Immunohistochemical examination reveals that MA reduces TH-IR in the striatum and other dopaminergic terminal fields in the forebrain (Hess et al, 1990;Pu and Vorhees, 1993;Pu et al, 1994;Trulson et al, 1985). Furthermore, astrogliosis and argyrophilia, indices of neuronal damage, are present in areas corresponding to the loss of TH-IR after MA treatment, thereby supporting the conclusion that MA injures dopaminergic terminals (Bowyer et al, 1994;Hess et al, 1990;Miller and O'Callaghan, 1994;O'Callaghan and Miller, 1994;Pu and Vorhees, 1993;Pu et al, 1994;Ricaurte et al, 1982).…”

Section: Introductionmentioning

confidence: 95%

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Methamphetamine selectively damages dopaminergic innervation to the nucleus accumbens core while sparing the shell

Broening

Vorhees

1997

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Dopaminergic innervation to the nucleus accumbens was investigated following a neurotoxic regimen of methamphetamine (MA) treatment. Four 10 mg/kg doses of MA were administered s.c. to male Sprague-Dawley rats with a 2 h interval between doses. Rectal temperatures were monitored for the induction of MA-induced hyperthermia. Three days or 2 weeks after MA treatment the animals were sacrificed by transcardial perfusion and processed for tyrosine hydroxylase (TH-IR) and glial fibrillary acidic protein immunoreactivity (GFAP-IR). MA treatment produced a severe loss of TH-IR throughout the striatum, including the nucleus accumbens. However, within the nucleus accumbens, there was substantial sparing of TH-IR in the shell, while in the core immunoreactivity was almost entirely lost. Furthermore, astrogliosis, as demonstrated by GFAP-IR, was prevalent in the core but present only in sparse patches in the medial and lateral shell. Thus, dopaminergic innervation to the nucleus accumbens core undergoes degeneration following MA treatment, while innervation to the shell is resistant to the neurodegenerative effects of MA.

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Section: Introductionmentioning

confidence: 84%

Section: Introductionmentioning

confidence: 95%

Methamphetamine selectively damages dopaminergic innervation to the nucleus accumbens core while sparing the shell

Broening

Vorhees

1997

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“…In rodents, methamphetamine administration has been shown to increase glial cells (Hess et al 1990;Pu and Vorhees 1993), and the increased levels of Cho are found in glial cells (Urenjak et al 1993). Therefore, the decrease in CrϩPCr/Cho could be accounted by the elevated Cho level in methamphetamine users.…”

Section: Discussionmentioning

confidence: 99%

Metabolite Alterations in Basal Ganglia Associated with Methamphetamine-related Psychiatric Symptoms A Proton MRS Study

Sekine

Minabe

Kawai

et al. 2002

Neuropsychopharmacology

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Following the chronic use of methamphetamine, some individuals experience psychosis and anxiety. One reason may be the persistence of metabolite abnormalities in the brain of currently abstinent former methamphetamine users.In this study, N-acetylaspartate (NAA), creatine plus phosphocreatine (Cr ϩ PCr), and choline-containing compound (Cho) levels were measured in the left and right basal ganglia using proton magnetic resonance spectroscopy (MRS) The number of abusers of the highly addictive drug methamphetamine has risen substantially worldwide and this has raised important concerns (Woolverton et al. 1984;Baberg et al. 1996;Shaw 1999). For example, chronic methamphetamine users show psychosis and anxiety following intoxication and withdrawal (Seivewright 2000). In addition, in some individuals, these psychiatric states may be present for months or even years after cessation of methamphetamine use (Sato et al. 1992;Iwanami et al. 1994;Buffenstein et al. 1999;Iyo et al. 1999). Although there are growing clinical observations on the neurotoxicology of chronic methamphetamine use, the mechanism by which the residual psychiatric problems arise from chronic methamphetamine NO . 3 use remains unknown. In rodents and baboons, methamphetamine has been shown to be toxic to dopaminergic and serotonergic neurons (Nakayama et al. 1993;Villemagne et al. 1998;Kokoshka et al. 1998). These neurotoxic effects include decreased concentrations of dopamine and serotonin in the brain and a reduction of dopamine and serotonin transporters, as well as loss of ATP and mitochondrial dysfunction in dopaminergic neurons (Chan et al. 1994;Burrows et al. 2000;Lotharius and O'Malley 2001). Human positron emission tomography (PET) studies have reported a significant reduction of dopamine transporter density in methamphetamine users Volkow et al. 2001), and that the reduction observed in methamphetamine users is associated with psychomotor impairment (Volkow et al. 2001). Recently, we have also found that the dopamine transporter density in methamphetamine users is inversely related to the length of methamphetamine use and the magnitude of psychiatric symptoms, including psychotic symptoms (Sekine et al. 2001).In vivo proton magnetic resonance spectroscopy ( 1 H MRS) and its variant 1 H MRS techniques provide insight into the metabolism of several endogenous brain chemicals (Miller 1991;Jackson 1992). A recent 1 H MRS study showed evidence for long-term metabolite alterations in currently abstinent former methamphetamine users, that is, reduced concentration of both N-acetylaspartate (NAA) and creatine plus phosphocreatine (Cr ϩ PCr) in the right basal ganglia (Ernst et al. 2000). However, it is unclear whether these abnormalities detected by 1 H MRS are related to psychiatric symptoms that are frequently observed in abstinent methamphetamine users.In this study, we investigated changes of the chemistry in the basal ganglia of abstinent methamphetamine users by 1 H MRS, and examined any relationship between the changes and clinical cha...

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“…In animal studies, METH administration indeed has been associated with reduced glial glutamate uptake and / or recycling (Yamamoto and Bankson, 2005). Additionally, METH causes activation of glial cells (Hess et al, 1990;Pu and Vorhees, 1993), specifically microglia (Asanuma et al, 2003;Escubedo et al, 1998), which in turn may lead to inhibition of glutamate uptake (Zou and Crews, 2005) and glutamine synthesis (Muscoli et al, 2005). Inhibition of glial glutamate recycling also might increase extracellular glutamate and therefore lead to excitotoxicity.…”

Section: Discussionmentioning

confidence: 99%

Adaptation of Brain Glutamate Plus Glutamine during Abstinence from Chronic Methamphetamine Use

Ernst

Chang

2008

J Neuroimmune Pharmacol

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Methamphetamine (METH) is a stimulant drug that is toxic primarily to dopaminergic and serotonergic neurons, and may lead to inflammatory changes in the brain. Additionally, the glutamatergic system is altered following METH exposure. Therefore, concentrations of brain glutamate+glutamine (GLX) were assessed during abstinence from chronic METH abuse. 25 subjects with a history of METH-dependence (age 31.8 ± 7.4 years, 14 females and 11 males) and 28 control subjects without a history of drug abuse (age 32.6 ± 8.8 years, 14 females) were enrolled. Twelve of the METH subjects were followed and rescanned 5-months later. METH users had used the drug 5.9 ± 1.7 times / week, for 109 ± 69 months, and had been abstinent for 2.1 ± 3.0 months. GLX was measured in the basal ganglia and frontal gray and white matter, using proton magnetic resonance spectroscopy. While overall GLX concentrations at baseline were similar between METH and control subjects, METH users with ≤ 1 month of abstinence showed reduced frontal gray matter GLX (p=0.01). Time of abstinence correlated positively with GLX in frontal gray (p<0.0001) and white matter (p=0.03). After 5-months, changes in frontal gray matter GLX showed a trend to correlate inversely with duration of abstinence (p=0.07). Subjects with craving symptoms had lower frontal gray matter GLX than those without craving (−8%, p=0.05). These findings suggest dynamic abnormalities in brain GLX in recently abstinent methamphetamine users, with a depletion of the glutamatergic system in METH users within the first two months of abstinence, and some normalization during prolonged abstinence. Since craving may contribute to relapse, medications that normalize GLX may minimize craving in METH users.

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Acute neuropathological changes in the caudate nucleus caused by MPTP and methamphetamine: Immunohistochemical studies

Cited by 70 publications

References 9 publications

Methamphetamine selectively damages dopaminergic innervation to the nucleus accumbens core while sparing the shell

Methamphetamine selectively damages dopaminergic innervation to the nucleus accumbens core while sparing the shell

Metabolite Alterations in Basal Ganglia Associated with Methamphetamine-related Psychiatric Symptoms A Proton MRS Study

Adaptation of Brain Glutamate Plus Glutamine during Abstinence from Chronic Methamphetamine Use

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