Influence of methamphetamine and neuroleptic drugs on tyrosine hydroxylase activity

Buening, Mildred K.; Gibb, James W.

doi:10.1016/0014-2999(74)90070-3

Cited by 74 publications

(26 citation statements)

References 11 publications

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“…Metabolites of dopamine generate toxic free radicals, which contribute to this damage (Cadet and Brannock, 1998). The connection between METH-induced dopamine terminal toxicity and elevated dopamine levels was established using pharmacological agents that blocked post-synaptic dopamine receptors or pre-synaptic dopamine transporters, such agents were found to protect from METH (Buening and Gibb, 1974;Gibb and Kogan, 1979;Hotchkiss and Gibb, 1980;Sonsalla et al, 1986;O'Dell et al, 1993;Xu et al, 2005). Microinjections of the dopamine agonist, SKF38393, administered centrally into the rat brain are toxic to striatal neurons (Kelley et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Methamphetamine-induced cell death: Selective vulnerability in neuronal subpopulations of the striatum in mice

2006

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Methamphetamine (METH) is an illicit and potent psychostimulant, which acts as an indirect dopamine agonist. In the striatum, METH has been shown to cause long lasting neurotoxic damage to dopaminergic nerve terminals and recently, the degeneration and death of striatal cells. The present study was undertaken to identify the type of striatal neurons that undergo apoptosis after METH. Male mice received a single high dose of METH (30 mg/kg, i.p.) and were killed 24 h later. To demonstrate that METH induces apoptosis in neurons, we combined terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining with immunohistofluorescence for the neuronal marker neuron-specific nuclear protein (NeuN). Staining for TUNEL and NeuN was colocalized throughout the striatum. METH induces apoptosis in approximately 25% of striatal neurons. Cell counts of TUNEL-positive neurons in the dorsomedial, ventromedial, dorsolateral and ventrolateral quadrants of the striatum did not reveal anatomical preference. The type of striatal neuron undergoing cell death was determined by combining TUNEL with immunohistofluorescence for selective markers of striatal neurons: dopamine-and cAMP-regulated phosphoprotein, of apparent M r 32,000, parvalbumin, choline acetyltransferase and somatostatin (SST). METH induces apoptosis in approximately 21% of dopamine-and cAMP-regulated phosphoprotein, of apparent M r 32,000-positive neurons (projection neurons), 45% of GABA-parvalbumin-positive neurons in the dorsal striatum, and 29% of cholinergic neurons in the dorsal-medial striatum. In contrast, the SST-positive interneurons were refractory to METH-induced apoptosis. Finally, the amount of cell loss determined with Nissl staining correlated with the amount of TUNEL staining in the striatum of METH-treated animals. In conclusion, some of the striatal projection neurons and the GABAparvalbumin and cholinergic interneurons were removed by apoptosis in the aftermath of METH. This imbalance in the populations of striatal neurons may lead to functional abnormalities in the output and processing of neural information in this part of the brain. Keywords methamphetamine; apoptosis; striatum; projection neurons; interneurons Methamphetamine (METH) is a potent and addictive psychostimulant. The neurotoxic effects of this substituted amphetamine are associated with its ability to induce an overflow of dopamine in the synapse by displacing vesicular dopamine stores (Raiteri et al., 1979; Liang and Rutledge, 1982a,b;Schmidt et al., 1985;Sulzer et al., 1995). Displaced dopamine molecules and its metabolites can be readily oxidized to reactive quinones and semiquinones (Cadet and Brannock, 1998) and nitrogen radicals (Lipton and Rosenberg, 1994;Imam et al., 1999) that affect a wide range of modifications of proteins, sugars, and lipids. Augmented levels of dopamine in the synapse induced by METH have been shown in humans (Wilson et al., 1996;McCann et al., 1998), non-human primates (Seiden et al., 1976;Villemagne et al., 1998;Harvey e...

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Section: Discussionmentioning

confidence: 99%

Methamphetamine-induced cell death: Selective vulnerability in neuronal subpopulations of the striatum in mice

2006

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“…It is well established that high-dose administration of the amphetamine analog METH causes DA deficits persisting months and even years after drug treatment in rodents, nonhuman primates, and perhaps humans (Buening and Gibb, 1974;Seiden et al, 1976;Hotchkiss et al, 1979;Morgan and Gibb, 1980;Eisch et al, 1992;Wilson et al, 1996;Villemagne et al, 1998). In contrast, administration of the amphetamine analog MDMA is far less toxic to DA systems (Johnson et al, 1988;Insel et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

Methylenedioxymethamphetamine Decreases Plasmalemmal and Vesicular Dopamine Transport: Mechanisms and Implications for Neurotoxicity

Hansen¹,

Riddle²,

Sandoval³

et al. 2002

J Pharmacol Exp Ther

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Administration of a high-dose regimen of methamphetamine (METH) rapidly and profoundly decreases plasmalemmal and vesicular dopamine (DA) transport in the striatum, as assessed in synaptosomes and purified vesicles, respectively. To determine whether these responses were common to other amphetamines of abuse, effects of methylenedioxymethamphetamine (MDMA) on the plasmalemmal DA transporter (DAT) and vesicular monoamine transporter-2 (VMAT-2) were assessed. Similar to effects of METH reported previously, multiple high-dose MDMA administrations rapidly (within 1 h) decreased plasmalemmal DA uptake, as assessed ex vivo in synaptosomes prepared from treated rats. Unlike effects of multiple METH injections, this deficit was reversed completely 24 h after drug treatment. Also in contrast to effects of multiple METH injections, 1) MDMA caused little or no decrease in binding of the DAT ligand WIN35428, and 2) neither prevention of hyperthermia nor prior depletion of DA prevented the MDMA-induced reduction in plasmalemmal DA transport. However, a role for phosphorylation was suggested because pretreatment with protein kinase C inhibitors attenuated the deficit caused by MDMA in an in vitro model system. In addition to affecting DAT function, MDMA rapidly decreased vesicular DA transport as assessed in striatal vesicles prepared from treated rats. Unlike effects of multiple METH injections reported previously, this decrease partially recovered by 24 h after drug treatment. Taken together, these results reveal several differences between effects of MDMA and previously reported METH on DAT and VMAT-2; differences that may underlie the dissimilar neurotoxic profile of these agents.

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“…Nif, Nic and Flu, on either the PCP-or MAP-induced abnormal behaviors were investigated. It has been well documented that the relationship between the therapeutic index of neuroleptics, and the potency of inhibition on the MAP-or PCP-induced abnormal behaviors are closely parallel [18][19][20]. The decision was based on the fact that the functional mechanisms of MAP, especially on the striatal DA neuronal system, have been well documented [12].…”

Section: Discussionmentioning

confidence: 99%

Differentiation of the Inhibitory Effects of Calcium Antagonists on Abnormal Behaviors Induced by Methamphetamine or Phencyclidine

Hori¹,

Takeda²,

Tsuji³

et al. 1998

Pharmacology

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The abnormal behaviors induced by methamphetamine (MAP: 1 mg/kg) or phencyclidine (PCP: 10 mg/kg) were measured using behavioral analysis following the microinjection of one of three calcium (Ca) antagonists (nifedipine: Nif, nicardipine: Nic and flunarizine: Flu) into the rat caudate putamen or amygdala. The intraperitoneal administration of MAP or PCP induced abnormal behaviors in a time-dependent manner; the maximum locomotor activity was measured 30–45 min after the administration of MAP or PCP. This hyperactivity was sustained for more than 2 h. Following microinjection of these Ca antagonists into the caudate putamen, each showed a different pattern of inhibition on MAP- or PCP-induced abnormal behaviors. Nic and Flu were effective at reducing these abnormal behaviors, in contrast, Nif was ineffective. In particular, the inhibitory effect of Nic was stronger than that of Flu. Microinjection of these Ca antagonists into the amygdala did not show any reductive effect on the hyperactivity induced by MAP or PCP. These results demonstrate that these Ca antagonists have different pharmacological properties and that both L- and T-type Ca²⁺ channels modulate the dopamine release in the rat caudate putamen. These results further lead us to suggest the presence of a subtype of L-type Ca²⁺ channels in the caudate putamen.

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Influence of methamphetamine and neuroleptic drugs on tyrosine hydroxylase activity

Cited by 74 publications

References 11 publications

Methamphetamine-induced cell death: Selective vulnerability in neuronal subpopulations of the striatum in mice

Methamphetamine-induced cell death: Selective vulnerability in neuronal subpopulations of the striatum in mice

Methylenedioxymethamphetamine Decreases Plasmalemmal and Vesicular Dopamine Transport: Mechanisms and Implications for Neurotoxicity

Differentiation of the Inhibitory Effects of Calcium Antagonists on Abnormal Behaviors Induced by Methamphetamine or Phencyclidine

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