Long-term effects of repeated methylamphetamine administration on dopamine and serotonin neurons in the rat brain: A regional study

Ricaurte, George A.; Schuster, Charles R.; Seiden, Lewis S.

doi:10.1016/0006-8993(80)90952-x

Cited by 464 publications

(255 citation statements)

References 22 publications

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“…In both mice and rats, acute repeated injections of METH produce long-lasting decreases in DA levels [145, 149-153], and long-term reductions in several DA markers, such as TH [144, 154, 155], DAT [152, 156, 157], and VMAT-2 [155, 157-159] within the striatum. Morphological studies demonstrate that the persistent loss of integrity of DA biochemical markers is due to the degeneration of DA axon terminals [145-149].…”

Section: Methamphetamine-induced Dopaminergic Toxicitymentioning

confidence: 99%

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The Effects of Locus Coeruleus and Norepinephrine in Methamphetamine Toxicity

Ferrucci

Giorgi

Bartalucci

et al. 2013

Current Neuropharmacology

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The activity of locus coeruleus (LC) neurons has been extensively investigated in a variety of behavioural states. In fact this norepinephrine (NE)-containing nucleus modulates many physiological and pathological conditions including the sleep-waking cycle, movement disorders, mood alterations, convulsive seizures, and the effects of drugs such as psychostimulants and opioids. This review focuses on the modulation exerted by central NE pathways on the behavioural and neurotoxic effects produced by the psychostimulant methamphetamine, essentially the modulation of the activity of mesencephalic dopamine (DA) neurons. In fact, although NE in itself mediates some behavioural effects induced by methamphetamine, NE modulation of DA release is pivotal for methamphetamine-induced behavioural states and neurotoxicity. These interactions are discussed on the basis of the state of the art of the functional neuroanatomy of central NE- and DA systems. Emphasis is given to those brain sites possessing a remarkable overlapping of both neurotransmitters.

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Section: Methamphetamine-induced Dopaminergic Toxicitymentioning

confidence: 99%

“…Morphological studies demonstrate that the persistent loss of integrity of DA biochemical markers is due to the degeneration of DA axon terminals [145-149]. …”

Section: Methamphetamine-induced Dopaminergic Toxicitymentioning

confidence: 99%

The Effects of Locus Coeruleus and Norepinephrine in Methamphetamine Toxicity

Ferrucci

Giorgi

Bartalucci

et al. 2013

Current Neuropharmacology

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“…Repeated exposure to moderate-to-high doses of methamphetamine (mAMPH) produces long-term damage to presynaptic dopaminergic and serotonergic terminals in rodents (Wagner et al, 1980;Ricaurte et al, 1980) and in humans (Wilson et al, 1996;McCann et al, 1998). Additionally, mAMPH produces degeneration of nonmonoaminergic cell bodies in somatosensory cortex (Commins and Seiden, 1986;O'Dell and Marshall, 2000).…”

Section: Introductionmentioning

confidence: 99%

Impaired Object Recognition Memory Following Methamphetamine, but not p-Chloroamphetamine- or d-Amphetamine-Induced Neurotoxicity

Belcher

O’Dell

Marshall

2005

Neuropsychopharmacol

106

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Repeated moderate doses of methamphetamine (mAMPH) damage forebrain monoaminergic terminals and nonmonoaminergic cells in somatosensory cortex, and impair performance in a novelty preference task of object recognition (OR). This study aimed to determine whether the memory deficit seen after a neurotoxic mAMPH regimen results from damage to dopamine (DA) and/or serotonin (5-HT) terminals. Animals were given a neurotoxic regimen of mAMPH, p-chloroamphetamine (PCA, preferentially damages 5-HT terminals), damphetamine (d-AMPH, preferentially damages DA terminals), or saline. After 1 week, animals were trained and tested for OR memory. Rats treated with mAMPH showed no recognition memory during the short-term memory (STM) test, whereas both PCA-and d-AMPH-treated rats showed OR STM scores comparable to controls. After behavioral testing, the specificity of monoaminergic lesions was determined by postmortem [ 125 I]RTI-55 binding to dopamine (DAT) and serotonin (SERT) transporter proteins. Tissue from a separate group of animals killed 3 days after drug treatment was processed for Fluoro-Jade (F-J) fluorescence histochemistry to detect damaged cortical neurons. mAMPH-treated rats showed reductions in striatal DAT and hippocampal (HC) and perirhinal (pRh) SERT, as well as degeneration of neurons in primary somatosensory cortex. In PCA-treated rats, HC and pRh SERT were substantially depleted, but striatal DAT and cortical neuron survival were unaffected. By contrast, d-AMPH-treated animals showed marked depletions in striatal DAT and cortical neurodegeneration, but HC and pRh SERT were unaffected. This pattern of results indicates that no single feature of mAMPH-induced neurotoxicity is sufficient to produce the OR impairments seen after mAMPH treatment.

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“…There is evidence that high or repeated doses of d-N, a-dimethylphenylethylamine (methamphetamine, Meth) induce long-term deficits in basal ganglia neurotransmission, both in rodents and humans, mainly affecting the monoamines dopamine (DA; Fibiger and McGeer 1971;Seiden et al 1976;Ricaurte et al 1980;Marek et al 1990) and serotonin (5-hydroxytryptamine, 5-HT; Ricaurte et al 1980;Haughey et al 2000), but also amino acids (Sonsalla et al 1989;Nash and Yamamoto 1992;Marshall et al 1993;Abekawa et al 1994;Meshul 1997, 1999) and neuropeptides (Castel et al 1994;Smith and McGinty 1994;McGinty 1995, 1996;Alburges et al 2001aAlburges et al , 2001b. The long-term effects of Meth are largely restricted to the nigrostriatal DA system (Ricaurte et al 1980;Marshall and Navarrete 1990;Marshall et al 1993;Burrows and Meshul 1997).…”

mentioning

confidence: 99%

“…The long-term effects of Meth are largely restricted to the nigrostriatal DA system (Ricaurte et al 1980;Marshall and Navarrete 1990;Marshall et al 1993;Burrows and Meshul 1997). Short-and long-term effects have also been described in limbic and cortical systems, but these systems are less and differently affected than the neostriatum (Axt and Molliver 1991;Brunswick et al 1992;Eisch et al 1996).…”

mentioning

confidence: 99%

Effect of single and repeated methamphetamine treatment on neurotransmitter release in substantia nigra and neostriatum of the rat

Bustamante

You²,

Castel

et al. 2002

Journal of Neurochemistry

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The main purpose of this study was to characterize the initial neurotransmission cascade elicited by methamphetamine, analysing simultaneously with in vivo microdialysis monoamine, amino acid and neuropeptide release in substantia nigra and neostriatum of the rat. The main effect of a single systemic dose of methamphetamine (15 mg/kg, subcutaneously) was an increase in dopamine levels, both in substantia nigra ( 10-fold) and neostriatum ( 40-fold), accompanied by a significant, but lesser, increase in dynorphin B ( two-fold, in both regions), and a decrease in monoamine metabolites. A similar effect was also observed after local administration of methamphetamine (100 lM) via the microdialysis probes, but restricted to the treated region. In other experiments, rats were repeatedly treated with methamphetamine or saline, with the last dose administered 12 h before microdialysis. Dopamine K + -stimulated release was decreased following repeated methamphetamine administration compared with that following saline, both in the substantia nigra (by 65%) and neostriatum (by 20%). In contrast, the effect of K + -depolarization on glutamate, aspartate and GABA levels was increased following repeated administration of methamphetamine. In conclusion, apart from an impairment of monoamine neurotransmission, repeated methamphetamine produces changes in amino acid homeostasis, probably leading to NMDA-receptor overstimulation.

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Long-term effects of repeated methylamphetamine administration on dopamine and serotonin neurons in the rat brain: A regional study

Cited by 464 publications

References 22 publications

The Effects of Locus Coeruleus and Norepinephrine in Methamphetamine Toxicity

The Effects of Locus Coeruleus and Norepinephrine in Methamphetamine Toxicity

Impaired Object Recognition Memory Following Methamphetamine, but not p-Chloroamphetamine- or d-Amphetamine-Induced Neurotoxicity

Effect of single and repeated methamphetamine treatment on neurotransmitter release in substantia nigra and neostriatum of the rat

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