Long-Term Monoamine Depletion, Differential Recovery, and Subtle Behavioral Impairment Following Methamphetamine-Induced Neurotoxicity

Friedman, Seth D.; Castañeda, Edward; Hodge, Gordon K.

doi:10.1016/s0091-3057(98)00066-5

Cited by 132 publications

(132 citation statements)

References 33 publications

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“…In contrast to previously published observations using the acute toxic dosing model (i.e., four injections of METH every 2 h; Daberkow et al, 2005;Eyerman and Yamamoto, 2005;Friedman et al, 1998;Ricaurte et al 1982;Straiko et al, 2007;Wallace et al, 2001), METH administration to rats not exposed to CUS did not produce depletions in 5-HT tissue content (Fig. 3B).…”

Section: Discussioncontrasting

confidence: 99%

“…The neurotoxic effects are evidenced by long-term depletions in striatal dopamine (DA) and serotonin (5-HT) concentrations, and their uptake sites (Friedman et al, 1998;Ricaurte et al, 1982;Wagner et al, 1980), decreases in tryptophan and tyrosine hydroxylase activity (Bakhit et al, 1981), and cell loss (Deng et al, 2007;Sonsalla et al, 1996;Thiriet et al, 2005;Yu et al, 2004;Zhu et al, 2006). In addition to the hypotheses of oxidative stress and apoptosis as mechanisms of METH-induced neurotoxicity (for review, see Davidson et al, 2001;Kita et al, 2003;Quinton and Yamamoto, 2006), increases in the extracellular concentrations of glutamate (GLU) have been also suggested to play an important role (Abekawa et al, 1994;Nash and Yamamoto, 1992;Sonsalla et al, 1989;Stephans and Yamamoto, 1994).…”

Section: Introductionmentioning

confidence: 99%

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Chronic stress enhances methamphetamine‐induced extracellular glutamate and excitotoxicity in the rat striatum

Tata

Yamamoto

2008

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Striking parallels exist between the neurochemical and toxic effects of stress and methamphetamine. Despite these similarities, no studies have examined how stress may promote the toxic effects of methamphetamine (METH). The current study tested the hypothesis that chronic stress enhances METH toxicity by augmenting glutamate (GLU) release and excitotoxicity in response to METH administration. Adult male Sprague-Dawley rats were exposed to 10 days of unpredictable stress and then received either saline or METH (7.5 mg/kg, i.p., once every 2 h × four injections). Prior exposure to unpredictable stress acutely enhanced the striatal extracellular GLU concentrations in response to METH, and eventually caused proteolysis of the cytoskeleton protein spectrin. Administration of the corticosterone synthesis inhibitor, metyrapone (25 mg/kg, i.p., prior to each stressor), during unpredictable stress attenuated the enhanced striatal GLU release in response to METH, blocked spectrin proteolysis, and attenuated METH-associated toxicity measured by long-term depletions in the dopamine and serotonin tissue content as well as depletions in dopamine and serotonin transporter immunoreactivity of the striatum. In summary, prior exposure to unpredictable stress enhances METH-induced elevations of GLU in the striatum, resulting in long-term excitotoxic damage and an augmentation of damage to dopamine and serotonin terminals. These studies provide a neurochemical basis for how stress contributes to the deleterious effects of METH abuse.

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Section: Discussioncontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Chronic stress enhances methamphetamine‐induced extracellular glutamate and excitotoxicity in the rat striatum

Tata

Yamamoto

2008

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“…In sufficient doses, mAMPH causes long-term damage to DA terminals in the striatum and to forebrain 5-HT terminals, as evidence by long-term depletions in these two neurotransmitters, their synthetic enzymes, metabolites, and plasma membrane transporters (Koda and Gibb, 1973;Hotchkiss and Gibb, 1980;Schmidt et al, 1985;Wagner et al, 1979;Ricaurte et al, 1982;Axt and Molliver, 1991;Friedman et al, 1998;Chapman et al, 2001). The mAMPH-induced depletions of DA reverse with a very slow time course (Cass and Manning, 1999).…”

Section: Discussionmentioning

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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“…While it might be suspected that rats exposed to doses of ( + )-methamphetamine that produce seizures and neurotoxicity would have nonspecific behavioral alterations, the contrary is more apparent. For example, novel object recognition is impaired in animals treated with ( + )-methamphetamine; however, novel place recognition and spatial learning and memory are intact (Belcher et al, 2005;Bisagno et al, 2002;Friedman et al, 1998;Schroder et al, 2003). It should be noted that Friedman et al (1998) showed that animals treated with ( + )-methamphetamine had a small deficit in latency to the platform in the MWM, but this was only apparent on one of the 5 days tested and no differences were noted in the probe phase.…”

Section: Effects Of 5-meo-diptmentioning

confidence: 99%

“…For example, novel object recognition is impaired in animals treated with ( + )-methamphetamine; however, novel place recognition and spatial learning and memory are intact (Belcher et al, 2005;Bisagno et al, 2002;Friedman et al, 1998;Schroder et al, 2003). It should be noted that Friedman et al (1998) showed that animals treated with ( + )-methamphetamine had a small deficit in latency to the platform in the MWM, but this was only apparent on one of the 5 days tested and no differences were noted in the probe phase. One residual effect that neurotoxic doses of ( + )-methamphetamine administration in adult animals Effects of 5-MEO-DIPT MT Williams et al does seem to produce reliably is a reduction in locomotor behavior, but this is likely the result of the reductions in dopamine produced by ( + )-methamphetamine (Wallace et al, 1999).…”

Section: Effects Of 5-meo-diptmentioning

confidence: 99%

Alterations in Body Temperature, Corticosterone, and Behavior Following the Administration of 5-Methoxy-Diisopropyltryptamine (‘Foxy’) to Adult Rats: a New Drug of Abuse

Williams

Herring

Schaefer

et al. 2006

Neuropsychopharmacol

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Many drugs are used or abused in social contexts without understanding the ramifications of their use. In this study, we examined the effects of a newly popular drug, 5-methoxy-diisopropyltryptamine (5-MEO-DIPT; 'foxy' or 'foxy-methoxy'). Two experiments were performed. In the first, 5-MEO-DIPT (0, 10, or 20 mg/kg) was administered to rats four times on a single day and animals were examined 3 days later. The animals that received 5-MEO-DIPT demonstrated hypothermia during the period of drug administration and delayed mild hyperthermic rebound for at least 48 h. Corticosterone levels in plasma were elevated in a dose-dependent manner compared to saline-treated animals with minor changes in 5-HT turnover and no changes in monoamine levels. In experiment 2, rats were examined in behavioral tasks following either 0 or 20 mg/kg of 5-MEO-DIPT. The animals treated with 5-MEO-DIPT showed hypoactivity and an attenuated response to ( + )-methamphetamine-induced stimulation (1 mg/kg). In a test of path integration (Cincinnati water maze), 5-MEO-DIPT-treated animals displayed deficits in performance compared to the saline-treated animals. No differences were noted in the ability of the animals to perform in the Morris water maze or on tests of novel object or place recognition. The data demonstrate that 5-MEO-DIPT alters the ability of an animal to perform certain cognitive tasks, while leaving others intact and disrupts the endocrine system. 5-MEO-DIPT may have the potential to induce untoward effects in humans.

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Long-Term Monoamine Depletion, Differential Recovery, and Subtle Behavioral Impairment Following Methamphetamine-Induced Neurotoxicity

Cited by 132 publications

References 33 publications

Chronic stress enhances methamphetamine‐induced extracellular glutamate and excitotoxicity in the rat striatum

Chronic stress enhances methamphetamine‐induced extracellular glutamate and excitotoxicity in the rat striatum

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

Alterations in Body Temperature, Corticosterone, and Behavior Following the Administration of 5-Methoxy-Diisopropyltryptamine (‘Foxy’) to Adult Rats: a New Drug of Abuse

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