Neuronal degeneration in rat forebrain resulting from d-amphetamine-induced convulsions is dependent on seizure severity and age

Bowyer, John F.; Peterson, Steven L.; Rountree, Robert; Tor-Agbidye, John; Wang, Guang Jian

doi:10.1016/s0006-8993(98)00846-4

Cited by 66 publications

(64 citation statements)

References 30 publications

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“…To this end, neurotoxicity to either dopaminergic or serotonergic terminals was induced using two amphetamine analogues with more specific profiles of damage, p-chloroamphetamine (PCA) and d-amphetamine (d-AMPH). In high doses, d-AMPH damages dopaminergic terminals in the striatum and cell bodies in parietal cortex (Bowyer et al, 1998), while largely sparing serotonin (5-HT) terminals. By contrast, PCA causes long-term depletions in markers of serotonergic activity (Pletscher et al, 1963;Fuller et al, 1965;Sanders-Bush et al, 1972) and structural alterations in serotonergic neurons (Harvey et al, 1975) while largely sparing dopaminergic terminals.…”

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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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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“…These initial studies (24) (3,8,25), d-Fenfluramine (28), and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (12 Figure 1F). These animals also had degenerating noncatecholaminergic neurons within the thalamus.…”

Section: Introductionmentioning

confidence: 99%

Fluoro-Jade: Novel Fluorochromes for Detecting Toxicant-Induced Neuronal Degeneration

2000

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“…Animal models of methamphetamine use have shown a marked neurodegeneration in the limbic system, including hippocampus, in association with the limbic-originated seizures [18]. The breakdown of the blood-brain-barrier and the activation of glial cells by the released neurotransmitters are some of the hypotheses that were proposed for the degeneration [19].…”

Section: Discussionmentioning

confidence: 99%

Anterograde Amnesia after Methamphetamine Lab Exposure

Sanders¹

2016

JNSK

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Anterograde Amnesia after Methamphetamine Lab Exposure Background: Some known toxic exposures can produce detrimental cognitive deficits. Yet, very few substances have been linked to the development of anterograde amnesia. Here, we report a novel case of a middle-age man who presented with a profound and apparently permanent anterograde amnesia following his exposure to a clandestine methamphetamine laboratory. Case Report: A 47 year-old, righthanded man presented in 2013 with a history of memory loss and seizures since 2001, when he was exposed during his work as a firefighter to the fumes of spilled material intended to synthesize methamphetamine in a clandestine laboratory. Following the exposure, he suffered a major and immediate impairment of multiple cognitive domains, with anterograde memory being most impaired. A formal neurobehavioral status examination NBSE showed a profound impairment in episodic/verbal memory and lesser impairment of executive function. The patient clinical course has to date been stable without further deterioration or improvement. Discussion: This case highlights a clear temporal relationship of methamphetamine laboratory exposure and the development of deficits in memory and executive dysfunction suggestive of involvement of both prefrontalstriatal circuits and medial temporal areas. This is in concordance with prior animal studies, and warrants further investigation in the future.

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Neuronal degeneration in rat forebrain resulting from d-amphetamine-induced convulsions is dependent on seizure severity and age

Cited by 66 publications

References 30 publications

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

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

Fluoro-Jade: Novel Fluorochromes for Detecting Toxicant-Induced Neuronal Degeneration

Anterograde Amnesia after Methamphetamine Lab Exposure

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