Self-injurious behavior produced in rats by daily caffeine and continuous amphetamine

Mueller, Kathyrne; Saboda, Stephanie; Palmour, Roberta M.; Nyhan, William L.

doi:10.1016/0091-3057(82)90332-x

Cited by 65 publications

(19 citation statements)

References 12 publications

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“…Finally, stimulantinduced stereotypic and appearance self-injurious behavior is dependent on changes in dopaminergic and serotonergic activity in the striatum (Allen & Davis, 1999;Halladay et al, 2003;Shishido, Watanabe, Kato, Horikoshi, & Niwa, 2000). The induction of self-injurious behavior following high doses of psychomotor stimulants such as amphetamine has been shown to mimic the behaviors seen in Lesch-Nyhan Syndrome and autism-like stereotyped behaviors (Jinnah, Gage, & Friedmann, 1990;Mueller, Saboda, Palmour, & Nyhan, 1982). While VPA-treated animals did not show increased behavioral sensitivity to amphetamine as adults; both groups demonstrated a high rate of self-injurious behavior (~69%) and stereotypy (100%) following amphetamine treatment.…”

Section: Discussionmentioning

confidence: 97%

A New Neurobehavioral Model of Autism in Mice: Pre- and Postnatal Exposure to Sodium Valproate

Wagner

Reuhl

Cheh

et al. 2006

J Autism Dev Disord

241

173

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Autism symptoms, including impairments in language development, social interactions, and motor skills, have been difficult to model in rodents. Since children exposed in utero to sodium valproate (VPA) demonstrate behavioral and neuroanatomical abnormalities similar to those seen in autism, the neurodevelopmental effects of this antiepileptic agent were examined in mice following its pre- or postnatal administration. Exposed pups were evaluated in a battery of neurodevelopmental procedures designed to assess VPA-induced retardation (wherein a behavior fails to mature on schedule), regression (wherein a behavior does mature on time but then deteriorates), or intrusions (wherein normal behaviors are overshadowed by stereotypic or self-injurious behaviors). The resulting observations were interpreted in the context of this new strategy to model autism.

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Section: Discussionmentioning

confidence: 97%

A New Neurobehavioral Model of Autism in Mice: Pre- and Postnatal Exposure to Sodium Valproate

Wagner

Reuhl

Cheh

et al. 2006

J Autism Dev Disord

241

173

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“…In both rodents and primates, SB and SIB have been shown to occur after systemic administration of high doses of drugs that stimulate dopamine release such as amphetamine, methamphetamine, or pemoline [19][20][21][22][23][24]. Alternatively, these behaviors can be provoked by chronic administration of lower doses of these drugs, or chronic administration of the dopamine uptake inhibitor, GBR 12909 [25].…”

Section: Introductionmentioning

confidence: 99%

Self-Biting Induced by Activation of L-Type Calcium Channels in Mice: Dopaminergic Influences

Kasim¹,

Jinnah²

2003

Dev Neurosci

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The L-type calcium channel activator ±Bay K 8644 induces repetitive self-biting and self-injurious behavior in young mice. Since dopaminergic systems have been implicated in prior studies of these behaviors in both humans and animals, the present experiments were designed to test whether drugs influencing the dopaminergic systems could modify the behavioral responses to ±Bay K 8644. The ability of ±Bay K 8644 to provoke self-biting and self-injurious behavior was increased by amphetamine and GBR 12909, drugs that augment synaptic dopaminergic concentrations by blocking the reuptake and/or stimulating the release of dopamine. Conversely, self-biting and self-injurious behavior were decreased by tetrabenazine or reserpine, two drugs that deplete vesicular stores of dopamine. These results suggest that dopaminergic systems may play a role in the ability of ±Bay K 8644 to provoke self-biting and self-injurious behavior.

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“…SB and SIB also occur in rodents after stimulation of dopamine receptors if brain dopamine neurons are destroyed during early development (9). Clonidine (10, 11) and the methylxanthines caffeine and theophylline can also provoke these behaviors at high doses, though the mechanism by which they do so remains unclear (6,12,13).To date, calcium channels have received little attention as mediators or potential therapeutic targets for SB or SIB. Calcium channels are expressed throughout the nervous system and in other organs, where they play an important role in stimulusresponse coupling.…”

mentioning

confidence: 99%

mentioning

confidence: 99%

“…The neurobiology of these peculiar behaviors is incompletely understood, and several animal models have been developed to study pathophysiology and potential treatments (3). For example, SB and SIB may be provoked in rodents after high doses or chronic administration of drugs that promote dopamine release such as amphetamine, GBR-12909, and pemoline (4)(5)(6)(7)(8). SB and SIB also occur in rodents after stimulation of dopamine receptors if brain dopamine neurons are destroyed during early development (9).…”

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confidence: 99%

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Calcium channel activation and self-biting in mice

Jinnah

Yitta

Drew

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

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The L type calcium channel agonist (؎)Bay K 8644 has been reported to cause characteristic motor abnormalities in adult mice. The current study shows that administration of this drug can also cause the unusual phenomenon of self-injurious biting, particularly when given to young mice. Self-biting is provoked by injecting small quantities of (؎)Bay K 8644 directly into the lateral ventricle of the brain, suggesting a central effect of the drug. Similar behaviors can be provoked by administration of another L type calcium channel agonist, FPL 64176. The self-biting provoked by (؎)Bay K 8644 can be inhibited by pretreating the mice with dihydropyridine L type calcium channel antagonists such as nifedipine, nimodipine, or nitrendipine. However, self-biting is not inhibited by nondihydropyridine antagonists including diltiazem, flunarizine, or verapamil. The known actions of (؎)Bay K 8644 as an L type calcium channel agonist, the reproduction of similar behavior with another L type calcium channel agonist, and the protection afforded by certain L type calcium channel antagonists implicate calcium channels in the mediation of the self-biting behavior. This phenomenon provides a model for studying the neurobiology of this unusual behavior. S elf-biting (SB) and other self-injurious behavior (SIB) may occur in a number of different human disorders (1, 2). They are most commonly seen in developmentally disabled individuals with severe mental retardation or autism. These behaviors also occur in specific neurogenetic diseases such as Lesch-Nyhan syndrome, Cornelia de Lange syndrome, Rett's syndrome, Tourette's syndrome, and neuroacanthocytosis. The neurobiology of these peculiar behaviors is incompletely understood, and several animal models have been developed to study pathophysiology and potential treatments (3). For example, SB and SIB may be provoked in rodents after high doses or chronic administration of drugs that promote dopamine release such as amphetamine, GBR-12909, and pemoline (4-8). SB and SIB also occur in rodents after stimulation of dopamine receptors if brain dopamine neurons are destroyed during early development (9). Clonidine (10, 11) and the methylxanthines caffeine and theophylline can also provoke these behaviors at high doses, though the mechanism by which they do so remains unclear (6,12,13).To date, calcium channels have received little attention as mediators or potential therapeutic targets for SB or SIB. Calcium channels are expressed throughout the nervous system and in other organs, where they play an important role in stimulusresponse coupling. Several calcium channel subtypes are currently recognized by their different pharmacological and electrophysiological properties (14). The L type calcium channel is voltage-gated and allows a transient influx of calcium in response to cell membrane depolarization. Within the brain, these channels are expressed at particularly high levels in the striatum, cortex, and hippocampus (15-18).(Ϯ)Bay K 8644 functions as an L type calcium channel activator tha...

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Self-injurious behavior produced in rats by daily caffeine and continuous amphetamine

Cited by 65 publications

References 12 publications

A New Neurobehavioral Model of Autism in Mice: Pre- and Postnatal Exposure to Sodium Valproate

A New Neurobehavioral Model of Autism in Mice: Pre- and Postnatal Exposure to Sodium Valproate

Self-Biting Induced by Activation of L-Type Calcium Channels in Mice: Dopaminergic Influences

Calcium channel activation and self-biting in mice

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