Effect of lithium and other drugs on the amphetamine chlordiazepoxide hyperactivity in mice

Poitou, P; Boulu, R; Bohuon, C

doi:10.1007/bf01924701

Cited by 31 publications

(11 citation statements)

References 21 publications

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“…The finding that the administration of L-DOPA completely counteracted the neuroleptic effect of lithium on avoidance behavior indicate a causal relationship between the behavioral and biochemical effect of acute lithium administration and give further support for the contention that lithium may act by interfering with central catecholaminergic neurotransmission. Moreover, like a-MT, lithium can suppress amphetamine-induced hyperactivity (Cox et al, 1971;Davies et aI., 1974;Poitou et al, 1975;Berggren et al, 1978), and we have recently found that this effect of lithium also can be counteracted by small doses of L-DOPA (Berggren et al, 1978). In addition we have previously reported that lithium, like e-MT, can potentiate the behavioral effect of haloperidol on food-reinforced lever-pressing behavior (Ahlenius and Engel, 1974) and thus in some cases lithium seems to have a behavioral profile similar to that of a-MT.…”

Section: Discussionmentioning

confidence: 98%

Effects of acute lithium administration on conditioned avoidance behavior and monoamine synthesis in rats

Berggren

Ahlénius

Engel

1980

J. Neural Transmission

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The effect of a single injection of various doses of lithium chloride was tested on conditioned avoidance behavior and on the accumulation of DOPA and 5-HTP after inhibition of aromatic amino acid decarboxylase. Lithium specifically suppressed conditioned avoidance behavior and reduced formation of DOPA, but not 5-HTP. The behavioral effect of lithium could be completely antagonized with additional L-DOPA treatment. The results indicate that lithium has a neuroleptlike effect on avoidance behavior, and it is suggested that some of the behavioral effects of lithium may be mediated via interference with central catecholaminergic mechanisms.

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Section: Discussionmentioning

confidence: 98%

Effects of acute lithium administration on conditioned avoidance behavior and monoamine synthesis in rats

Berggren

Ahlénius

Engel

1980

J. Neural Transmission

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“…The benzodiazepine derivative chlordiazepoxide (CDP), which has anxiolytic and sedative effects alone, has been used in combination with amphetamine as a rodent model of mania (Poitou et al, 1975, Arban et al, 2005). However, the most common behavioral output measure used is still locomotor activity, since amphetamine and chlordiazepoxide (AMP + CDP) treatment increases activity in both rats and mice.…”

Section: Pharmacological Models Of Maniamentioning

confidence: 99%

Animal models of bipolar mania: The past, present and future

2016

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Bipolar disorder (BD) is the sixth leading cause of disability in the world according to the World Health Organization and affects nearly 6 million (~2.5% of the population) adults in the United State alone each year. BD is primarily characterized by mood cycling of depressive (e.g., helplessness, reduced energy and activity, and anhedonia) and manic (e.g., increased energy and hyperactivity, reduced need for sleep, impulsivity, reduced anxiety and depression), episodes. The following review describes several animal models of bipolar mania with a focus on more recent findings using genetically modified mice, including several with the potential of investigating the mechanisms underlying ‘mood’ cycling (or behavioral switching in rodents). We discuss whether each of these models satisfy criteria of validity (i.e., face, predictive, and construct), while highlighting their strengths and limitations. Animal models are helping to address critical questions related to pathophysiology of bipolar mania, in an effort to more clearly define necessary targets of first-line medications, lithium and valproic acid, and to discover novel mechanisms with the hope of developing more effective therapeutics. Future studies will leverage new technologies and strategies for integrating animal and human data to reveal important insights into the etiology, pathophysiology, and treatment of BD.

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“…In rodents, a mixture of amphetamine and chlordiazepoxide reportedly increases exploratory behavior, and lithium has been reported to reverse this effect (Cox et al, 1971;Davies et al, 1974;Poitou et al, 1975;Murphy, 1977). To test the effect of chronic lithium treatment on exploratory behavior in the absence of other drugs, we assessed exploratory behavior in lithium-treated and control mice in a hole board apparatus, in which the number of holes explored in the floor of a chamber is recorded over 10 min (File and Wardill, 1975).…”

Section: Exploratory Behaviormentioning

confidence: 99%

“…Many of these studies have tested whether lithium modifies behaviors caused by other drugs. For example, amphetamine-chlordiazepoxide (Cox et al, 1971;Poitou et al, 1975;Murphy, 1977) or MAP kinase inhibitors (Einat et al, 2003) cause hyperactivity and increased exploration that is reduced in rodents pretreated with lithium. Furthermore, many previous studies have used acute dosing, although the beneficial effects of lithium in BPD are only observed after a lag of days to weeks and persist after treatment is withdrawn.…”

Section: Introductionmentioning

confidence: 99%

Glycogen Synthase Kinase-3β Haploinsufficiency Mimics the Behavioral and Molecular Effects of Lithium

O’Brien

Harper²,

Jové³

et al. 2004

J. Neurosci.

403

376

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Lithium is widely used to treat bipolar disorder, but its mechanism of action in this disorder is unknown. Several molecular targets of lithium have been identified, but these putative targets have not been shown to be responsible for the behavioral effects of lithium in vivo. A robust model for the effects of chronic lithium on behavior in mice would greatly facilitate the characterization of lithium action. We describe behaviors in mice that are robustly affected by chronic lithium. Remarkably, these lithium-sensitive behaviors are also observed in mice lacking one copy of the gene encoding glycogen synthase kinase-3␤ (Gsk-3␤), a well established direct target of lithium. In addition, chronic lithium induces molecular changes consistent with inhibition of GSK-3 within regions of the brain that are paralleled in Gsk-3␤ ϩ/Ϫ heterozygous mice. We also show that lithium therapy activates Wnt signaling in vivo, as measured by increased Wntdependent gene expression in the amygdala, hippocampus, and hypothalamus. These observations support a central role for GSK-3␤ in mediating behavioral responses to lithium.

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Effect of lithium and other drugs on the amphetamine chlordiazepoxide hyperactivity in mice

Cited by 31 publications

References 21 publications

Effects of acute lithium administration on conditioned avoidance behavior and monoamine synthesis in rats

Effects of acute lithium administration on conditioned avoidance behavior and monoamine synthesis in rats

Animal models of bipolar mania: The past, present and future

Glycogen Synthase Kinase-3β Haploinsufficiency Mimics the Behavioral and Molecular Effects of Lithium

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