Transcranial magnetic stimulation in an amphetamine hyperactivity model of mania

Shaldivin, A.; Kaptsan, Alexander; Belmaker, Robert H.; Einat, Haim; Grisaru, Nimrod

doi:10.1034/j.1399-5618.2001.030104.x

Cited by 23 publications

(9 citation statements)

References 18 publications

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“…Shaldivin et al [57] used an amphetamine-induced hyperactivity model of mania in rats, and found that once-daily TMS treatment for up to 7 days significantly reduced amphetamine-induced hyperactivity whereas twice-daily TMS over the same time period enhanced hyperactivity. Taken together, evidence for the use of TMS as a treatment for mania is disappointing.…”

Section: Tms In Maniamentioning

confidence: 99%

Transcranial Magnetic Stimulation in the Management of Mood Disorders

Allan

Herrmann²,

Ebmeier³

2011

Neuropsychobiology

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Background: Many trials of transcranial magnetic stimulation (TMS) have used small samples and, therefore, lack power. Here we present an up-to-date meta-analysis of TMS in the treatment of depression. Methods: We searched Medline and Embase from 1996 until 2008 for randomized sham-controlled trials, with patients and investigators blinded to treatment, and outcome measured using a version of the Hamilton Depression Rating Scale (or similar). We identified 1,789 studies. Thirty-one were suitable for inclusion, with a cumulative sample of 815 active and 716 sham TMS courses. Results: We found a moderately sized effect in favour of TMS [Random Effects Model Hedges’ g = 0.64, 95% confidence interval (95% CI) = 0.50–0.79]. The corresponding Pooled Peto Odds Ratio for treatment response (≤50% reduction in depression scores) was 4.1 (95% CI = 2.9–5.9). There was significant variability between study effect sizes. Meta-regressions with relevant study variables did not reveal any predictors of treatment efficacy. Nine studies included follow-up data with an average follow-up time of 4.3 weeks; there was no mean change in depression severity between the end of treatment and follow-up (Hedges’ g = –0.02, 95% CI = –0.22 to +0.18) and no heterogeneity in outcome. Discussion: TMS appears to be an effective treatment; however, at 4 weeks’ follow-up after TMS, there had been no further change in depression severity. Problems with finding a suitably blind and ineffective placebo condition may have confounded the published effect sizes. If the TMS effect is specific, only further large double-blind randomized controlled designs with systematic exploration of treatment and patient parameters will help to define optimum treatment indications and regimen.

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Section: Tms In Maniamentioning

confidence: 99%

Transcranial Magnetic Stimulation in the Management of Mood Disorders

Allan

Herrmann²,

Ebmeier³

2011

Neuropsychobiology

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“…One facet of mania that is heavily modeled is hyperactivity as currently most models of mania focus only on this component of the behavior (Decker et al 2000;Einat et al 2000;Post and Weiss 1989;Ralph-Williams et al 2003;Shaldivin et al 2001;Shaldubina et al 2002). The most commonly used model is psychostimulant-induced hyperactivity and whereas this model has partial validity it also has a lot of limitations (Einat et al in press).…”

Section: Psychostimulants-induced Hyperactivitymentioning

confidence: 99%

Establishment of a Battery of Simple Models for Facets of Bipolar Disorder: A Practical Approach to Achieve Increased Validity, Better Screening and Possible Insights into Endophenotypes of Disease

Einat

2006

Behav Genet

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The lack of appropriate animal models for bipolar disorder (BPD) hinders the translation of novel molecular and genetic findings into the development of new more efficient treatments. Attempts to develop a comprehensive model for BPD did not result in a practical and valid model and at present most studies utilize a limited number of models for specific components of the disorder. Whereas there is a higher availability of models for the depression pole of BPD, only a few models represent the manic pole with the most frequently used being psychostimulant-induced hyperactivity. This last model had been important in studies of the disease and has some validity but it is clear that by itself cannot be considered to represent mania. Additional models for facets of BPD are needed to allow better screening of new drugs and new mutant mice. Such models may also support the exploration of endophenotypes of BPD and the mechanisms of the disease. An advantage of a battery approach is that each model can be only partially valid when used alone but the combination of a few models may result in strong validity. The present study suggests that such a battery can be based on existing models previously developed in the context of studying normal behavior or other disorders after an initial validation in the context of BPD. An example for this idea is described using the resident-intruder test for aggression. Present results show that 3 weeks oral treatment with 1.2-2.4% lithium (increasing doses), or 20 g/kg daily dose of valproate, significantly reduced aggressive behavior in resident mice without affecting non-aggressive social interactions. Accordingly, it is suggested that the simplified resident-intruder paradigm may model the aggression related to mania as part of a test battery for facets of BPD. It is further speculated that, pending further research, this paradigm can be combined with additional methods to explore changes in the LHPA axis that may be linked to an important endophenotype of BPD.

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“…Abnormal expression of the dopamine transporter (DAT) has been implicated in the neuropathophysiology of BD through genetic linkage studies (Greenwood et al 2001, 2006; Kelsoe et al 1996), with the functional consequences of an observed DAT mutation leading to reduced cell surface DAT expression (Horschitz et al 2005). Amphetamine, which inhibits the DAT and other monoamine transporters (Han and Gu 2006; Rothman and Baumann 2006), is one of the most common animal models of BD in mice (Arban et al 2005; Gould et al 2001), rats (Cappeliez and Moore 1990; Frey et al 2006; Shaldivin et al 2001), and humans (Asghar et al 2003; Silverstone et al 1998). Despite the prevalent use of amphetamine as a model of BD, however, there has been limited success in developing therapies specifically for BD.…”

Section: Introductionmentioning

confidence: 99%

GBR 12909 administration as a mouse model of bipolar disorder mania: mimicking quantitative assessment of manic behavior

et al. 2009

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RationaleMania is a core feature of bipolar disorder (BD) that traditionally is assessed using rating scales. Studies using a new human behavioral pattern monitor (BPM) recently demonstrated that manic BD patients exhibit a specific profile of behavior that differs from schizophrenia and is characterized by increased motor activity, increased specific exploration, and perseverative locomotor patterns as assessed by spatial d.ObjectivesIt was hypothesized that disrupting dopaminergic homeostasis by inhibiting dopamine transporter (DAT) function would produce a BD mania-like phenotype in mice as assessed by the mouse BPM.MethodsWe compared the spontaneous locomotor and exploratory behavior of C57BL/6J mice treated with the catecholamine transporter inhibitor amphetamine or the selective DAT inhibitor GBR 12909 in the mouse BPM. We also assessed the duration of the effect of GBR 12909 by testing mice in the BPM for 3 h and its potential strain dependency by testing 129/SvJ mice.ResultsAmphetamine produced hyperactivity and increased perseverative patterns of locomotion as reflected in reduced spatial d values but reduced exploratory activity in contrast to the increased exploration observed in BD patients. GBR 12909 increased activity and reduced spatial d in combination with increased exploratory behavior, irrespective of inbred strain. These effects persisted for at least 3 h.ConclusionsThus, selectively inhibiting the DAT produced a long-lasting cross-strain behavioral profile in mice that was consistent with that observed in manic BD patients. These findings support the use of selective DAT inhibition in animal models of the impaired dopaminergic homeostasis putatively involved in the pathophysiology of BD mania.

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Transcranial magnetic stimulation in an amphetamine hyperactivity model of mania

Abstract: The results suggest that TMS treatment to rats interacts with the effects of amphetamine; the specific effects may be dependent on the schedule of treatment.

Cited by 23 publications

References 18 publications

Transcranial Magnetic Stimulation in the Management of Mood Disorders

Transcranial Magnetic Stimulation in the Management of Mood Disorders

Establishment of a Battery of Simple Models for Facets of Bipolar Disorder: A Practical Approach to Achieve Increased Validity, Better Screening and Possible Insights into Endophenotypes of Disease

GBR 12909 administration as a mouse model of bipolar disorder mania: mimicking quantitative assessment of manic behavior

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