Intra- and interstrain differences in models of “behavioral despair”

Bai, Fengju; Li, Xia; Clay, Michael P.; Lindstrom, Terry D.; Skolnick, Phil

doi:10.1016/s0091-3057(01)00599-8

Cited by 230 publications

(131 citation statements)

References 18 publications

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“…These compounds (referred to as AMPA receptor-positive modulators or AMPA receptor potentiators, ARPs) do not activate AMPA receptors themselves, but slow the rate of receptor desensitization and/or deactivation in the presence of an agonist (e.g., glutamate and AMPA). ARPs have been reported to have antidepressant effects in animal models of antidepressant efficacy including the FST, TST, and a reduction in antidepressant-sensitive submissive behaviors (Alt et al, 2006;Bai et al, 2001;Knapp et al, 2002;Li et al, 2001). Similar to lithium, ARPs have been shown to have a robust augmentative effect on the actions of antidepressants in the FST (Li et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…It is important to discern the effect of lithium in additional behavioral tests beyond the FST, in order to allow the use of multiple tests to confirm any putative antidepressant-like mechanism of lithium, as well as to use an alternative test when using background mouse strains that are historically unresponsive to antidepressants in the FST Petit-Demouliere et al, 2005). Despite the face value similarities of behavioral endpoints, the spectrum of drugs that are active in the FST and TST are not identical, suggesting possible fundamental differences in the neurochemistry involved in the behavioral output (Bai et al, 2001;Lucki et al, 2001;Petit-Demouliere et al, 2005;Ripoll et al, 2003).Our aims in the current study include the investigation of the effects of both short-and longterm actions of lithium in the FST and TST. We additionally investigated the relationship between the antidepressant-like effects of lithium in these models and AMPA receptor blockade and cell surface expression.…”

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Involvement of AMPA receptors in the antidepressant-like effects of lithium in the mouse tail suspension test and forced swim test

et al. 2008

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In addition to its clinical antimanic effects, lithium also has efficacy in the treatment of depression. However, the mechanism by which lithium exerts its antidepressant effects is unclear. Our objective was to further characterize the effects of peripheral and central administration of lithium in mouse models of antidepressant efficacy as well as to investigate the role of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptors in these behaviors. We utilized the mouse forced swim test (FST) and tail suspension test (TST), intracerebroventricular (ICV) lithium administration, AMPA receptor inhibitors, and BS3 crosslinking followed by western blot. Both short-and long-term administration of lithium resulted in robust antidepressant-like effects in the mouse FST and TST. Using ICV administration of lithium, we show that these effects are due to actions of lithium on the brain, rather than to peripheral effects of the drug. Both ICV and rodent chow (0.4% LiCl) administration paradigms resulted in brain lithium concentrations within the human therapeutic range. The effects of lithium to decrease immobility in the FST and TST were blocked by administration of AMPA receptor inhibitors. Additionally, administration of lithium increased the cell surface expression of GluR1 and GluR2 in the mouse hippocampus. Collectively, these data show that lithium exerts centrally mediated antidepressant-like effects in the mouse FST and TST that require AMPA receptor activation. Lithium may exert its antidepressant effects in humans through AMPA receptors, thus further supporting a role of targeting AMPA receptors as a therapeutic approach for the treatment of depression. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Depression is a severe neuropsychiatric disorder that manifests both as a component of bipolar disorder and unipolar depressive disorder. Bipolar disorder affects at least 1% of the world's population when a strict definition (DSM IV bipolar I disorder) is applied. Major depression is more common than bipolar disorder in the overall population (~ 15% lifetime risk as defined by DSM IV) (Kessler et al., 2005;Sullivan et al., 2000). The recognition of the significant morbidity and mortality (suicide rate of 15%) associated with these severe mood disorders (Evans et al., 2005;Jamison, 2000;Kupfer, 2005), as well as the growing appreciation that a significant percentage of patients either do not respond fully to existing treatments or are intolerant of undesirable side effects, has made the challenge of discovering improved therapeutic agents increasing...

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Involvement of AMPA receptors in the antidepressant-like effects of lithium in the mouse tail suspension test and forced swim test

et al. 2008

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“…Although it is possible that A/J mice failed to show an increase in hippocampal cell proliferation in response to fluoxetine because of a ceiling effect (eg baseline proliferation is already at maximum), this is an unlikely interpretation: C57BL/6J (B6) mice have been shown to have a higher rate of hippocampal cell proliferation than A/J mice, but, unlike A/J, B6 mice are behaviorally responsive to the antidepressant effects of fluoxetine treatment (Kempermann et al, 1997(Kempermann et al, , 2006Bai et al, 2001;Hayes and Nowakowski, 2002). It is important to note, however, that our data suggest that the rate of baseline hippocampal cell proliferation is not correlated with baseline TST immobility: rather, the correlation between cell proliferation and TST activity is specific to the effect of fluoxetine.…”

Section: Discussionmentioning

confidence: 99%

Genetic Regulation of Behavioral and Neuronal Responses to Fluoxetine

Miller

Schultz

Gulati

et al. 2007

Neuropsychopharmacol

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Despite widespread use of antidepressants, the factors underlying the behavioral response to antidepressants are unknown. It has been shown that antidepressant treatment promotes the proliferation and survival of neurons in the adult hippocampus via enhanced serotonergic signaling, but it is unclear whether hippocampal neurogenesis is responsible for the behavioral response to antidepressants. Furthermore, a large subpopulation of patients fails to respond to antidepressant treatment due to presumed underlying genetic factors. In the present study, we have used the phenotypic and genotypic variability of inbred mouse strains to show that there is a genetic component to both the behavioral and neuronal effects of chronic fluoxetine treatment, and that this antidepressant induces an increase in hippocampal cell proliferation only in the strains that also show a positive behavioral response to treatment. Furthermore, the behavioral and neuronal responses are associated with an upregulation of genes known to promote neuronal proliferation and survival. These results suggest that inherent genetic predisposition to increased serotonin-induced neurogenesis may be a determinant of antidepressant efficacy.

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“…The TST has been shown to be sensitive to an array of antidepressant treatments, including tricyclics, SSRIs, monoamine oxidase inhibitors, atypical antidepressants, and electroconvulsive therapy (Perrault et al, 1992;Steru et al, 1985Steru et al, , 1987Teste et al, 1990Teste et al, , 1993. Inbred rodent strains show substantial variability in baseline performance and behavioral response to antidepressant administration in the TST (Bai et al, 2001;Gershenfeld, 2001, 2003;Rippoll et al, 2003; for a review, see Cryan et al, 2005). Baseline response was not correlated with the response to antidepressants Liu and Gershenfeld, 2003), so that mice with the greatest immobility values are not necessarily the most responsive to antidepressants.…”

Section: Introductionmentioning

confidence: 99%

Pharmacogenomic Evaluation of the Antidepressant Citalopram in the Mouse Tail Suspension Test

Crowley

Brodkin

Blendy

et al. 2006

Neuropsychopharmacol

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The identification of genetic variants regulating antidepressant response in human patients would allow for more individualized, rational, and successful drug treatments. We have previously identified the BALB/cJ inbred mouse strain as highly responsive to the selective serotonin reuptake inhibitor (SSRI) citalopram in the tail suspension test (TST), a widely used and well-established screening paradigm for detecting compounds with antidepressant activity. In contrast, A/J mice did not show a significant response to citalopram in this test despite exposure to equivalent plasma levels of the drug. To identify genetic determinants of this differential response, 506 F 2 mice from an intercross between BALB/cJ and A/J mice were phenotyped. Composite interval mapping of 92 mice from the phenotypic extremes revealed three loci on chromosomes 7, 12, and 19 affecting citalopram response in the TST. The quantitative trait locus (QTL) at the telomeric end of chromosome 19 showed the greatest level of significance. Three candidate genes residing in this locus include those for vesicular monoamine transporter 2 (VMAT2, slc18a2), alpha 2A adrenergic receptor (adra2a), and beta 1 adrenergic receptor (adrb1). The protein coding regions of these three genes in BALB/cJ and A/J mice were sequenced and two polymorphisms were found in VMAT2 (Leu117Pro and Ser505Pro), while the transcribed regions of adra2a and adrb1 were of identical sequence between strains. Follow-up studies are needed to determine if the VMAT2 polymorphisms are functional and if they could explain the chromosome 19 QTL. The present quantitative trait study suggests possible candidate genes for human pharmacogenetic studies of therapeutic responses to SSRIs such as citalopram.

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Intra- and interstrain differences in models of “behavioral despair”

Cited by 230 publications

References 18 publications

Involvement of AMPA receptors in the antidepressant-like effects of lithium in the mouse tail suspension test and forced swim test

Involvement of AMPA receptors in the antidepressant-like effects of lithium in the mouse tail suspension test and forced swim test

Genetic Regulation of Behavioral and Neuronal Responses to Fluoxetine

Pharmacogenomic Evaluation of the Antidepressant Citalopram in the Mouse Tail Suspension Test

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