Effects of repeated maternal separation on anxiety- and depression-related phenotypes in different mouse strains

Millstein, Rachel; Holmes, Andrew

doi:10.1016/j.neubiorev.2006.05.003

Cited by 353 publications

(347 citation statements)

References 115 publications

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“…4), as reported previously by others with B6 and mixed B6 strains (27,28). Taken together, the data indicate that maternal receptor deficit has no appreciable effect on offspring behavior in the B6 and B6-derived strains and are consistent with the reported resilience of B6 mice to environmental adversity (25,26,29).…”

Section: Genetic Inactivation Of P16 Ink4a Phenocopies Both the Cellusupporting

confidence: 91%

“…Nevertheless, the finding that p16 ink4a KO mimics both the cellular and behavioral phenotypes of the receptordeficient maternal genotype effect and specifically the prenatally determined EPM behavior suggests the involvement of early DG development in establishing the level of EPM anxiety. Although outbred strains such as the SW tend to respond to adverse or stimulating environments, inbred lines, in particular the C57BL6 (B6), are resilient to these effects (25,26). No anxiety in the EPM and enhanced stress response in the FST developed in response to the 5-HT 1A R-deficient maternal environment when the strain background was switched from SW to B6 (>99.9% isogeneity).…”

Section: Genetic Inactivation Of P16 Ink4a Phenocopies Both the Cellumentioning

confidence: 99%

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The serotonin _1A receptor gene as a genetic and prenatal maternal environmental factor in anxiety

Gleason

Liu²,

Bruening³

et al. 2010

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

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Low serotonin 1A receptor (5-HT 1A R) binding is a risk factor for anxiety and depression, and deletion of the 5-HT 1A R results in anxiety-like behavior in mice. Here we show that anxiety-like behavior in mice also can be caused, independently of the offspring's own 5-HT 1A R genotype, by a receptor deficit in the mother: a nongenetic transmission of a genetic defect. Some of the nongenetically transmitted anxiety manifestations were acquired prenatally and linked to a delay in dentate gyrus maturation in the ventral hippocampus of the offspring. Both the developmental delay and the anxiety-like phenotype were phenocopied by the genetic inactivation of p16 ink4a encoding a cyclin-dependent kinase inhibitor implicated in neuronal precursor differentiation. No maternal 5-HT 1A R genotype-dependent anxiety developed when the strain background was switched from Swiss Webster to C57BL/6, consistent with the increased resilience of this strain to early adverse environment. Instead, all anxiety manifestations were caused by the offspring's own receptor deficiency, indicating that the genetic and nongenetic effects converge to common anxiety manifestations. We propose that 5-HT 1A R deficit represents a dual risk for anxiety and that vulnerability to anxiety associated with genetic 5-HT 1A R deficiency can be transmitted by both genetic and nongenetic mechanisms in a population. Thus, the overall effect of risk alleles can be higher than estimated by traditional genetic assays and may contribute to the relatively high heritability of anxiety and psychiatric disorders in general.genetic risk | heritability | cross-fostering S tudies have identified mutant/polymorphic variants of genes, each with a relatively small contribution to the risk of depression, anxiety, schizophrenia, and other psychiatric diseases. However, demonstrable genetic influences explain only a small fraction of estimated heritability in psychiatric conditions. This "missing heritability" could be caused by a large number of undiscovered alleles or by mechanisms that amplify the effect of risk alleles but are not genetic in nature. We tested the hypothesis that mutant/polymorphic variants can have a larger effect if, besides their purely genetic effect, they have an additional "environmental" effect. For example, gene variants could influence maternal physiology, affecting the developmental program of the offspring, and consequently also increasing the risk for psychopathology. Indeed, adverse prenatal maternal and/or postnatal environment increases vulnerability to various diseases, including psychiatric disorders, in adulthood (1, 2), and one may extrapolate these findings to an abnormal maternal/parental environment related to disease-associated genes/gene variants.One of the few candidate genes whose function has been associated with anxiety and depression encodes the serotonin 1A receptor (5-HT 1A R) (3). Reduced binding or binding potential in the 5-HT 1A R has been linked to posttraumatic stress and panic disorders (3) and depression (4), and a...

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Section: Genetic Inactivation Of P16 Ink4a Phenocopies Both the Cellusupporting

confidence: 91%

Section: Genetic Inactivation Of P16 Ink4a Phenocopies Both the Cellumentioning

confidence: 99%

The serotonin _1A receptor gene as a genetic and prenatal maternal environmental factor in anxiety

Gleason

Liu²,

Bruening³

et al. 2010

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

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“…Thus, although the relatively stress-insensitive C57BL/6J strain [3,36,56] did not respond to stress while 'stress-sensitive' BALB/cByJ did, DBA/2J mice also responded, even though this strain is typically similar to C57BL/6J on measures of anxiety-like behavior and stress-reactivity [3,36,56]. While we did not conduct a strain comparison of glucocorticoid response profiles to our stress paradigm, these data suggest that the relationship between strain differences in stress reactivity and twobottle EtOH self-administration is likely to be complex and modulated by multiple factors.…”

Section: Nih Public Accessmentioning

confidence: 99%

“…Further studies will be needed to identify such a model in mice. This might entail the use of an alterative stressor (e.g., restraint, footshock) that has less of a physical component than swimming given evidence that physical exercise can itself affect EtOH-related behaviors in C57BL/6J mice [38]) and strain differences in swimming [37]. Another potentially fruitful approach would be to test stress effects on EtOH drinking after enforced abstinence, as successfully employed in rats [30].…”

Section: Nih Public Accessmentioning

confidence: 99%

“…Moreover, a number of studies have found marked differences in stress-related behaviors and stress-responsivity between inbred strains. Of note, on some, but not all, assays for anxiety and depression-related behaviors and stress-responsivity, the C57BL/6J strain scores low relative to certain other strains such as BALB/cByJ [3,15,36,56]. We recently reported that repeated exposure (14-days) to forced swim stress in the C57BL/6J inbred strain increased sensitivity to the sedative/ hypnotic and hypothermic effects of EtOH [5].…”

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confidence: 99%

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Effects of chronic swim stress on EtOH-related behaviors in C57BL/6J, DBA/2J and BALB/cByJ mice

Boyce-Rustay

Janos

Holmes

2008

Behavioural Brain Research

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There is a strong clinical relationship between stress and stress-related disorders and the incidence of alcohol abuse and alcoholism, and this relationship appears to be partly genetic in origin. There are marked strain differences in ethanol (EtOH)-related behaviors and reactivity to stress, but little investigation of the interaction between the two. The present study assessed the effects of chronic exposure to swim stress on EtOH-related behavior in three common inbred strains of mice, C57BL/ 6J, DBA/2J and BALB/cByJ. After establishing baseline (10%) EtOH self-administration in a twobottle free choice test, mice were exposed to daily swim stress for 14 consecutive days and EtOH consumption measured as a percent of baseline both during stress and for 10 days afterwards. A separate experiment examined the effects of 14 days of swim stress on sensitivity to the sedative/ hypnotic effects of an acute injection of 4 g/kg EtOH. Results showed that stress produced a marked and prolonged decrease in EtOH consumption in DBA/2J and BALB/cByJ, but not C57BL/6J mice. By contrast, stress increased sensitivity to the sedative/hypnotic effects of EtOH across all 3 strains. These findings demonstrate that chronic swim stress produces reductions in EtOH self-administration in a strain-dependent manner, and that these effects may be restricted to low-consuming strains. Present data also indicate a dissociation between effects of this stressor on EtOH self-administration and sensitivity to EtOH's sedative/hypnotic effects. In conclusion, strain differences, that are likely in large part genetic in nature, modify the effects of this stressor on EtOH's effects in a behaviorspecific manner. Keywords mouse; strain; ethanol; sedation; gene; drinking; swim stress; preference; two-bottle choice There is a strong epidemiological link between stress-related psychiatric disorders and alcoholism. Individuals suffering from depression or anxiety disorders, conditions often associated with stress, are more likely to abuse alcohol and become alcoholic, and tend to respond less well to therapeutic interventions [8,9,29,54]. Moreover, a history of adverse life events positively correlates with increased rates of alcoholism; although, interestingly, a proportion of individuals become abstinent following stress [19,35,46,51]. These clinic data lend support to the influential hypothesis that stress represent a significant risk factor for alcoholism [12,28]. *Corresponding author: R4N5 AP9A-L018, Abbott Laboratories, 100 Abbott Park Rd, Abbott Park, IL 60064, Ph. +1-847-937-2559, Fax +1-847-938-0072, E-mail: janel.boyce-rustay@abbott.com. 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 wh...

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Social Stress Effects on Defensive Behavior and Anxiety

Pearson

Blanchard

2011

The Handbook of Stress

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Effects of repeated maternal separation on anxiety- and depression-related phenotypes in different mouse strains

Cited by 353 publications

References 115 publications

The serotonin _1A receptor gene as a genetic and prenatal maternal environmental factor in anxiety

The serotonin _1A receptor gene as a genetic and prenatal maternal environmental factor in anxiety

Effects of chronic swim stress on EtOH-related behaviors in C57BL/6J, DBA/2J and BALB/cByJ mice

Social Stress Effects on Defensive Behavior and Anxiety

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Effects of repeated maternal separation on anxiety- and depression-related phenotypes in different mouse strains

Cited by 353 publications

References 115 publications

The serotonin 1A receptor gene as a genetic and prenatal maternal environmental factor in anxiety

The serotonin 1A receptor gene as a genetic and prenatal maternal environmental factor in anxiety

Effects of chronic swim stress on EtOH-related behaviors in C57BL/6J, DBA/2J and BALB/cByJ mice

Social Stress Effects on Defensive Behavior and Anxiety

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Product

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The serotonin _1A receptor gene as a genetic and prenatal maternal environmental factor in anxiety

The serotonin _1A receptor gene as a genetic and prenatal maternal environmental factor in anxiety