Sex differences in Mongolian gerbils in four tests of anxiety

Bridges, Nikola Jane; Starkey, Nicola J.

doi:10.1016/j.physbeh.2004.08.002

Cited by 14 publications

(12 citation statements)

References 32 publications

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“…Consistent with previous studies in voles (Grippo et al, 2007b, 2008; Pan et al, 2009) and in other rodent species (Wright et al, 1991), our data indicate that social isolation induced an anxiogenic response—indicative of an increased level of anxiety (Bridges and Starkey, 2004; Ferdman et al, 2007). Further, social isolation facilitated depression-like behaviors in female prairie voles, as has been reported in previous studies (Grippo et al, 2008, 2009).…”

Section: Discussionsupporting

confidence: 92%

Social isolation impairs adult neurogenesis in the limbic system and alters behaviors in female prairie voles

Lieberwirth

Liu

Jia

et al. 2012

Hormones and Behavior

104

108

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Disruptions in the social environment, such as social isolation, are distressing and can induce various behavioral and neural changes in the distressed animal. We conducted a series of experiments to test the hypothesis that long-term social isolation affects brain plasticity and alters behavior in the highly social prairie vole (Microtus ochrogaster). In Experiment 1, adult female prairie voles were injected with a cell division marker, 5-bromo-2′-deoxyuridine (BrdU), and then same-sex pair-housed (control) or single-housed (isolation) for 6 weeks. Social isolation reduced cell proliferation, survival, and neuronal differentiation and altered cell death in the dentate gyrus of the hippocampus and the amygdala. In addition, social isolation reduced cell proliferation in the medial preoptic area and cell survival in the ventromedial hypothalamus. These data suggest that long-term social isolation affects distinct stages of adult neurogenesis in specific limbic brain regions. In Experiment 2, isolated females displayed higher levels of anxiety-like behaviors in both the open field and elevated plus maze tests and higher levels of depression-like behavior in the forced swim test than controls. Further, isolated females showed a higher level of affiliative behavior than controls, but the two groups did not differ in social recognition memory. Together, our data suggest that social isolation not only impairs cell proliferation, survival, and neuronal differentiation in limbic brain areas, but also alters anxiety-like, depression-like, and affiliative behaviors in adult female prairie voles. These data warrant further investigation of a possible link between altered neurogenesis within the limbic system and behavioral changes.

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Section: Discussionsupporting

confidence: 92%

Social isolation impairs adult neurogenesis in the limbic system and alters behaviors in female prairie voles

Lieberwirth

Liu

Jia

et al. 2012

Hormones and Behavior

104

108

View full text Add to dashboard Cite

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“…However, male–male vs. female–female SI may have inherently different components, and more avoidance in the Vogel punished drinking paradigm might be compromised by enhanced female pain sensitivity [119]. Sex differences in anxiety-like behavior also depend on the species (with monogamous, alloparenting species such as Mongolian gerbils [66] and prairie voles [26] potentially proving to be better rodent models for sex differences in anxiety than mice and rats), strain [13, 309, 358], age [110, 175], and whether female data were pooled for all estrous stages or not. In fact, estrous stage appears to be a major determinant of conflict anxiety, with diestrus females acting more anxious than males or estrus, metaestrus, and proestrus females [125, 133, 234, 261].…”

Section: Sex Differences In Conflict Anxiety and Current Animal Modelsmentioning

confidence: 99%

Sex differences in anxiety and emotional behavior

Donner

Lowry

2013

Pflugers Arch - Eur J Physiol

303

168

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Research has elucidated causal links between stress exposure and the development of anxiety disorders, but due to the limited use of female or sex-comparative animal models, little is known about the mechanisms underlying sex differences in those disorders. This is despite an overwhelming wealth of evidence from the clinical literature that the prevalence of anxiety disorders is about twice as high in women compared to men, in addition to gender differences in severity and treatment efficacy. We here review human gender differences in generalized anxiety disorder, panic disorder, posttraumatic stress disorder and anxiety-relevant biological functions, discuss the limitations of classic conflict anxiety tests to measure naturally occurring sex differences in anxiety-like behaviors, describe sex-dependent manifestation of anxiety states after gestational, neonatal, or adolescent stressors, and present animal models of chronic anxiety states induced by acute or chronic stressors during adulthood. Potential mechanisms underlying sex differences in stress-related anxiety states include emerging evidence supporting the existence of two anatomically and functionally distinct serotonergic circuits that are related to the modulation of conflict anxiety and panic-like anxiety, respectively. We discuss how these serotonergic circuits may be controlled by reproductive steroid hormone-dependent modulation of crfr1 and crfr2 expression in the midbrain dorsal raphe nucleus and by estrous stage-dependent alterations of γ-aminobutyric acid (GABAergic) neurotransmission in the periaqueductal gray, ultimately leading to sex differences in emotional behavior.

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“…Gonadal hormones also play a role in the display of anxiety-related behavior in rodents as assessed by open field testing, exposure to a novel object, the elevated plus maze task, and Walf and Frye, 2005;Lund et al, 2005;Bridges and Starkey, 2004;Frye and Lacey, 2001). In general, increases in either T or E2 in both male and female rodents are correlated with a decrease in anxiety-related behaviors (Frye and Walf, 2004;Bing et al, 1998; Frye et al 2007).…”

Section: Anxiety-related Behaviormentioning

confidence: 99%

The role of androgen receptors in the masculinization of brain and behavior: What we've learned from the testicular feminization mutation

Zuloaga

Puts

Jordan

et al. 2008

Hormones and Behavior

213

156

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Many studies demonstrate that exposure to testicular steroids such as testosterone early in life masculinizes the developing brain, leading to permanent changes in behavior. Traditionally, masculinization of the rodent brain is believed to depend on estrogen receptors (ERs) and not androgen receptors (ARs). According to the aromatization hypothesis, circulating testosterone from the testes is converted locally in the brain by aromatase to estrogens, which then activate ERs to masculinize the brain. However, an emerging body of evidence indicates that the aromatization hypothesis cannot fully account for sex differences in brain morphology and behavior, and that androgens acting on ARs also play a role. The testicular feminization mutation (Tfm) in rodents, which produces a nonfunctional AR protein, provides an excellent model to probe the role of ARs in the development of brain and behavior. Tfm rodent models indicate that ARs are normally involved in the masculinization of many sexually dimorphic brain regions and a variety of behaviors, including sexual behaviors, stress response and cognitive processing. We review the role of ARs in the development of the brain and behavior, with an emphasis on what has been learned from Tfm rodents as well as from related mutations in humans causing complete androgen insensitivity. Keywordscomplete androgen insensitivity syndrome -CAIS; vasopressin; anxiety; spatial memory; bed nucleus; medial amygdala; SDN-POA; sexual behavior; aggression; VMH Exposure to testicular steroids such as testosterone (T) early in life masculinizes the developing brain, leading to permanent changes in behavior in a wide variety of animal models (Morris et al., 2004). According to the aromatization hypothesis, T is converted by aromatase into 17-β estradiol (E2), which then acts on estrogen receptors (ERs) to masculinize the brain (Naftolin et al., 1975). Traditionally, aromatization is believed to be the mechanism by which the rodent brain becomes masculinized and defeminized. Some sexually dimorphic regions within the hypothalamus adhere well to this hypothesis, including the sexually dimorphic nucleus of the preoptic area (SDN-POA) and anteroventral periventricular nucleus (AVPV). T spares neuronsCorresponding author: Damian Zuloaga, Neuroscience Program, 108 Giltner Hall, Michigan State University, East Lansing, MI 48824, Phone: Fax: (517) 432-2744, Email: E-mail: zuloagad@msu.edu. 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. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript from death in the SDN-POA...

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Sex differences in Mongolian gerbils in four tests of anxiety

Cited by 14 publications

References 32 publications

Social isolation impairs adult neurogenesis in the limbic system and alters behaviors in female prairie voles

Social isolation impairs adult neurogenesis in the limbic system and alters behaviors in female prairie voles

Sex differences in anxiety and emotional behavior

The role of androgen receptors in the masculinization of brain and behavior: What we've learned from the testicular feminization mutation

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