Posttraining androgens' enhancement of cognitive performance is temporally distinct from androgens' increases in affective behavior

Frye, Cheryl A.; Lacey, Elizabeth H.

doi:10.3758/cabn.1.2.172

Cited by 85 publications

(58 citation statements)

References 91 publications

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“…As such, in our laboratory, we have used gonadectomized adult male rodents, which have their primary endogenous sources of androgens, such as testosterone and its metabolite (i.e., 3a-androstanediol, a neurosteroid that is a positive modulator of GABA A receptors), the testes, removed (2 ± 1 s spent on the open arms of the plus maze), as negative controls. Androgen-replete rodents, those that are gonadally intact (28 ± 6 s) or gonadectomized and replaced with testosterone (4 mg kg À1 subcutaneously; 36 + 5 s, which produces physiological circulating testosterone and 3a-androstanediol levels) serve as positive controls 40,41 . PROCEDURE 1| Make sure maze is cleaned and dried before use and that video-tracking system is ready to be used.…”

Section: Methodsmentioning

confidence: 99%

“…We have used single exposure to the elevated plus maze with success to determine response to novelty/anxiety behavior of rodents in different hormone conditions to determine the antianxiety effects of steroid hormones, such as estrogen, progestins and androgens 22,[40][41][42][43][44][45][46][47][48][49][50] . The materials, methods and typical results obtained are as follows.…”

Section: Predictive Validity Of the Elevated Plus Mazementioning

confidence: 99%

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The use of the elevated plus maze as an assay of anxiety-related behavior in rodents

2007

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The elevated plus maze is a widely used behavioral assay for rodents and it has been validated to assess the anti-anxiety effects of pharmacological agents and steroid hormones, and to define brain regions and mechanisms underlying anxiety-related behavior. Briefly, rats or mice are placed at the junction of the four arms of the maze, facing an open arm, and entries/duration in each arm are recorded by a video-tracking system and observer simultaneously for 5 min. Other ethological parameters (i.e., rears, head dips and stretchedattend postures) can also be observed. An increase in open arm activity (duration and/or entries) reflects anti-anxiety behavior. In our laboratory, rats or mice are exposed to the plus maze on one occasion; thus, results can be obtained in 5 min per rodent. INTRODUCTIONThe elevated plus maze has been described as a simple method for assessing anxiety responses of rodents by File and co-workers 1 . A task, using a Y-shaped apparatus that included an elevated open alley, which produced a strong approach-avoidance conflict, and an enclosed alley, which did not, was first described by Montgomery 2 . This task was modified into an elevated maze with four arms (two open and two enclosed) that are arranged to form a plus shape and was described by Handley and Mithani 3 . These authors described the assessment of anxiety behavior of rodents by using the ratio of time spent on the open arms to the time spent on the closed arms. Unlike other behavioral assays used to assess anxiety responses that rely upon the presentation of noxious stimuli (i.e., electric shock, food/water deprivation, loud noises, exposure to predator odor, etc.) that typically produce a conditioned response, the elevated plus maze relies upon rodents' proclivity toward dark, enclosed spaces (approach) and an unconditioned fear of heights/open spaces (avoidance) 4 .There is great diversity in possible applications of the elevated plus maze. To name a few, prescreening of newly developed pharmacological agents for treatment of anxiety-related disorders can be carried out. The anxiolytic and anxiogenic effects of pharmacological agents, drugs of abuse and hormones can be investigated. The effects of reproductive senescence/aging and/or pre-, peri-or postnatal exposure to various stressors can be assessed. Furthermore, beyond its utility as a model to detect anxiolytic effects of benzodiazepine-related compounds, the elevated plus maze can be used as a behavioral assay to study the brain sites (e.g., limbic regions, hippocampus, amygdala, dorsal raphe nucleus, etc. 5,6 ) and mechanisms (e.g., GABA, glutamate, serotonin, hypothalamic-pituitary-adrenal axis neuromodulators, etc. 1,3,[7][8][9][10][11][12] ) underlying anxiety behavior. Indeed, the elevated plus maze has been used as a model of state, unconditioned anxiety for over two decades, and there are now over 2,000 papers related to this topic. Because a lengthy discussion of these key findings is beyond the scope of this protocol, readers are referred to several excellent an...

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Section: Methodsmentioning

confidence: 99%

Section: Predictive Validity Of the Elevated Plus Mazementioning

confidence: 99%

The use of the elevated plus maze as an assay of anxiety-related behavior in rodents

2007

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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%

“…Other facets of memory also appear to be influenced by androgens, such as object memory in rodents, which is strongly influenced by circulating androgens and estrogens in adulthood (Frye and Lacey, 2001;Walf et al, 2006). Use of the Tfm models would further elucidate the role of T and its mechanism of action in this and other memory tasks.…”

Section: Spatial Memorymentioning

confidence: 99%

“…Tfm male mice also show impaired MWM performance compared to partially androgen-insensitive Tfm carrier females, although sex differences in wt mice were not found (Rizk et al, 2005). Together, these findings suggest that the AR is necessary for the full masculinization of spatial memory.Other facets of memory also appear to be influenced by androgens, such as object memory in rodents, which is strongly influenced by circulating androgens and estrogens in adulthood (Frye and Lacey, 2001;Walf et al, 2006). Use of the Tfm models would further elucidate the role of T and its mechanism of action in this and other memory tasks.…”

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confidence: 99%

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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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Differential impacts on multiple forms of spatial and contextual memory in diazepam binding inhibitor knockout mice

Ujjainwala

Courtney

Wojnowski

et al. 2019

J of Neuroscience Research

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Learning and memory are fundamental processes that are disrupted in many neurological disorders including Alzheimer’s disease and epilepsy. The hippocampus plays an integral role in these functions, and modulation of synaptic transmission mediated by γ-aminobutyric acid (GABA) type-A receptors (GABAARs) impacts hippocampus-dependent learning and memory. The protein diazepam binding inhibitor (DBI) differentially modulates GABAARs in various brain regions, including hippocampus, and changes in DBI levels may be linked to altered learning and memory. The effects of genetic loss of DBI signaling on these processes, however, have not been determined. In these studies, we examined male and female constitutive DBI knockout mice and wild-type littermates to investigate the role of DBI signaling in modulating multiple forms of hippocampus-dependent spatial learning and memory. DBI knockout mice did not show impaired discrimination of objects in familiar and novel locations in an object location memory test, but did exhibit reduced time spent exploring the objects. Multiple parameters of Barnes maze performance, testing the capability to utilize spatial reference cues, were disrupted in DBI knockout mice. Furthermore, whereas most wild-type mice adopted a direct search strategy upon learning the location of the target hole, knockout mice showed higher rates of using an inefficient random strategy. In addition, DBI knockout mice displayed typical levels of contextual fear conditioning, but lacked a sex difference observed in wild-type mice. Together, these data suggest that DBI selectively influences certain forms of spatial learning and memory, indicating novel roles for DBI signaling in modulating hippocampus-dependent behavior in a task-specific manner.

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Posttraining androgens' enhancement of cognitive performance is temporally distinct from androgens' increases in affective behavior

Cited by 85 publications

References 91 publications

The use of the elevated plus maze as an assay of anxiety-related behavior in rodents

The use of the elevated plus maze as an assay of anxiety-related behavior in rodents

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

Differential impacts on multiple forms of spatial and contextual memory in diazepam binding inhibitor knockout mice

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