Testosterone modulates performance on a spatial working memory task in male rats

Sandstrom, Noah J.; Kim, Ju H.; Wasserman, Molly A.

doi:10.1016/j.yhbeh.2005.09.008

Cited by 99 publications

(97 citation statements)

References 67 publications

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“…We also found that testosterone-deprived rats impaired cognition and impaired hippocampal synaptic plasticity, but HFDinduced obesity did not aggravate those impairments in the testosterone-deprived condition. The present findings and other previous studies (Sakata et al 2000, Naghdi et al 2005, Sandstrom et al 2006, Spritzer et al 2011 indicated that testosterone plays an important role in cognitive function. Since brain mitochondrial function and brain insulin sensitivity were intact in NDO rats, these results indicate that they were not mainly contributed to Time (min)…”

Section: Discussionsupporting

confidence: 88%

“…Although vildagliptin increased brain insulin sensitivity and decreased brain mitochondrial dysfunction, it could not restore hippocampal synaptic plasticity and cognitive function in testosterone-deprived rats with or without obesity. Furthermore, findings from previous studies (Sandstrom et al 2006, Spritzer et al 2011, McConnell et al 2012) and the present study ( Fig. 5B and C) suggest that testosterone plays a critical role in maintaining the normal function of cognition.…”

Section: Figuresupporting

confidence: 78%

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Dipeptidyl peptidase 4 inhibitor improves brain insulin sensitivity, but fails to prevent cognitive impairment in orchiectomy obese rats

Pintana¹,

Pongkan²,

Pratchayasakul³

et al. 2015

Journal of Endocrinology

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It is unclear whether the dipeptidyl peptidase 4 (DPP4) inhibitor can counteract brain insulin resistance, brain mitochondrial dysfunction, impairment of hippocampal synaptic plasticity and cognitive decline in testosterone-deprived obese rats. We hypothesized that DPP4 inhibitor vildagliptin improves cognitive function in testosterone-deprived obese rats by restoring brain insulin sensitivity, brain mitochondrial function and hippocampal synaptic plasticity. Thirty male Wistar rats received either a sham-operated (S, nZ6) or bilateral orchiectomy (ORX, nZ24). ORX rats were divided into two groups and fed with either a normal diet (ND (NDO)) or a high-fat diet (HFO) for 12 weeks. Then, ORX rats in each dietary group were divided into two subgroups (nZ6/subgroup) to receive either a vehicle or vildagliptin (3 mg/kg per day, p.o.) for 4 weeks. After treatment, cognitive function, metabolic parameters, brain insulin sensitivity, hippocampal synaptic plasticity and brain mitochondrial function were determined in each rat. We found that HFO rats exhibited peripheral and brain insulin resistance, brain mitochondrial dysfunction, impaired hippocampal synaptic plasticity and cognitive decline. NDO rats did not develop peripheral and brain insulin resistance. However, impaired hippocampal synaptic plasticity and cognitive decline occurred. Vildagliptin significantly improved peripheral insulin sensitivity, restored brain insulin sensitivity and decreased brain mitochondrial reactive oxygen species production in HFO rats. However, vildagliptin did not restore hippocampal synaptic plasticity and cognitive function in both NDO and HFO rats. These findings suggest that vildagliptin could not counteract the impairment of hippocampal synaptic plasticity and cognitive decline in testosterone-deprived subjects, despite its effects on improved peripheral and brain insulin sensitivity as well as brain mitochondrial function.

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Section: Discussionsupporting

confidence: 88%

Section: Figuresupporting

confidence: 78%

Dipeptidyl peptidase 4 inhibitor improves brain insulin sensitivity, but fails to prevent cognitive impairment in orchiectomy obese rats

Pintana¹,

Pongkan²,

Pratchayasakul³

et al. 2015

Journal of Endocrinology

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“…Castration of male rats impairs spatial memory, while supplementation with T improves spatial memory [27]. Another study on castrated male rats showed impaired working memory, but an improved reference memory [28].…”

Section: Discussionmentioning

confidence: 97%

The effects of exogenous testosterone on spatial memory in rats

et al. 2010

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Testosterone (T) is known to affect spatial abilities in men and women. Studies focusing on this relationship showed that both endogenous variability of T and administration of exogenous T, altered mental rotation and spatial visualization. Organizational and activational effects of T can be separately identified. The aim of our study was to evaluate the activational effects of exogenous T on spatial memory in male and female rats. T was administered 3 times a week over a two week period in either 1 mg/kg for low testosterone group or 10 mg/kg for high testosterone group. The Morris water maze was performed to assess the rat's working and reference spatial memory. T and estradiol levels were measured in plasma. Increase in plasma T levels was confirmed in the experimental groups in comparison to the control groups (receiving sterile oil, 3 times a week over a two week period). Low dose T impaired working, but improved reference memory in female rats. In male rats the negative effects of T (both doses) on reference memory were shown. This experiment showed that the activational effects of exogenous testosterone on spatial memory of rats were gender and dose-dependent.© Versita Sp. z o.o.

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“…Adult circulating androgens and estrogens can also affect certain aspects of spatial memory performance and these effects may, at least partially, be mediated through activation of ARs in adulthood (Gibbs, 2005;Sandstrom et al, 2006;Naghdi et al, 2001). To further explore the role of ARs in spatial memory, performance in the MWM has been examined in both the rat and mouse Tfm models.…”

Section: Spatial Memorymentioning

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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Testosterone modulates performance on a spatial working memory task in male rats

Cited by 99 publications

References 67 publications

Dipeptidyl peptidase 4 inhibitor improves brain insulin sensitivity, but fails to prevent cognitive impairment in orchiectomy obese rats

Dipeptidyl peptidase 4 inhibitor improves brain insulin sensitivity, but fails to prevent cognitive impairment in orchiectomy obese rats

The effects of exogenous testosterone on spatial memory in rats

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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