Androgens Increase Spine Synapse Density in the CA1 Hippocampal Subfield of Ovariectomized Female Rats

Léránth, Csaba; Hajszán, Tibor; MacLusky, Neil J.

doi:10.1523/jneurosci.4516-03.2004

Cited by 189 publications

(141 citation statements)

References 48 publications

Supporting

Mentioning

128

Contrasting

Unclassified

Order By: Relevance

“…In addition, drugs that inhibit actin filaments within spine heads interfere with LTP, which is thought to be important for memory coding and consolidation within the hippocampus (Mesches et al, 1999;Ackermann and Matus, 2003). While ovarian hormones and androgens induce changes in both spine density and shape in rodents Woolley et al, 1997;Leranth et al, 2004;Li et al, 2004;Gonzalez-Burgos et al, 2005), these data show that chronic stress modulates CA1 spine shape as well.…”

Section: Effects Of Chronic Stress On Hippocampal Morphologymentioning

confidence: 95%

Chronic stress enhances spatial memory in ovariectomized female rats despite CA3 dendritic retraction: Possible involvement of CA1 neurons

et al. 2005

View full text Add to dashboard Cite

Emerging data report sex differences in how the brain responds to chronic stress. Here, we investigated the effects of chronic restraint stress (6 h/day/21 days) on hippocampal morphology and function in ovariectomized female rats. Chronic restraint stress caused CA3 apical dendritic retraction in short-and long-shafted neurons, while it reduced basal dendritic arbors in long-shafted neurons only. Chronic restraint did not affect CA1 dendritic arborization, although it increased the proportion of CA1 spine heads compared with controls. Both stressed and control animals performed well on the Y-maze, a spatial memory task. However, chronic stress enhanced Y-maze performance compared with controls, which may reflect facilitated spatial memory or reduced habituation. Ymaze performance correlated with CA1 spine head proportion. This relationship suggests that spatial ability in females may be more tightly coupled with CA1 morphology, which may override the influence of CA3 dendritic retraction. Thus, this research provides additional evidence that CA3 morphology does not always parallel spatial memory.

show abstract

Section: Effects Of Chronic Stress On Hippocampal Morphologymentioning

confidence: 95%

Chronic stress enhances spatial memory in ovariectomized female rats despite CA3 dendritic retraction: Possible involvement of CA1 neurons

et al. 2005

View full text Add to dashboard Cite

show abstract

“…Androgens also increase the pyramidal cell dendritic spine density (PSSD) in CA1 of the hippocampus in male and female rats Leranth et al, 2004; Hajszan et al., in this issue). In females, estrogens can also increase CA1 PSSD, though they have no effect in males (Leranth et al, 2003;MacLusky et al, 2005).…”

Section: Hippocampusmentioning

confidence: 96%

“…Jones and Watson (2005) found that Tfm male rats show a greater GCL volume than do females, although there was no sex difference in GCL volume. Why GCL volume is greatest in Tfm rats is unclear, but the authors suggest it may result from increased ER activation within the GCL due to the higher levels of T in Tfm male rats.Androgens also increase the pyramidal cell dendritic spine density (PSSD) in CA1 of the hippocampus in male and female rats Leranth et al, 2004; Hajszan et al., in this issue). In females, estrogens can also increase CA1 PSSD, though they have no effect in males (Leranth et al, 2003;MacLusky et al, 2005).…”

mentioning

confidence: 96%

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

View full text Add to dashboard Cite

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...

show abstract

“…86 Androgens improve spine-synapse density in the CA1 of rodents. 91 Taken together, androgen could improve insulin resistance by binding androgen receptor in brain, enhance synaptic failure, and promote synaptogenesis in the AD brain.…”

Section: Androgen Receptor Could Control Insulin Resistance and Synapmentioning

confidence: 99%

The Novel Implication of Androgen in Diabetes-induced Alzheimer's Disease

Song

Jung

Kim

2017

J Lipid Atheroscler

View full text Add to dashboard Cite

Alzheimer's disease (AD) is characterized by the accumulation of amyloid beta (Aβ) and the hyperphosphorylation of tau protein in the brain, leading to the increase in inflammation and neuronal loss. Recently, evidences to support the association between type 2 diabetes mellitus (T2DM) and AD have markedly increased by clinical researches and experimental studies. Reduced insulin action and impaired glucose metabolism in the brain leads to diabetes induced AD. Androgen, a male sex hormone, was known to regulate inflammatory response, Aβ deposition in AD, insulin signaling, and synaptic plasticity in brain. Clinical studies demonstrated that androgen deficiency results in the increased risk of AD and its severe progression in male subjects. We reviewed the significant evidences to support that low testosterone levels are linked to diabetes-induced AD based on previous studies. Thus, we highlight the therapeutic potential of androgen in diabetes induced AD. Corresponding Author: Oh Yoen Kim, Department of Food Sciences and Nutrition, Human Life Research Center, Dong-A University, 37 550 beon-gil Nakdong-daero, Busan 49315,.kr *These authors contributed equally to this work. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. INTRODUCTION THE ASSOCIATION BETWEEN DIABETES AND ADIn the T2DM, the impairment of glycemic control and insulin resistance triggers mild cognitive impairment ANDROGEN PROTECTS NEURONAL CELLS AND INVOLVES Aβ ACCUMULATION IN THE AD BRAINThe accumulation of amyloid plaques is the neuro- CONFLICTS OF INTERESTThe authors have no conflict of interest to declare. ACKNOWLEDGEMENTS

show abstract

Androgens Increase Spine Synapse Density in the CA1 Hippocampal Subfield of Ovariectomized Female Rats

Cited by 189 publications

References 48 publications

Chronic stress enhances spatial memory in ovariectomized female rats despite CA3 dendritic retraction: Possible involvement of CA1 neurons

Chronic stress enhances spatial memory in ovariectomized female rats despite CA3 dendritic retraction: Possible involvement of CA1 neurons

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

The Novel Implication of Androgen in Diabetes-induced Alzheimer's Disease

Contact Info

Product

Resources

About