Androgens modulate neuronal vulnerability to kainate lesion

Ramsden, Martin; Shin, Taekyun; Pike, Christian J.

doi:10.1016/j.neuroscience.2003.08.048

Cited by 102 publications

(86 citation statements)

References 27 publications

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“…Although still somewhat controversial, many studies have shown that the expression of AMPA-, KA-and NMDA-sensitive receptors as well as the GABA A receptor is either constant or variably diminished in many different brain regions including the hippocampus during aging (Gonzales et al, 1991;Pittaluga et al, 1993;Le Jeune et al, 1996;Nicolle et al, 1996;EcklesSmith et al, 2000;Kuehl-Kovarik et al, 2000;Magnusson, 2000;Sonntag et al, 2000;Wenk and Barnes, 2000;Adams et al, 2001;Clayton and Browning, 2001;Clayton et al, 2002;Lerma et al, 2001). Differences in a variety of other factors, including voltage-gated calcium channels (Vigues et al, 1999;Kelly et al, 2003), androgen levels (Mejias-Aponte et al, 2002;Ramsden et al, 2003;Ciriza et al, 2004), and GABA receptor function (MacGregor et al, 1997;Ma et al, 2001) which have been shown to modulate kainate-induced seizure activity in young animals, may modulate susceptibility in aged animals as well.…”

Section: Discussionmentioning

confidence: 99%

Effect of age on kainate-induced seizure severity and cell death

et al. 2008

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While the onset and extent of epilepsy increases in the aged population, the reasons for this increased incidence remain unexplored. The present study used two inbred strains of mice (C57BL/6J and FVB/NJ) to address the genetic control of age-dependent neurodegeneration by building upon previous experiments that have identified phenotypic differences in susceptibility to hippocampal seizure-induced cell death. We determined if seizure induction and seizure-induced cell death are affected differentially in young adult, mature, and aged male C57BL/6J and FVB/NJ mice administered the excitotoxin, kainic acid. Dose response testing was performed in three-four groups of male mice from each strain. Following kainate injections, mice were scored for seizure activity and brains from mice in each age group were processed for light microscopic histopathologic evaluation seven days following kainate administration to evaluate the severity of seizure-induced brain damage. Irrespective of the dose of kainate administered or the age group examined, resistant strains of mice (C57BL/6J) continued to be resistant to seizure-induced cell death. In contrast, aged animals of the FVB/NJ strain were more vulnerable to the induction of behavioral seizures and associated neuropathology after systemic injection of kainic acid than young or middle-aged mice.Results from these studies suggest that the age-related increased susceptibility to the neurotoxic effects of seizure induction and seizure-induced injury is regulated in a strain-dependent manner, similar to previous observations in young adult mice. Keywords mouse strain; excitotoxicity; kainic acid; epilepsy; cell death; aging Knowledge about the influence of aging on the susceptibility of the brain to seizure disorders is of critical importance in geriatric medicine and public health. Epilepsy is the most common neurological disorder after stroke, affecting more than 50 million persons worldwide and with a 2-3% life time risk of being given a diagnosis of epilepsy (Browne and Holmes, 2001). Currently it is well known that there is a significant incidence of epilepsy in children. However, less clearly recognized but of increasing importance is the significant incidence of epilepsy in 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 the elderly population. Recent studies in the United States and Europe indicate that the agespecific incidence of epilepsy is higher in those over the age of 65 years than in those in the first decade of life (Talli...

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Section: Discussionmentioning

confidence: 99%

Effect of age on kainate-induced seizure severity and cell death

et al. 2008

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“…Dihydrotestosterone has been found to regulate cellular growth, differentiation, survival, or death through both genomic and non-genomic signaling pathways [160]. Androgens, including T and DHT, can protect neurons from various insults in culture, including kainic acid toxicity [161], β-amyloid toxicity [162; 163] and serum deprivation [164], and have been shown to rapidly activate the cytoprotection-associated ERK/MAPK pathway [161; 163]. The receptor mediating these protective effects is thought to be AR due to the fact that AR antagonists block the neuroprotective effects [163; 164].…”

Section: Neuroprotective Verses Neuroendangering -Genomic Verses Nongmentioning

confidence: 99%

Non-genomic actions of androgens

Foradori

Weiser

Handa

2008

Frontiers in Neuroendocrinology

407

244

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Previous work in the endocrine and neuroendocrine fields has viewed androgen receptors (AR) as a transcription factor activated by testosterone or one of its many metabolites. The bound androgen receptor acts as transcription factor and binds to specific DNA response elements in target gene promoters, causing activation or repression of transcription and subsequently protein synthesis. Over the past two decades evidence has begun to accumulate to implicate androgens, dependent or independent of the AR, in rapid actions at the cellular and organism level. Androgen's rapid time course of action; effects in the absence or inhibition of the cellular machinery necessary for transcription/translation; and/or the effects of androgens not able to translocate to the nucleus suggest a method of androgen action not initially dependent on genomic mechcanisms (i.e. non-genomic in nature). In the present paper the non-genomic effects of androgens are reviewed, along with a discussion of the possible role non-genomic androgen actions have on animal physiology and behavior.

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“…This suggests that T and/or its metabolites could play a neuroprotective role in rescuing HVC from the regression induced by the withdrawal of systemic T and exposure to SD photoperiod, not unlike the hormone-mediated neuroprotection that is seen in several in vivo animal models of neurodegenerative insult (Ramsden et al 2003;Pike et al 2006). Consistent with this, we found that direct intracerebral infusion of T near HVC unilaterally in castrated male white-crowned sparrows transferred to SD photoperiod and systemic Twithrdrawal seems to ameliorate neurodegeneration of the ipsilateral HVC (unpublished data, C.K.…”

Section: Neurodegenerative Mechanisms Of Hvc Regression and Steroidalmentioning

confidence: 99%

Seasonal-like growth and regression of the avian song control system: Neural and behavioral plasticity in adult male Gambel’s white-crowned sparrows

Meitzen

Thompson

2008

General and Comparative Endocrinology

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Birdsong is regulated by a series of discrete brain nuclei known as the song control system. In seasonally-breeding male songbirds, seasonal changes in steroid sex hormones regulate the structure and electrophysiology of song control system neurons, resulting in dramatic changes in singing behavior. Male songbirds can be brought into the laboratory, where circulating levels of steroid hormone and photoperiod can be abruptly manipulated, providing controlled conditions under which rapid "seasonal-like" changes in behavior and morphology can be carefully studied. In this minireview, we will discuss the steroidal and cellular mechanisms underlying seasonal-like growth and regression of the song control system in adult male Gambel's white-crowned sparrows (Zonotrichia leucophrys gambelii), and its impact on song behavior. Specifically, we discuss recent advances concerning: 1) the role of androgen and estrogen receptors in inducing seasonal-like growth of the song control system; 2) how photoperiod modulates the time course of testosterone-induced growth of the song control system; 3) how bilateral intracerebral infusion of androgen and estrogen receptor antagonists near the song control nucleus HVC prevents seasonal-like increases in song stereotypy but not song rate; and 4) the steroidal and cellular mechanisms that mediate rapid regression of the song control system. Throughout this mini-review we compare data collected from white-crowned sparrows to that from other songbird species. We conclude by outlining avenues of future research.

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Androgens modulate neuronal vulnerability to kainate lesion

Cited by 102 publications

References 27 publications

Effect of age on kainate-induced seizure severity and cell death

Effect of age on kainate-induced seizure severity and cell death

Non-genomic actions of androgens

Seasonal-like growth and regression of the avian song control system: Neural and behavioral plasticity in adult male Gambel’s white-crowned sparrows

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