Estradiol reduces cytochrome c translocation and minimizes hippocampal damage caused by transient global ischemia in rat

Bagetta, Giacinto; Chiappetta, O; Amantea, Diana; Iannone, Michelangelo; Rotiroti, Domenicantonio; Costa, Alfredo; Nappi, Giuseppe; Corasaniti, Maria Tiziana

doi:10.1016/j.neulet.2004.06.062

Cited by 51 publications

(43 citation statements)

References 37 publications

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“…Our results also corroborate the findings of many studies that have reported estradiol-mediated neuroprotection in animal models of both focal ischemia (Dubal et al, 1998;Rusa et al, 1999) and global ischemia (Bagetta et al, 2004;Jover et al, 2002;Shughrue and Merchenthaler, 2003;Sudo et al, 1997). Studies of the neuroprotective effects of estradiol using transient global ischemia have typically administered the hormone for multiple weeks prior to the ischemic insult (Gulinello et al, 2006;Jover et al, 2002;Kondo et al, 1997;Miller et al, 2005;Plamondon et al, 2006;Wang et al, 1999).…”

Section: Discussionsupporting

confidence: 89%

Acute pretreatment with estradiol protects against CA1 cell loss and spatial learning impairments resulting from transient global ischemia

Sandstrom

Rowan

2007

Hormones and Behavior

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Estradiol can act to protect against hippocampal damage resulting from transient global ischemia, but little is known about the functional consequences of such neuroprotection. The present study examines whether acute estradiol administered prior to the induction of transient global ischemia protects against hippocampal cell death and deficits in performance on a spatial learning task. Ovariectomized female rats were primed with estradiol benzoate or oil vehicle 48 and 24 hrs prior to experiencing one of three durations of 4-vessel occlusion (0, 5, or 10 min). Performance on the cued and hidden platform versions of the Morris water maze was assessed one week following ischemia. On the cued platform task, neither hormone treatment nor ischemia significantly influenced acquisition. When tested on the hidden platform task, however, oil-treated rats exhibited impairments in spatial learning after either 5 or 10 min of ischemia while estradiol-treated rats showed no impairments after 5 min of ischemia and only mild impairments after 10 min of ischemia. Immediately following behavioral testing, rats were perfused and survival of CA1 pyramidal cells was assessed. Ischemia was associated with the loss of CA1 pyramidal cells but rats that received estradiol prior to ischemia showed less severe damage. Furthermore, the extent of cell loss was correlated with degree of spatial bias expressed on a probe trial following hidden platform training. These findings indicate that acute exposure to estradiol prior to ischemia is both neuroprotective and functionally protective. Keywords estrogen; ischemia; cardiac arrest; hippocampus; neuroprotection; spatial learning; water maze Acute pretreatment with estradiol protects against CA1 cell loss and spatial learning impairments resulting from transient global ischemiaTransient global ischemia leads to the dramatic loss of neurons in the CA1 region of the hippocampus in humans (Horn and Schlote, 1992;Tanabe et al., 1999;Taraszewska et al., 2002), non-human primates (Zola-Morgan et al., 1992), and rodents (Pulsinelli et al., 1982). This neuronal damage can be accompanied by severe impairments in cognition. For example, human survivors of ischemic strokes typically exhibit disruptions in performance on tasks requiring attention, learning and memory (Elwan et al., 1994;Volpe et al., 1986; Address Correspondence to: Noah J. Sandstrom, Department of Psychology, Williams College, 18 Hoxsey Street, Williamstown, MA 01267, Phone: 413-597-4107, Fax: 413-597-2085, E-mail: Noah.Sandstrom@williams.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...

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Section: Discussionsupporting

confidence: 89%

Acute pretreatment with estradiol protects against CA1 cell loss and spatial learning impairments resulting from transient global ischemia

Sandstrom

Rowan

2007

Hormones and Behavior

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“…The increase in neonatal testosterone in response to birth hypoxia is consistent with a possible protective role for this hormone. This suggestion is supported by observations indicating that testosterone may have neuroprotective properties, acting either directly or indirectly through conversion to estradiol via aromatase [37, 38]. …”

Section: Discussionmentioning

confidence: 65%

Global Birth Hypoxia Increases the Neonatal Testosterone Surge in the Rat

Boksa

Zhang

2008

Neuroendocrinology

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Background/Aims: Global birth hypoxia in rats has been shown to produce long-term changes in central nervous system functions, known to be influenced by neonatal testosterone secretion. Birth hypoxia alters levels of several circulating hormones, but it is unknown if it affects neonatal testosterone. Methods: Using a rat model of acute global hypoxia during cesarean section (C-section) birth, this study tested whether birth hypoxia affects neonatal testosterone. We then evaluated whether the observed hypoxia-induced changes in neonatal testosterone may be mediated via N-methyl-D-aspartate (NMDA) receptor activation and/or altered luteinizing hormone (LH), adrenocorticotropic hormone (ACTH) or corticosterone levels. Longer-term effects of birth hypoxia on testosterone-related function were also assessed. Results: Rats born by C-section + 15 min of anoxia had significantly higher plasma testosterone at 2 and 3 h after birth compared to controls born either vaginally or by C-section. Administration of an NMDA receptor antagonist at birth increased neonatal testosterone in both anoxic pups and controls. Pups exposed to birth anoxia under hypothermic conditions also showed increased neonatal testosterone. Circulating LH, follicle-stimulating hormone and corticosterone in neonates, and testosterone at adulthood were unaffected by birth hypoxia. However, plasma ACTH was significantly increased in anoxic neonates at 2 h after birth. Birth condition had no effect on anogenital distance or juvenile play behavior. Conclusion: It is concluded that birth hypoxia augments plasma testosterone during the critical period of the neonatal testosterone surge, by a mechanism that is independent of NMDA-mediated LH secretion, but may involve increased circulating ACTH.

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“…The present study demonstrated the therapeutic action of estrogen on the bio-psycho-social onset of PSD. Previous studies have reported that estrogen regulates the cell cycle at the G1/S transition, boosts neurogenesis following ER activation (36), and promotes B-cell lymphoma 2 expression and a decrease in apoptosis (37,38). The inflammatory reaction following stroke causes expansive damage in the brain (39), …”

Section: Discussionmentioning

confidence: 99%

Estrogen therapy increases BDNF expression and improves post-stroke depression in ovariectomy-treated rats

Cheng

Jin

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. The present study investigated the effect of exogenous estrogen on post-stroke depression. Rats were exposed to chronic mild stress following middle cerebral artery occlusion. The occurrence of post-stroke depression was evaluated according to the changes in preference for sucrose and performance in a forced swimming test. Estrogen therapy significantly improved these neurological symptoms, indicating that estrogen is effective in treating post-stroke depression. Increased brain-derived neurotrophic factor (BDNF) expression was reported in the hippocampus of rats that had been treated with estrogen for two weeks, suggesting that BDNF expression may be an important contributor to the improvement of post-stroke depression that is observed following estrogen therapy. IntroductionDepression is a common complication of stroke, occurring in ~33% of patients (1,2); the clinical symptoms of this include feelings of guilt, low self-esteem, reduction in food intake, sleep disorders and fatigue. There are between 1.6-2.0 million new stroke patients in China every year and post-stroke depression (PSD) is closely associated with the increased risk of mortality following a stroke (3). PSD negatively impacts upon subsequent rehabilitation; in a previous study by Sinyor et al, PSD patients demonstrated greater functional impairment than patients without depression, also scoring lower on behavioral action and functional status (4). The severity of depression is closely associated with health-associated quality of life and functional recovery in stroke survivors (5). PSD patients demonstrate a negative mood during rehabilitation and achieve poorer outcomes during functional recovery therapy. These patients also have greater difficulty in restoring social activities (6). Several studies have described a higher mortality rate in stroke patients with depression (7), and certain studies have reported that PSD patients using antidepressant drugs demonstrate improved ability to function than those without antidepressant therapy. The treatment of depression has been demonstrated to aid functional recovery (8), meaning that the early diagnosis and effective treatment of PSD are crucial to recovery from a stroke.Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family, which regulates neurogenesis (9), apoptosis (10), the expression level of monoamine transmitters (11), and the function and plasticity of synapses (12). Neurotrophins may be key in the development of depression (13); BDNF, for instance, can activate intracellular mitogen-activated protein kinase/extracellular signal-regulated kinase cascade signaling pathways (14), affecting synaptic plasticity (12) and alleviating the symptoms of depression (15), and BDNF may thus be important in the maintenance of emotional stability. Deletion of the BDNF receptor induces a reduction in neurogenesis and increases anxious behavior (16). Additionally, BDNF expression is associated with 5-hydroxytryptamine receptor expression in the brain, particularly the hi...

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Estradiol reduces cytochrome c translocation and minimizes hippocampal damage caused by transient global ischemia in rat

Cited by 51 publications

References 37 publications

Acute pretreatment with estradiol protects against CA1 cell loss and spatial learning impairments resulting from transient global ischemia

Acute pretreatment with estradiol protects against CA1 cell loss and spatial learning impairments resulting from transient global ischemia

Global Birth Hypoxia Increases the Neonatal Testosterone Surge in the Rat

Estrogen therapy increases BDNF expression and improves post-stroke depression in ovariectomy-treated rats

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