17β-estradiol suppresses expression of long-term depression in aged rats

Vouimba, Rose-Marie; Foy, Michael R.; Foy, Judith G.; Thompson, Richard F.

doi:10.1016/s0361-9230(00)00377-4

Cited by 68 publications

(50 citation statements)

References 35 publications

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“…E2 also improves other forms of memory formation such as spatial reference memory and trace conditioning controlled by the hippocampus and forms of visual memory and strategy solving tasks controlled by the cerebral cortex (Frick et al, 2002;Luine et al, 2003;Leuner et al, 2004;Rhodes and Frye, 2004). In the hippocampus, E2 has also been shown to facilitate the formation of new synapses (Woolley and McEwen, 1993) and to exert a positive impact on induction of LTP (Cordoba Montoya and Carrer, 1997;Good et al, 1999;Vouimba et al, 2000). Thus, although short-term potentiating mechanisms such as those mediated by levels of calcium concentration and activation of kinases and phosphatases can vary substantially between hippocampal and cerebellar learning (Cordoba Montoya and Carrer, 1997;Good et al, 1999;Vouimba et al, 2000), sex hormone-related mechanisms appear to be able to overrule these differences and exert general effects in different brain regions.…”

Section: Discussionmentioning

confidence: 99%

“…The gonadal hormone estradiol (E2) has beneficial effects on the formation of hippocampus-dependent memory (Farr et al, 1995;O'Neal et al, 1996;Gibbs et al, 1998;Shors et al, 1998;Leuner et al, 2004;Rhodes and Frye, 2004). During the estrous cycle, pyramidal cells in the hippocampus are subject to major changes including morphological changes (Woolley and McEwen, 1993;Adams et al, 2001) and modifications in synaptic efficacy (Warren et al, 1995;Cordoba Montoya and Carrer, 1997;Good et al, 1999;Vouimba et al, 2000;Mukai et al, 2007). Yet, it is not known whether E2 also affects cerebellar memory formation, despite the prominent presence of estrogen receptors (ERs) in the cerebellum (Shughrue et al, 1997;Price and Handa, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Estradiol Improves Cerebellar Memory Formation by Activating Estrogen Receptor β

Andreescu¹,

Milojkovic²,

Haasdijk³

et al. 2007

J. Neurosci.

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Learning motor skills is critical for motor abilities such as driving a car or playing piano. The speed at which we learn those skills is subject to many factors. Yet, it is not known to what extent gonadal hormones can affect the achievement of accurate movements in time and space. Here we demonstrate via different lines of evidence that estradiol promotes plasticity in the cerebellar cortex underlying motor learning. First, we show that estradiol enhances induction of long-term potentiation at the parallel fiber to Purkinje cell synapse, whereas it does not affect long-term depression; second, we show that estradiol activation of estrogen receptor ␤ receptors in Purkinje cells significantly improves gain-decrease adaptation of the vestibulo-ocular reflex, whereas it does not affect general eye movement performance; and third, we show that estradiol increases the density of parallel fiber to Purkinje cell synapses, whereas it does not affect the density of climbing fiber synapses. We conclude that estradiol can improve motor skills by potentiating cerebellar plasticity and synapse formation. These processes may be advantageous during periods of high estradiol levels of the estrous cycle or pregnancy.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Estradiol Improves Cerebellar Memory Formation by Activating Estrogen Receptor β

Andreescu¹,

Milojkovic²,

Haasdijk³

et al. 2007

J. Neurosci.

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“…However, not all studies find that E 2 facilitates LTD in male and female rodents. In hippocampal slices pretreated with E 2 for at least 30 min, the induction of LTD by patterned stimulation was unaltered in gonadally intact male rats (Vouimba et al 2000) and blocked by E 2 in young ovariectomized rats (Sharrow et al 2002). It has been suggested that the inconsistency between these studies and those showing that E 2 enhances LTP may result from differential influences of discrepant E 2 treatments on intracellular calcium or on activation of classical and nonclassical ER mechanisms (Sharrow et al 2002;Shiroma et al 2005;Foy et al 2008).…”

Section: Synaptic Plasticitymentioning

confidence: 99%

“…For example, chronic E 2 treatment blocked the induction of LTD induced by patterned stimulation in hippocampal slices from aged ovariectomized rats that had undergone extensive behavioral testing (Foster et al 2003). Similarly, 30 min of E 2 suppressed LTD induced by patterned stimulation in hippocampal slices from aged males (Vouimba et al 2000;Foy et al 2008). Enhanced LTD in aged rats is thought to play a role in age-related memory decline (Norris et al 1996;Foster 1999), and E 2 is an important trophic factor that protects against such decline (Frick 2009).…”

Section: Synaptic Plasticitymentioning

confidence: 99%

Sex steroid hormones matter for learning and memory: estrogenic regulation of hippocampal function in male and female rodents

et al. 2015

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Ample evidence has demonstrated that sex steroid hormones, such as the potent estrogen 17b-estradiol (E 2 ), affect hippocampal morphology, plasticity, and memory in male and female rodents. Yet relatively few investigators who work with male subjects consider the effects of these hormones on learning and memory. This review describes the effects of E 2 on hippocampal spinogenesis, neurogenesis, physiology, and memory, with particular attention paid to the effects of E 2 in male rodents. The estrogen receptors, cell-signaling pathways, and epigenetic processes necessary for E 2 to enhance memory in female rodents are also discussed in detail. Finally, practical considerations for working with female rodents are described for those investigators thinking of adding females to their experimental designs.Hormones have long been known to play key roles in regulating learning and memory. Many hormones, including epinephrine, glucocorticoids, and insulin influence learning and memory via inverted U-shaped dose-response relationships in which memory is enhanced by moderate, but not low or high, hormone levels (Roozendaal 2000;Korol and Gold 2007;McNay and Recknagel 2011). Research from the past two decades has demonstrated that sex steroid hormones, particularly the potent estrogen 17b-estradiol (E 2 ), also regulate learning and memory in male and female rodents via an inverted U-shaped dose-response function that is influenced by estrogen receptor expression (Packard and Teather 1997a;Packard 1998;Foster 2012). Yet E 2 has not gained widespread acceptance as a hormonal modulator of memory in both females and males, perhaps because the majority of this research has been conducted in female rodents. Moreover, the common view of E 2 as a "female" hormone may contribute to the misperception that E 2 is not relevant for cognitive function in males. However, considerable evidence supports a vital role for E 2 in mediating neural function and behavior in male rodents. Therefore, it is important for investigators working with males to understand the ways in which E 2 and other sex steroid hormones (e.g., androgens, progestins, and other estrogens) may influence their brain regions and behaviors of interest.Another reason for investigators to be cognizant of sex steroid hormone-induced regulation of learning and memory is that males and females may respond differently to various treatments and environmental factors. A classic example is that of acute stress, which enhances classical conditioning and increases apical CA1 dendritic spine density in male rats, but impairs classical conditioning and decreases CA1 spine density in female rats (Wood and Shors 1998;Shors et al. 2001). Therefore, investigators hoping to comply with National Institutes of Health policies that encourage the inclusion of females in biomedical research must be aware that adding females to a study is not as simple as adding another group. In some ways, females are fundamentally different from males, the most obvious of which is the presence of reproductive...

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“…lower stimulus frequencies or fewer stimulus pulses) (for review see 4,6,16 ). Also, some labs, including ours, have observed increased susceptibility to LTD induction in aged rats 2,[17][18][19] , while other groups have found no difference or reduced susceptibility in their aged animals. As discussed briefly below (see Discussion), subtle but critical differences in experimental protocol may account for these discrepancies.…”

Section: Elicit and Record Ca3-ca1 Synaptic Responsesmentioning

confidence: 61%

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Mathis

Furman

Norris

2011

JoVE

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The rodent hippocampal slice preparation is perhaps the most broadly used tool for investigating mammalian synaptic function and plasticity. The hippocampus can be extracted quickly and easily from rats and mice and slices remain viable for hours in oxygenated artificial cerebrospinal fluid. Moreover, basic electrophysisologic techniques are easily applied to the investigation of synaptic function in hippocampal slices and have provided some of the best biomarkers for cognitive impairments. The hippocampal slice is especially popular for the study of synaptic plasticity mechanisms involved in learning and memory. Changes in the induction of long-term potentiation and depression (LTP and LTD) of synaptic efficacy in hippocampal slices (or lack thereof) are frequently used to describe the neurologic phenotype of cognitively-impaired animals and/ or to evaluate the mechanism of action of nootropic compounds. This article outlines the procedures we use for preparing hippocampal slices from rats and transgenic mice for the study of synaptic alterations associated with brain aging and Alzheimer's disease (AD) [1][2][3] . Use of aged rats and AD model mice can present a unique set of challenges to researchers accustomed to using younger rats and/or mice in their research. Aged rats have thicker skulls and tougher connective tissue than younger rats and mice, which can delay brain extraction and/or dissection and consequently negate or exaggerate real age-differences in synaptic function and plasticity. Aging and amyloid pathology may also exacerbate hippocampal damage sustained during the dissection procedure, again complicating any inferences drawn from physiologic assessment. Here, we discuss the steps taken during the dissection procedure to minimize these problems. Examples of synaptic responses acquired in "healthy" and "unhealthy" slices from rats and mice are provided, as well as representative synaptic plasticity experiments. The possible impact of other methodological factors on synaptic function in these animal models (e.g. recording solution components, stimulation parameters) are also discussed. While the focus of this article is on the use of aged rats and transgenic mice, novices to slice physiology should find enough detail here to get started on their own studies, using a variety of rodent models. Video LinkThe video component of this article can be found at https://www.jove.com/video/2330/ Protocol Preparing Ice-cold Oxygenated Artificial Cerebrospinal Fluid (ACSF)1. Prepare 2 L of "Ca 2+ -free" ACSF. In a 2L Erlenmeyer flask, add approximately 1.5 L of sterile or double-distilled H 2 O, and begin stirring vigorously on a stir plate. Add the following ACSF components (in mM): 124 NaCl, 2 KCl, 1.25 KH 2 PO 4 , 2 MgSO 4 , 26 NaHCO 3 , and 10 dextrose (see Table 1). Bring to a volume of 2 L with distilled H 2 O. 2. Using an aquarium bubbler and tubing attached to a 95% O 2 /5% CO 2 air tank, oxygenate ACSF vigorously for approximately 20-30 min.Check the pH, and if necessary, adjust to 7.4 using N...

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17β-estradiol suppresses expression of long-term depression in aged rats

Cited by 68 publications

References 35 publications

Estradiol Improves Cerebellar Memory Formation by Activating Estrogen Receptor β

Estradiol Improves Cerebellar Memory Formation by Activating Estrogen Receptor β

Sex steroid hormones matter for learning and memory: estrogenic regulation of hippocampal function in male and female rodents

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

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