Effects of 17β-estradiol on chemically induced long-term depression

Shiroma, S.; Yamaguchi, Tsutomu; Kometani, Kaoru

doi:10.1016/j.neuropharm.2005.02.002

Cited by 18 publications

(20 citation statements)

References 26 publications

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“…Mechanisms for estrogen modulation of LTD and memory consolidation E 2 has been previously shown to enhance mGluR-LTD in CA1 through activation of classical ERs (Shiroma et al, 2005). Consistent with these findings, G1 was unable to induce Arc synthesis or GluA1 internalization in this area, and hence it is unlikely that GPER1 is involved in these effects.…”

Section: Role Of the Ups In Mglur-ltdsupporting

confidence: 61%

“…Although the mechanisms by which E 2 regulates synaptic plasticity in CA1 have been extensively studied, less attention has been paid to its effects in other hippocampal areas, such as CA3 or dentate gyrus (DG). Likewise, E 2 modulates different forms of longterm depression (LTD) in hippocampus (Shiroma et al, 2005;Mukai et al, 2007;Murakami et al, 2015), but the underlying mechanism remains largely unknown.…”

Section: Introductionmentioning

confidence: 99%

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A novel form of synaptic plasticity in field CA3 of hippocampus requires GPER1 activation and BDNF release

Briz¹,

Liu²,

Zhu³

et al. 2015

J Exp Med

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Section: Role Of the Ups In Mglur-ltdsupporting

confidence: 61%

Section: Introductionmentioning

confidence: 99%

A novel form of synaptic plasticity in field CA3 of hippocampus requires GPER1 activation and BDNF release

Briz¹,

Liu²,

Zhu³

et al. 2015

J Exp Med

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“…The effects of E 2 on LTD in ovariectomized females required NMDA receptors and depended on conditioning frequency, as 2-or 4-Hz pairedpulse conditioning facilitated LTD induction, whereas 10-Hz conditioning blocked LTD induction (Zamani et al 2000). These data have been interpreted to suggest that E 2 decreases the threshold for inducing LTD in adult females by activating group I mGlu receptors (Zamani et al 2000;Shiroma et al 2005). Similarly, 30 min of E 2 pretreatment enhanced NMDA-induced LTD in CA1, CA3, and the dentate gyrus of adult male rats (Mukai et al 2007;Murakami et al 2014).…”

Section: Synaptic Plasticitymentioning

confidence: 95%

“…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%

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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“…Both facilitation and inhibition of synaptic transmission in various brain regions have been observed after application of E 2 (for review, see Woolley, 1999 andKelly et al, 2003). Some studies seem to indicate that the effect of estradiol on synaptic transmission within central nervous system nuclei is predominantly excitatory (Wong and Moss, 1992;Rudick and Woolley, 2003;Shiroma et al, 2005). However, in a previous study (Fatehi et al, 2006), we provided evidence that E 2 at a much higher concentrations (10-100 mM) attenuated excitatory neurotransmission in the parabrachial nucleus of male rats.…”

Section: Facilitation Of Excitatory Neurotransmissionmentioning

confidence: 64%

Effects of 17β-Estradiol on Neuronal Cell Excitability and Neurotransmission in the Suprachiasmatic Nucleus of Rat

Fatehi

Fatehi‐Hassanabad

2007

Neuropsychopharmacol

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17b-Estradiol receptors have been found in several brain nuclei including the suprachiasmatic nucleus (SCN) of mammalian species. The SCN is believed to act as brain clock regulating circadian and circannual biological rhythms, such as body temperature, sleep, and mood. Here, we examined whether 17b-estradiol (E 2 ) could affect cell excitability and synaptic transmission in the SCN. Bath application of E 2 (0.03-3 mM) increased the spontaneous firing frequency and depolarized cell membrane of the SCN neurons significantly. Furthermore, E 2 (0.03-3 mM) increased (by about 25-150% of control) frequency of the miniature excitatory postsynaptic currents. Amplitude of the evoked excitatory postsynaptic currents was enhanced (by about 32% of control) after exposure to 1 mM E 2 . The paired-pulse ratio was reduced by E 2 . These effects were prevented by the estrogen receptor antagonist, ICI 182780. Exposure to the biologically inactive 17a-estradiol did not cause any significant changes in the parameters mentioned above. These findings are in favor of an implication of estrogen in modulation of neuronal activity in SCN and possibly regulating circadian rhythms.

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Effects of 17β-estradiol on chemically induced long-term depression

Cited by 18 publications

References 26 publications

A novel form of synaptic plasticity in field CA3 of hippocampus requires GPER1 activation and BDNF release

A novel form of synaptic plasticity in field CA3 of hippocampus requires GPER1 activation and BDNF release

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

Effects of 17β-Estradiol on Neuronal Cell Excitability and Neurotransmission in the Suprachiasmatic Nucleus of Rat

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