17β estradiol recruits GluN2B-containing NMDARs and ERK during induction of long-term potentiation at temporoammonic-CA1 synapses

Smith, Caroline C.; Smith, Lindsey A.; Bredemann, Teruko M.; McMahon, Lori L.

doi:10.1002/hipo.22495

Cited by 27 publications

(32 citation statements)

References 51 publications

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“…We also observed that TA-CA1 LTP magnitude was not different between female rats in the two different stages of the menstrual cycle. These results are consistent with a recent study from Smith et al that estradiol administration to ovariectomized female rats increased both AMPA and NMDA receptor-mediated currents, but did not increase LTP magnitude, at TA-CA1 synapses [62]. In sum, our results indicate that reduced LLTP expression at TA-CA1 synapses in female rats is likely not attributable to varying estrogen levels across the estrus cycle.…”

Section: Discussionsupporting

confidence: 93%

Sex Differences in Long-Term Potentiation at Temporoammonic-CA1 Synapses: Potential Implications for Memory Consolidation

Zhang

et al. 2016

PLoS ONE

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Sex differences in spatial memory have long been observed in humans, non-human primates and rodents, but the underlying cellular and molecular mechanisms responsible for these differences remain obscure. In the present study we found that adolescent male rats outperformed female rats in 7 d and 28 d retention probes, but not in learning trials and immediate probes, in the Morris water maze task. Male rats also had larger long-term potentiation (LTP) at hippocampal temproammonic-CA1 (TA-CA1) synapses, which have been implicated to play a key role in place field and memory consolidation, when protocols designed to elicit late-stage LTP (LLTP) were used. Interestingly, the ratio of evoked AMPA/NMDA currents was found to be smaller at TA-CA1 synapses in male rats compared to female rats. Protein biotinylation experiments showed that male rats expressed more surface GluN1 receptors in hippocampal CA1 stratum lacunosum-moleculare (SLM) than female rats, although GluA1 expression was also slightly higher in male rats. Taken together, our results suggest that differences in the expression of AMPA and NMDA receptors may affect LTP expression at TA-CA1 synapses in adolescent male and female rats, and thus possibly contribute to the observed sex difference in spatial memory.

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Section: Discussionsupporting

confidence: 93%

Sex Differences in Long-Term Potentiation at Temporoammonic-CA1 Synapses: Potential Implications for Memory Consolidation

Zhang

et al. 2016

PLoS ONE

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“…Both are associated with dual effects of estrogen on NRs depending on the status of glutamatergic neurotransmission. That is, estrogen inhibits NRs upon excitotoxic assaults (Garcia-Segura, Azcoitia, & DonCarlos, 2001;Heron & Daya, 2001;Hilton et al, 2006;Snyder et al, 2011;Spampinato et al, 2012;Weaver et al, 1997), but reverses hypoactivity of NRs (Foy et al, 1999;Lewis et al, 2008;Smith & McMahon, 2006;Smith, Vedder, & McMahon, 2009;Smith et al, 2016;Snyder et al, 2011;Zamani, Desmond, & Levy, 2000). The evidence indicates that NR2 subunits are the major targets through which estrogen confers neuroprotection and synaptic potentiation.…”

Section: Discussionmentioning

confidence: 99%

“…For instance, E2 dramatically reduces brain infarction volume after stroke (Groger & Plesnila, 2014), and through inhibiting NMDA receptors, it attenuates death of hippocampal neurons caused by quinolinic acid (Heron & Daya, 2001), NMDA (Park-Chung, Gibbs, & Farb, 1997), and glutamate (Hilton, Nunez, Bambrick, Thompson, & McCarthy, 2006). In addition to neuroprotection, E2 promotes recovery of neurological function from stroke (Groger & Plesnila, 2014), and reverses malfunction in synaptic plasticity by modulating NMDA receptors (Galvin & Ninan, 2014;Smith, Smith, Bredemann, & McMahon, 2016;Smith & McMahon, 2006;Snyder, Cooke, & Woolley, 2011). Therefore, we hypothesized that E2 might have therapeutic potential for TBI in both neuroprotection and recovery of neurological function.…”

mentioning

confidence: 99%

17β‐estradiol rescues damages following traumatic brain injury from molecule to behavior in mice

Jin

et al. 2017

Journal Cellular Physiology

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Traumatic brain injury (TBI) is a public health concern, and causes cognitive dysfunction, emotional disorders, and neurodegeration, as well. The currently available treatments are all symptom-oriented with unsatifying efficacy. It is highly demanded to understand its underlying mechanisms. Controlled cortical impact (CCI) was used to induce TBI in aged female mice subjected to ovariectomy. Brain damages were assessed with neurological severity score, brain infarction and edema. Morris water maze and elevated plus maze were applied to evaluate the levels of anxiety. Apoptosis in the hippocampus was assayed with Fluoro-Jade B staining and TUNEL staining. Western blot was employed to measure the expression of NMDA receptor subunits and phosphorylation of ERK1/2, and biochemical assays were used to estimate oxidative stress. 17beta-Estradiol (E2) was intraperitoneally administered at 10-80 μg/kg once per day for 7 consecutive days before or after CCI. Chronic administration of E2 both before and immediately after CCI conferred neuroprotection, reducing neurological severity score, brain infarction, and edema in TBI mice. Additionally, E2 improved many aspects of deleterious effects of TBI on the hippocampus, including neuronal apoptosis, dysfunction in spatial memory, reduction in NR2B, enhancement of oxidative stress, and activation of ERK1/2 pathway. The present study provides clue for the notion that E2 has therapeutic potential for both prevention and intervention of TBI-induced brain damages.

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“…(TA-CA1) neurons (Smith et al, 2016), however the contribution of GPER1 to this effect of E2 is not known.…”

Section: Activation Of Erβ But Not Erα Is Reported To Mediate the Fmentioning

confidence: 99%

Emerging roles for the novel estrogen-sensing receptor GPER1 in the CNS

2017

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Keywords: G protein coupled estrogen receptor, hippocampal synaptic function; receptor trafficking; learning and memory; neuroprotection; synaptic plasticity. Estrogens play a key role in regulating reproductive and neuroendocrine function by activating classical nuclear steroid receptors that act as ligand gated transcription factors.However evidence is growing that estrogens also promote rapid non-genomic responses via activation of membrane-associated estrogen receptors. The G protein-coupled estrogen receptor (GPER1; also known as GPR30) has been identified as one of the main estrogensensitive receptors responsible for the rapid non-genomic actions of estrogen. In recent years, our understanding of the CNS actions of GPER1s has significantly increased following the development of selective pharmacological tools and via the use of transgenic technologies to knockout GPER1 in mice. Here we review recent advances that have been made to uncover the role of GPER1s in the CNS.Introduction.

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17β estradiol recruits GluN2B-containing NMDARs and ERK during induction of long-term potentiation at temporoammonic-CA1 synapses

Cited by 27 publications

References 51 publications

Sex Differences in Long-Term Potentiation at Temporoammonic-CA1 Synapses: Potential Implications for Memory Consolidation

Sex Differences in Long-Term Potentiation at Temporoammonic-CA1 Synapses: Potential Implications for Memory Consolidation

17β‐estradiol rescues damages following traumatic brain injury from molecule to behavior in mice

Emerging roles for the novel estrogen-sensing receptor GPER1 in the CNS

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