17-β Estradiol rapidly enhances extracellular signal-regulated kinase 2 phosphorylation in the rat brain

Bryant, Damani N.; Bosch, Martha A.; Rønnekleiv, Online K.; Dorsa, Daniel M.

doi:10.1016/j.neuroscience.2005.02.024

Cited by 59 publications

(36 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similar stereo-specificity for the modulatory actions of estradiol has been observed in several other studies (eg Li and Hay, 2000;Bryant et al, 2005;Fatehi et al, 2005). This means that the biologically active form of the hormone is capable of controlling or regulating of such vital responses in the neuronal networks.…”

Section: Involvement Of Estrogen Receptors and Stereo-specificity Of supporting

confidence: 82%

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

Fatehi

Fatehi‐Hassanabad

2007

Neuropsychopharmacol

View full text Add to dashboard Cite

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.

show abstract

Section: Involvement Of Estrogen Receptors and Stereo-specificity Of supporting

confidence: 82%

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

Fatehi

Fatehi‐Hassanabad

2007

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…Like αCaMKII, all three are involved in neuronal differentiation and neurite outgrowth, and ERK1/2 and CREB have also been shown to play a role in LTP and memory processes (Trifilieff, 2006). E2 action has previously been linked to ERK1/2 and CREB phosphorylation in various populations of neurons and in vivo (Lee, 2004;Bryant, 2005;Szego, 2006), and we have provided evidence that αCaMKII action mediates their phosphorylation stimulated by E2 in NLT neurons and primary hippocampal neurons. CREB can be directly phosphorylated by αCaMKII (Wu, 2001), although in our studies it appears that CREB is indirectly affected by αCaMKII-mediated ERK1/2 activity since its phosphorylation by E2 was blocked by U0126 pre-treatment.…”

supporting

confidence: 53%

Leg Muscle Usage Effects on Tibial Elasticity During Running

Antich¹

2006

View full text Add to dashboard Cite

Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. (From -To) REPORT DATE (DD-MM-YYYY) 01-03-2008 REPORT TYPE Annual Summary DATES COVERED SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited SUPPLEMENTARY NOTES ABSTRACT:The ER modulates various signaling cascades involved in the survival and differentiation of a wide range of tissues, both reproductive and nonreproductive. In our studies, we confirmed that 17ß-estradiol (E2) and other ER-specific ligands rapidly phosphorylate ERK1/2 in breast cancer and neuronal cell lines. Subsequently, we found that E2 rapidly stimulates aCaMKII autophosphorylation in immortalized GnRH neurons and primary hippocampal neurons in a calmodulin and Ca2+ influx-dependent manner. Interestingly, ERa associates with aCaMKII and their interaction attenuates the positive effect of E2 on aCaMKII autophosphorylation, suggesting that ERa plays a complex role in modulating aCaMKII activity. However, it appears that the activating signal of E2 is dominant since there is a clear, positive downstream response to E2-activated aCaMKII; pharmacological inhibitors and RNAi technology demonstrated ERa-mediated aCaMKII signaling targets ERK1/2, CREB, and MAP2 for phosphorylation. In vivo, E2 or PPT administration to ovariectomized female rats significantly enhances aCaMKII activity in the hippocampus after 1 hr or 24 hr of exposure. Additionally, E2 administration induces ERK1/2 phosphorylation in vivo in the uterine horn and brain extracts. Functionally, E2-induced aCaMKII signaling influences neurite outgrowth of primary hippocampal neurons. Our findings suggest a novel model for the modulation of aCaMKII signaling by ERa, which provides a molecular link as to how E2 might influence brain function. Ultimately, the characterization of this signaling pathway could be exploited to create new selective estrogen receptor modulators that enhance cognitive function in postmenopausal women without affecting breast tissue or increasing the risk of developing breast cancer.

show abstract

“…Furthermore, examining the effects of ER AS-ODN treatment to vehicleadministered ovx rats would provide additional information about the importance of ER function for these behavioral effects. Indeed, the downstream effectors of ERs, which may be membrane-bound and/or have membrane actions that potentiate intracellular events, such as extracellular regulated kinase/mitogen-activated protein kinase, need to be elucidated (Wade and Dorsa, 2003;Bryant et al, 2005;Vasudevan et al, 2001Vasudevan et al, , 2005Mhyre and Dorsa, 2006). In the future, it would be important to address these points.…”

Section: Discussionmentioning

confidence: 99%

Antisense Oligodeoxynucleotides for Estrogen Receptor-β and α Attenuate Estradiol's Modulation of Affective and Sexual Behavior, Respectively

Walf

Ciriza

Garcia-Segura

et al. 2007

Neuropsychopharmacol

View full text Add to dashboard Cite

Estradiol (E 2 ) modulates affective and socio-sexual behavior of female rodents. E 2 's functional effects may involve actions through a and b isoforms of estrogen receptor (ERs). The importance of E 2 's actions at these isoforms for anxiety (open field, elevated plus maze), depression (forced swim test), and sexual behavior (lordosis) was investigated using an antisense oligonucleotide (AS-ODN) strategy. If ERb is required for anti-anxiety and antidepressant-like effects, and ERa is required for sexual receptivity, of E 2 , then intracerebroventricular administration of AS-ODNs against these ERs should attenuate these effects and reduce immunoreactivity of ERs in brain regions that mediate these behaviors, such as the hippocampus and ventral medial hypothalamus (VMH). Ovariectomized rats were primed with 17b-E 2 (10 mg) 48 h before testing (hour 0). At hours 0, 24, and 47.5, rats were infused with saline vehicle, scrambled control AS-ODNs, or AS-ODNs targeted against ERa and/or ERb, and were tested at hour 48. Rats infused with ERb AS-ODNs, alone, or with ERa AS-ODNs had significantly decreased open field central entries, decreased plus maze open arm time and entries, increased time spent immobile, and decreased time spent swimming in the forced swim test, and decreased ERb immunoreactivity in the brain than did rats administered ERa AS-ODNs, vehicle, or scrambled AS-ODNs. Rats that were administered ERa AS-ODNs, alone, or with ERb AS-ODNs had significantly decreased lordosis and decreased ERa immunoreactivity in the brain compared to rats administered ERb AS-ODNs, vehicle, or scrambled AS-ODNs. Thus, ERb and ERa may be required for E 2 's modulation of affective and sexual behavior, respectively.

show abstract

17-β Estradiol rapidly enhances extracellular signal-regulated kinase 2 phosphorylation in the rat brain

Cited by 59 publications

References 50 publications

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

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

Leg Muscle Usage Effects on Tibial Elasticity During Running

Antisense Oligodeoxynucleotides for Estrogen Receptor-β and α Attenuate Estradiol's Modulation of Affective and Sexual Behavior, Respectively

Contact Info

Product

Resources

About