Estrogenic stimulation of neurite growth in midbrain dopaminergic neurons depends on cAMP/protein kinase A signalling

Beyer, Cordian; Karolczak, Magdalena

doi:10.1002/(sici)1097-4547(20000101)59:1<107::aid-jnr13>3.0.co;2-w

Cited by 121 publications

(53 citation statements)

References 74 publications

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“…The authors observed a 33-48% abolition of anti-apoptotic effects with PD98059 [21]; therefore the response was in part MEK 1-dependent. Also, Beyer and Karolczak demonstrated the role of membraneassociated estrogen action in dendritic growth involving phosphorylation of the cyclic AMPresponsive nuclear factor, cAMP-response element binding protein (CREB) [47]. In addition, nontranscriptional pathways have been suggested to be important for cell growth [48].…”

Section: Is There a Novel Membrane-based Estrogen Receptor?mentioning

confidence: 99%

“…This difference argues for the existence of an unidentified estrogen-binding factor, because both ERα and ERβ are sensitive to ICI 182 780, which blocks both AF-1 and AF-2-mediated responses. Membrane-based estrogen signaling has been shown to trigger distinct signaling cascades involving cAMP [49], release of intracellular Ca 2+ stores [47], Ca 2+ fluxes [50], MAPK [30] and phosphorylation of CREB [51]. The compelling demonstration of immediate membrane-based responses, albeit involving diverse second messenger cascades, raises the possibility that estrogen might pass through the outer cell membrane by a process of facilitated transfer using a distinct carrier system.…”

Section: Is There a Novel Membrane-based Estrogen Receptor?mentioning

confidence: 99%

See 1 more Smart Citation

Estrogen action and cytoplasmic signaling cascades. Part I: membrane-associated signaling complexes

Segars

Driggers

2002

Trends in Endocrinology & Metabolism

168

102

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Remarkable progress in recent years has suggested that estrogen action in vivo is complex and often involves activation of cytoplasmic signaling cascades in addition to genomic actions mediated directly through estrogen receptors α and β. Rather than a linear response mediated solely through estrogen-responsive DNA elements, in vivo estrogen might simultaneously activate distinct signaling cascades that function as networks to coordinate tissue responses to estrogen. This complex signaling system provides for exquisite control and plasticity of response to estrogen at the tissue level, and undoubtedly contributes to the remarkable tissue-specific responses to estrogens. In part I of this series, we summarize cytoplasmic signaling modules involving estrogen or estrogen receptors, with particular focus on recently described membrane-associated signaling complexes.Knowledge of the molecular mechanism of estrogen action has evolved rapidly during the past two decades. It is now accepted that two proteins serve as receptors for 17β estradiol (E 2 ), estrogen receptors α and β (ERα, ERβ). These receptors function as ligand-dependent transcription factors to increase gene transcription from promoters by direct binding of the receptor to specific DNA target sequences, designated estrogen response elements (EREs). Association of receptors with the gene transcription machinery involves essential coregulatory proteins that contribute to estrogen action and that can enhance or repress ER action (see Refs [1][2][3]). The importance of this signaling pathway in vivo has been substantiated using several approaches, including targeted gene disruption (knockout) in mice [4][5][6][7][8]. Within the ER proteins, there are two activating functions corresponding to the N-terminus (AF-1) or ligand-binding region (AF-2) of the molecule [9] (and Refs therein). In addition, ER function is modified by its phosphorylation [10,11]. The genomic actions of E 2 proceeding through augmentation or repression of ERE-containing promoters by ERs α and β have been designated the classic pathway of estrogen action [12]. In addition, ER acts through AP-1 and SP-1 to affect transcription.* segarsj@mail.nih.gov. In spite of the clarity with which the ER has been shown to act as a transcription factor, it has been apparent for several years that not all physiological effects of E 2 are accomplished through a direct effect on gene transcription [13]. Definition of the classic estrogen-signaling pathway highlighted the fact that, in many instances, another signaling pathway(s) involving cytoplasmic proteins, growth factors and/or membrane-initiated responses contributed to estrogen action (reviewed in Refs [14][15][16][17][18]). In Part I of this review, we focus on membraneassociated estrogen action, particularly cellular responses observed within minutes of estrogen exposure. Part II (to be published in the December issue of TEM) covers cytoplasmic cascades initiated by growth factors, and involvement of the ER in second messenger signaling casc...

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Section: Is There a Novel Membrane-based Estrogen Receptor?mentioning

confidence: 99%

Section: Is There a Novel Membrane-based Estrogen Receptor?mentioning

confidence: 99%

Estrogen action and cytoplasmic signaling cascades. Part I: membrane-associated signaling complexes

Segars

Driggers

2002

Trends in Endocrinology & Metabolism

168

102

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“…Shingo and Kito (2005), demonstrated that 17β-estradiol (E 2 ) conjugated to bovine serum albumin (BSA), a molecule that cannot penetrate the cell membrane, activated PKA 45 seconds after bath application, in vitro. A role for PKA in E 2 -induced differentiation in dopaminergic neurons, and in cerebellar granule cells, has also been reported (Belcher, Le, Spurling, & Wong, 2005;Beyer & Karolczak, 2000). To date, no published studies have examined the involvement of PKA in the effects of E 2 on hippocampal-dependent memory.…”

mentioning

confidence: 92%

Estradiol-induced enhancement of object memory consolidation involves NMDA receptors and protein kinase A in the dorsal hippocampus of female C57BL/6 mice.

Lewis¹,

Kerr²,

Orr³

et al. 2008

Behavioral Neuroscience

137

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This study examined the role of dorsal hippocampal NMDA receptors and PKA activation in 17β-estradiol (E 2 )-induced enhancement of object memory consolidation. Mice explored two identical objects during training, after which they immediately received intraperitoneal injections of 0.2 mg/ kg E 2 , and bilateral dorsal hippocampal infusions of Vehicle, the NMDA receptor antagonist APV (2.5 μg/side), or the cAMP inhibitor Rp-cAMPS (18.0 μg/side). Retention was tested 48 hours later. The enhanced object memory and increased ERK phosphorylation observed with E 2 alone was reduced by APV and Rp-cAMPS, suggesting that estrogenic enhancement of object memory involves NMDA receptors and PKA activation within the dorsal hippocampus.

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“…Studies have further identified how estrogen acts on the dopamine system. Estrogen modulates the development of dopaminergic neurons and neurotransmission (Bourque, 147 2009) by promoting neurite plasticity (Beyer et al, 2000). These effects are either mediated through a direct action on dopaminergic neurons or interactions with local astroglia (Ivanova et al, 2001(Ivanova et al, , 2002.…”

Section: Dopamine Neurotransmissionmentioning

confidence: 99%

Estrogen and Brain Protection

Ju¹,

Metzger²,

Jung³

2012

Sex Steroids

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Estrogenic stimulation of neurite growth in midbrain dopaminergic neurons depends on cAMP/protein kinase A signalling

Cited by 121 publications

References 74 publications

Estrogen action and cytoplasmic signaling cascades. Part I: membrane-associated signaling complexes

Estrogen action and cytoplasmic signaling cascades. Part I: membrane-associated signaling complexes

Estradiol-induced enhancement of object memory consolidation involves NMDA receptors and protein kinase A in the dorsal hippocampus of female C57BL/6 mice.

Estrogen and Brain Protection

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