1
40
6
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.psyneuen.2010.12.007" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.psyneuen.2010.12.007</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
955-969
Issue
7
Volume
36
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Title
A name given to the resource
Sex differences in methamphetamine toxicity in mice: Effect on brain dopamine signaling pathways
Publisher
An entity responsible for making the resource available
Psychoneuroendocrinology
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-08
Subject
The topic of the resource
dopamine; mice; Psychiatry; Akt; 3; 2; 1-methyl-4-phenyl-1; Neurosciences & Neurology; Endocrinology & Metabolism; cell-death; activation; neurotoxicity; induced; rat striatum; kinase; striatum; Methamphetamine; evoked striatal dopamine; neurotoxicity; cd-1; element-binding protein; Sex difference; transporter function; 6-tetrahydropyridine mice
Creator
An entity primarily responsible for making the resource
Bourque M; Liu B; Dluzen D E; Di Paolo T
Description
An account of the resource
Mate mice were reported to display greater methamphetamine-induced neurotoxicity than females. The present study evaluated the involvement of phosphatidylinositol-3 kinase (PI3K)/Akt and extracellular signal-regulated kinase (ERK1/2) pathways in this sex-dependent methamphetamine toxicity. Intact female and male mice were administered methamphetamine (20 or 40 mg/kg) and euthanized a week later. Dopamine transporter (DAT) and vesicular monoamine transporter 2 (VMAT2) autoradiography in the lateral striatum showed a greater sensitivity in male mice treated with 20 mg/kg methamphetamine compared to female mice. Striatal dopamine concentration and DAT autoradiography showed a more extensive depletion in male mice given 40 mg/kg methamphetamine compared to female mice. Mice administered 40 mg/kg methamphetamine showed no sex difference in striatal VMAT2 autoradiography. In the substantia nigra, DAT specific binding was decreased only in male mice treated with 40 mg/kg methamphetamine and DAT mRNA levels decreased in methamphetamine-treated female and male mice. Methamphetamine-treated male mice presented a dose-dependent decrease of VMAT2 mRNA levels. Methamphetamine reduced insulin-like growth factor 1 receptor levels in females at both methamphetamine doses tested whereas it elevated G protein-coupled estrogen receptor 1 (GPER1) only in male mice. Phosphorylated Akt levels decreased only in male mice treated with 40 mg/kg methamphetamine. Glycogen synthase kinase 30 levels were reduced in male mice at both methamphetamine doses tested and in females receiving 40 mg/kg. Bcl-2 Levels were increased in male mice treated with methamphetamine, whereas ERK1/2 and BAD levels were unchanged. These results implicate some of the signaling pathways associated with the sex differences in methamphetamine-induced toxicity. (C) 2011 Elsevier Ltd. All rights reserved.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.psyneuen.2010.12.007" target="_blank" rel="noreferrer noopener">10.1016/j.psyneuen.2010.12.007</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
1-Methyl-4-phenyl-1
2
2011
3
6-tetrahydropyridine mice
activation
Akt
Bourque M
cd-1
cell-death
Di Paolo T
Dluzen D E
Dopamine
element-binding protein
Endocrinology & Metabolism
evoked striatal dopamine
Induced
Journal Article or Conference Abstract Publication
Kinase
Liu B
Methamphetamine
Mice
Neurosciences & Neurology
Neurotoxicity
Psychiatry
Psychoneuroendocrinology
rat striatum
Sex difference
striatum
transporter function
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.yfrne.2012.02.003" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.yfrne.2012.02.003</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
169-178
Issue
2
Volume
33
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The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Signaling pathways mediating the neuroprotective effects of sex steroids and SERMs in Parkinson's disease
Publisher
An entity responsible for making the resource available
Frontiers in Neuroendocrinology
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-04
Subject
The topic of the resource
Signaling; Neuroprotection; MPTP; mice; Akt; 3; 2; 1-methyl-4-phenyl-1; 6-tetrahydropyridine; receptor; Neurosciences & Neurology; Endocrinology & Metabolism; nervous-system; plasma-membrane; estrogen-receptor-alpha; er-alpha; gender-differences; rat-brain; striatum; estrogen; ERK; estradiol; growth-factor-i; protein-coupled receptor-30; selective estrogen; SERMs; Substantia nigra
Creator
An entity primarily responsible for making the resource
Bourque M; Dluzen D E; Di Paolo T
Description
An account of the resource
Studies with the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) animal model of Parkinson's disease have shown the ability of 17 beta-estradiol to protect the nigrostriatal dopaminergic system. This paper reviews the signaling pathways mediating the neuroprotective effect of 17 beta-estradiol against MPTP-induced toxicity. The mechanisms of 17 beta-estradiol action implicate activation of signaling pathways such as the phosphatidylinositol-3 kinase/Akt and the mitogen-activated protein kinase pathways. 17 beta-estradiol signaling is complex and integrates multiple interactions with signaling molecules that act to potentiate a protective effect. 17 beta-estradiol signaling is mediated via estrogen receptors, including GPER1, but others receptors, such as the IGF-1 receptor, are implicated in the neuroprotective effect. Glial and neuronal crosstalk is a critical factor in the maintenance of dopamine neuronal survival and in the neuroprotective action of 17 beta-estradiol. Compounds that stimulate GPER1 such as selective estrogen receptor modulators and phytoestrogens show neuroprotective activity and are alternatives to 17 beta-estradiol. (C) 2012 Published by Elsevier Inc.
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An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.yfrne.2012.02.003" target="_blank" rel="noreferrer noopener">10.1016/j.yfrne.2012.02.003</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
1-Methyl-4-phenyl-1
2
2012
3
6-tetrahydropyridine
Akt
Bourque M
Di Paolo T
Dluzen D E
Endocrinology & Metabolism
er-alpha
ERK
estradiol
estrogen
estrogen-receptor-alpha
Frontiers in Neuroendocrinology
gender-differences
growth-factor-i
Journal Article or Conference Abstract Publication
Mice
MPTP
nervous-system
Neuroprotection
Neurosciences & Neurology
plasma-membrane
protein-coupled receptor-30
rat-brain
Receptor
selective estrogen
SERMs
Signaling
striatum
SUBSTANTIA nigra
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.neuropharm.2012.02.009" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.neuropharm.2012.02.009</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
2363-2372
Issue
7
Volume
62
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The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Sex and temporally-dependent effects of methamphetamine toxicity on dopamine markers and signaling pathways
Publisher
An entity responsible for making the resource available
Neuropharmacology
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-06
Subject
The topic of the resource
dopamine; Akt; Neurosciences & Neurology; Pharmacology & Pharmacy; gene-expression; estrous-cycle; striatum; protein-phosphorylation; markers; glycogen-synthase kinase-3-beta; Methamphetamine; Sex difference; evoked striatal dopamine; induced neurotoxicity; monoamine; neuronal apoptosis; neurotoxicity; physiological functions; terminal; transporters
Creator
An entity primarily responsible for making the resource
Bourque M; Dluzen D E; Di Paolo T
Description
An account of the resource
Methamphetamine induces a greater neurodegenerative effect in male versus female mice. In order to investigate this sex difference we studied the involvement of Akt and extracellular signal-regulated kinase (ERK1/2) in methamphetamine toxicity as a function of time post-treatment (30 min, 1 and 3 days). Methamphetamine-induced decreases in dopamine concentrations and dopamine transporter (DAT) specific binding in the medial striatum were similar in female and male mice when evaluated 1 day post-methamphetamine (40 mg/kg). At 3 days post-methamphetamine, striatal dopamine concentration and DAT specific binding continued to decline in males, whereas females showed a recovery with increases in dopamine content and DAT specific binding in medial striatum at day 3 versus day 1 post-methamphetamine. The reduction in striatal vesicular monoamine transporter 2 specific binding observed at 1 and 3 days post-methamphetamine showed neither a sex- nor temporal-dependant effect. Under the present experimental conditions, methamphetamine treatments had modest effects on dopamine markers measured in the substantia nigra. Proteins assessed by Western blots showed similar reductions in both female and male mice for DAT proteins at 1 and 3 days post-methamphetamine. An increase in the phosphorylation of striatal Akt (after 1 day), glycogen synthase kinase 3 beta (at 1 and 3 days) and ERK1/2 (30 min post-methamphetamine) was only observed in females. Striatal glial fibrillary acidic protein levels were augmented in both females and males at 3 days post-methamphetamine. These results reveal some of the sex- and temporally-dependent effects of methamphetamine toxicity on dopaminergic markers and suggest some of the signaling pathways associated with these responses. (C) 2012 Elsevier Ltd. All rights reserved.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.neuropharm.2012.02.009" target="_blank" rel="noreferrer noopener">10.1016/j.neuropharm.2012.02.009</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2012
Akt
Bourque M
Di Paolo T
Dluzen D E
Dopamine
estrous-cycle
evoked striatal dopamine
gene-expression
glycogen-synthase kinase-3-beta
induced neurotoxicity
Journal Article or Conference Abstract Publication
markers
Methamphetamine
monoamine
neuronal apoptosis
Neuropharmacology
Neurosciences & Neurology
Neurotoxicity
Pharmacology & Pharmacy
physiological functions
protein-phosphorylation
Sex difference
striatum
terminal
transporters
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.yfrne.2009.04.014" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.yfrne.2009.04.014</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
142-157
Issue
2
Volume
30
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The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Neuroprotective actions of sex steroids in Parkinson's disease
Publisher
An entity responsible for making the resource available
Frontiers in Neuroendocrinology
Date
A point or period of time associated with an event in the lifecycle of the resource
2009
2009-07
Subject
The topic of the resource
parkinsons-disease; Neuroprotection; MPTP; Akt; Neurosciences & Neurology; Endocrinology & Metabolism; estrogen-receptor-alpha; rat cortical-neurons; methamphetamine-induced neurotoxicity; activated protein-kinase; mptp-induced neurotoxicity; glycogen-synthase kinase-3-beta; Androgens; estrogen; induced cell-death; MAPK/ERK; Methamphetamine; nigrostriatal dopaminergic system; Progesterone; regulates bcl-2 expression; Sex difference; vesicular monoamine transporter
Creator
An entity primarily responsible for making the resource
Bourque M; Dluzen D E; Di Paolo T
Description
An account of the resource
The sex difference in Parkinson's disease, with a higher susceptibility in men, suggests a modulatory effect of sex steroids in the brain. Numerous studies highlight that sex steroids have neuroprotective properties against various brain injuries. This paper reviews the protective effects of sex hormones, particularly estradiol, progesterone and androgens, in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) animal model of Parkinson's disease as compared to methamphetamine toxicity. The molecular mechanisms underlying beneficial actions of sex steroids on the brain have been investigated showing steroid, dose, timing and duration specificities and presently focus is on the dopamine signaling pathways, the next frontier. Both genomic and non-genomic actions of estrogen converge to promote survival factors and show sex differences. Neuroprotection by estrogen involves activation of signaling molecules such as the phosphatidylinositol-3 kinase/Akt and the mitogen-activated protein kinase pathways. Interaction with growth factors, such as insulin-like growth factor 1, also contributes to protective actions of estrogen. (C) 2009 Elsevier Inc. All rights reserved.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.yfrne.2009.04.014" target="_blank" rel="noreferrer noopener">10.1016/j.yfrne.2009.04.014</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2009
activated protein-kinase
Akt
androgens
Bourque M
Di Paolo T
Dluzen D E
Endocrinology & Metabolism
estrogen
estrogen-receptor-alpha
Frontiers in Neuroendocrinology
glycogen-synthase kinase-3-beta
induced cell-death
Journal Article or Conference Abstract Publication
MAPK/ERK
Methamphetamine
methamphetamine-induced neurotoxicity
MPTP
mptp-induced neurotoxicity
Neuroprotection
Neurosciences & Neurology
nigrostriatal dopaminergic system
parkinsons-disease
progesterone
rat cortical-neurons
regulates bcl-2 expression
Sex difference
Vesicular monoamine transporter
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1111/j.1365-2826.2011.02193.x" target="_blank" rel="noreferrer noopener">http://doi.org/10.1111/j.1365-2826.2011.02193.x</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
48-61
Issue
1
Volume
24
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Oestrogen Receptors and Signalling Pathways: Implications for Neuroprotective Effects of Sex Steroids in Parkinson's Disease
Publisher
An entity responsible for making the resource available
Journal of Neuroendocrinology
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-01
Subject
The topic of the resource
17 ss-oestradiol; Akt; beta messenger-rna; central-nervous-system; dopamine transporter; Endocrinology & Metabolism; er-alpha; GPER1; growth-factor receptor; GSK3 ss; induced dopamine depletion; ischemic brain-injury; monoamine transporter; MPTP; Neurosciences & Neurology; plasma-membrane; protein-coupled receptor; rat-brain; vesicular
Creator
An entity primarily responsible for making the resource
Al Sweidi S; Sanchez M G; Bourque M; Morissette M; Dluzen D; Di Paolo T
Description
An account of the resource
Parkinsons disease (PD) is an age-related neurodegenerative disorder with a higher incidence in the male population. In the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD, 17 beta-oestradiol but not androgens were shown to protect dopamine (DA) neurones. We report that oestrogen receptors (ER)a and beta distinctly contribute to neuroprotection against MPTP toxicity, as revealed by examining the membrane DA transporter (DAT), the vesicular monoamine transporter 2 (VMAT2) and tyrosine hyroxylase in ER wild-type (WT) and knockout (ERKO) C57Bl/6 male mice. Intact ERKO beta mice had lower levels of striatal DAT and VMAT2, whereas ERKOa mice were the most sensitive to MPTP toxicity compared to WT and ERKO beta mice and had the highest levels of plasma androgens. In both ERKO mice groups, treatment with 17 beta-oestradiol did not provide neuroprotection against MPTP, despite elevated plasma 17 beta-oestradiol levels. Next, the recently described membrane G protein-coupled oestrogen receptor (GPER1) was examined in female Macaca fascicularis monkeys and mice. GPER1 levels were increased in the caudate nucleus and the putamen of MPTP-monkeys and in the male mouse striatum lesioned with methamphetamine or MPTP. Moreover, neuroprotective mechanisms in response to oestrogens transmit via Akt/glycogen synthase kinase-3 (GSK3) signalling. The intact and lesioned striata of 17 beta-oestradiol treated monkeys, similar to that of mice, had increased levels of pAkt (Ser 473)/beta III-tubulin, pGSK3 (Ser 9)/beta III-tubulin and Akt/beta III-tubulin. Hence, ERa, ER beta and GPER1 activation by oestrogens is imperative in the modulation of ER signalling and serves as a basis for evaluating nigrostriatal neuroprotection.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1111/j.1365-2826.2011.02193.x" target="_blank" rel="noreferrer noopener">10.1111/j.1365-2826.2011.02193.x</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
17 ss-oestradiol
2012
Akt
Al Sweidi S
beta messenger-rna
Bourque M
central-nervous-system
Di Paolo T
Dluzen D
Dopamine transporter
Endocrinology & Metabolism
er-alpha
GPER1
growth-factor receptor
GSK3 ss
induced dopamine depletion
ischemic brain-injury
Journal Article or Conference Abstract Publication
Journal of neuroendocrinology
monoamine transporter
Morissette M
MPTP
Neurosciences & Neurology
plasma-membrane
protein-coupled receptor
rat-brain
Sanchez M G
vesicular
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1074/jbc.M114.624270" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M114.624270</a>
Pages
20128–20146
Issue
33
Volume
290
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Mutation in Osteoactivin Promotes Receptor Activator of NFkappaB Ligand (RANKL)-mediated Osteoclast Differentiation and Survival but Inhibits Osteoclast Function.
Publisher
An entity responsible for making the resource available
The Journal of biological chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-08
Subject
The topic of the resource
*Mutation; Akt; Animals; bone; bone marrow; Bone Remodeling; Cell Differentiation/*physiology; Cell Survival/*physiology; Eye Proteins/*genetics; Inbred DBA; MAP kinases (MAPKs); Membrane Glycoproteins/*genetics; Mice; osteoactivin; osteoclast; Osteoclasts/*cytology; osteopetrosis; RANK Ligand/metabolism/*physiology; Signal Transduction; X-Ray Microtomography
Creator
An entity primarily responsible for making the resource
Abdelmagid Samir M; Sondag Gregory R; Moussa Fouad M; Belcher Joyce Y; Yu Bing; Stinnett Hilary; Novak Kimberly; Mbimba Thomas; Khol Matthew; Hankenson Kurt D; Malcuit Christopher; Safadi Fayez F
Description
An account of the resource
We previously reported on the importance of osteoactivin (OA/Gpnmb) in osteogenesis. In this study, we examined the role of OA in osteoclastogenesis, using mice with a nonsense mutation in the Gpnmb gene (D2J) and wild-type controls (D2J/Gpnmb(+)). In these D2J mice, micro-computed tomography and histomorphometric analyses revealed increased cortical thickness, whereas total porosity and eroded surface were significantly reduced in D2J mice compared with wild-type controls, and these results were corroborated by lower serum levels of
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.M114.624270" target="_blank" rel="noreferrer noopener">10.1074/jbc.M114.624270</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Mutation
2015
Abdelmagid Samir M
Akt
Animals
Belcher Joyce Y
Bone
bone marrow
Bone Remodeling
Cell Differentiation/*physiology
Cell Survival/*physiology
Department of Anatomy & Neurobiology
Eye Proteins/*genetics
Hankenson Kurt D
Inbred DBA
Khol Matthew
Malcuit Christopher
MAP kinases (MAPKs)
Mbimba Thomas
Membrane Glycoproteins/*genetics
Mice
Moussa Fouad M
NEOMED College of Medicine
Novak Kimberly
OSTEOACTIVIN
osteoclast
Osteoclasts/*cytology
osteopetrosis
RANK Ligand/metabolism/*physiology
Safadi Fayez F
Signal Transduction
Sondag Gregory R
Stinnett Hilary
The Journal of biological chemistry
X-Ray Microtomography
Yu Bing