1
40
2
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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.neuro.2017.06.005" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.neuro.2017.06.005</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
256-266
Volume
64
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
The effect of manganese exposure in Atp13a2-deficient mice.
Publisher
An entity responsible for making the resource available
Neurotoxicology
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-01
Subject
The topic of the resource
Female; Male; Animals; Mice; *Parkinson's disease; *Alpha-synuclein; Mice; Membrane Proteins/genetics/*metabolism; Motor Activity; *Lipofuscin; *Manganese; *Sensorimotor function; Behavior; Inbred C57BL; Animal; Knockout; Adenosine Triphosphatases/genetics/*metabolism; alpha-Synuclein/metabolism; Brain/*drug effects/*metabolism; Manganese/metabolism/*toxicity
Creator
An entity primarily responsible for making the resource
Fleming Sheila M; Santiago Nicholas A; Mullin Elizabeth J; Pamphile Shanta; Karkare Swagata; Lemkuhl Andrew; Ekhator Osunde R; Linn Stephen C; Holden John G; Aga Diana S; Roth Jerome A; Liou Benjamin; Sun Ying; Shull Gary E; Schultheis Patrick J
Description
An account of the resource
Loss of function mutations in the P5-ATPase ATP13A2 are associated with Kufor-Rakeb Syndrome and Neuronal Ceroid Lipofuscinosis. While the function of ATP13A2 is unclear, in vitro studies suggest it is a lysosomal protein that interacts with the metals manganese (Mn) and zinc and the presynaptic protein alpha-synuclein. Loss of ATP13A2 function in mice causes sensorimotor deficits, enhanced autofluorescent storage material, and accumulation of alpha-synuclein. The present study sought to determine the effect of Mn administration on these same outcomes in ATP13A2-deficient mice. Wildtype and ATP13A2-deficient mice received saline or Mn at 5-9 or 12-19 months for 45days. Sensorimotor function was assessed starting at day 30. Autofluorescence was quantified in multiple brain regions and alpha-synuclein protein levels were determined in the ventral midbrain. Brain Mn, iron, zinc, and copper concentrations were measured in 5-9 month old mice. The results show Mn enhanced sensorimotor function, increased autofluorescence in the substantia nigra, and increased insoluble alpha-synuclein in the ventral midbrain in older ATP13A2-deficient mice. In addition, the Mn regimen used increased Mn concentration in the brain and levels were higher in Mn-treated mutants than controls. These results indicate loss of ATP13A2 function leads to increased sensitivity to Mn in vivo.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.neuro.2017.06.005" target="_blank" rel="noreferrer noopener">10.1016/j.neuro.2017.06.005</a>
*Alpha-synuclein
*Lipofuscin
*Manganese
*Parkinson's disease
*Sensorimotor function
2018
Adenosine Triphosphatases/genetics/*metabolism
Aga Diana S
alpha-Synuclein/metabolism
Animal
Animals
Behavior
Brain/*drug effects/*metabolism
Department of Pharmaceutical Sciences
Ekhator Osunde R
Female
Fleming Sheila M
Holden John G
Inbred C57BL
Karkare Swagata
Knockout
Lemkuhl Andrew
Linn Stephen C
Liou Benjamin
Male
Manganese/metabolism/*toxicity
Membrane Proteins/genetics/*metabolism
Mice
Motor Activity
Mullin Elizabeth J
NEOMED College of Pharmacy
Neurotoxicology
Pamphile Shanta
Roth Jerome A
Santiago Nicholas A
Schultheis Patrick J
Shull Gary E
Sun Ying
-
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.neuro.2017.06.005" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.neuro.2017.06.005</a>
Pages
256–266
Volume
64
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
The effect of manganese exposure in Atp13a2-deficient mice.
Publisher
An entity responsible for making the resource available
Neurotoxicology
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-01
Subject
The topic of the resource
*Alpha-synuclein; *Lipofuscin; *Manganese; *Mice; *Parkinson's disease; *Sensorimotor function
Creator
An entity primarily responsible for making the resource
Fleming Sheila M; Santiago Nicholas A; Mullin Elizabeth J; Pamphile Shanta; Karkare Swagata; Lemkuhl Andrew; Ekhator Osunde R; Linn Stephen C; Holden John G; Aga Diana S; Roth Jerome A; Liou Benjamin; Sun Ying; Shull Gary E; Schultheis Patrick J
Description
An account of the resource
Loss of function mutations in the P5-ATPase ATP13A2 are associated with Kufor-Rakeb Syndrome and Neuronal Ceroid Lipofuscinosis. While the function of ATP13A2 is unclear, in vitro studies suggest it is a lysosomal protein that interacts with the metals manganese (Mn) and zinc and the presynaptic protein alpha-synuclein. Loss of ATP13A2 function in mice causes sensorimotor deficits, enhanced autofluorescent storage material, and accumulation of alpha-synuclein. The present study sought to determine the effect of Mn administration on these same outcomes in ATP13A2-deficient mice. Wildtype and ATP13A2-deficient mice received saline or Mn at 5-9 or 12-19 months for 45days. Sensorimotor function was assessed starting at day 30. Autofluorescence was quantified in multiple brain regions and alpha-synuclein protein levels were determined in the ventral midbrain. Brain Mn, iron, zinc, and copper concentrations were measured in 5-9 month old mice. The results show Mn enhanced sensorimotor function, increased autofluorescence in the substantia nigra, and increased insoluble alpha-synuclein in the ventral midbrain in older ATP13A2-deficient mice. In addition, the Mn regimen used increased Mn concentration in the brain and levels were higher in Mn-treated mutants than controls. These results indicate loss of ATP13A2 function leads to increased sensitivity to Mn in vivo.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.neuro.2017.06.005" target="_blank" rel="noreferrer noopener">10.1016/j.neuro.2017.06.005</a>
Rights
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).
*Alpha-synuclein
*Lipofuscin
*Manganese
*Mice
*Parkinson's disease
*Sensorimotor function
2018
Aga Diana S
Department of Pharmaceutical Sciences
Ekhator Osunde R
Fleming Sheila M
Holden John G
Karkare Swagata
Lemkuhl Andrew
Linn Stephen C
Liou Benjamin
Mullin Elizabeth J
NEOMED College of Pharmacy
Neurotoxicology
Pamphile Shanta
Roth Jerome A
Santiago Nicholas A
Schultheis Patrick J
Shull Gary E
Sun Ying