Allopregnanolone reinstates tyrosine hydroxylase immunoreactive neurons and motor performance in an MPTP-lesioned mouse model of Parkinson's disease
Restorative/protective therapies to restore dopamine neurons in the substantia nigra pars compacta (SNpc) are greatly needed to effectively change the debilitating course of Parkinson's disease. In this study, we tested the therapeutic potential of a neurogenic neurosteroid, allopregnanolone, i...
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Published in | PloS one Vol. 7; no. 11; p. e50040 |
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Main Authors | , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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Public Library of Science
29.11.2012
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Abstract | Restorative/protective therapies to restore dopamine neurons in the substantia nigra pars compacta (SNpc) are greatly needed to effectively change the debilitating course of Parkinson's disease. In this study, we tested the therapeutic potential of a neurogenic neurosteroid, allopregnanolone, in the restoration of the components of the nigrostriatal pathway in MPTP-lesioned mice by measuring striatal dopamine levels, total and tyrosine hydroxylase immunoreactive neuron numbers and BrdU-positive cells in the SNpc. An acute treatment (once/week for two weeks) with allopregnanolone restored the number of tyrosine hydroxylase-positive and total cell numbers in the SNpc of MPTP-lesioned mice, even though this did not increase striatal dopamine. It was also noted that MPTP treated mice to which allopregnanolone was administered had an increase in BrdU-positive cells in the SNpc. The effects of allopregnanolone in MPTP-lesioned mice were more apparent in mice that underwent behavioral tests. Interestingly, mice treated with allopregnanolone after MPTP lesion were able to perform at levels similar to that of non-lesioned control mice in a rotarod test. These data demonstrate that allopregnanolone promotes the restoration of tyrosine hydroxylase immunoreactive neurons and total cells in the nigrostriatal tract, improves the motor performance in MPTP-treated mice, and may serve as a therapeutic strategy for Parkinson's disease. |
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AbstractList | Restorative/protective therapies to restore dopamine neurons in the substantia nigra pars compacta (SNpc) are greatly needed to effectively change the debilitating course of Parkinson's disease. In this study, we tested the therapeutic potential of a neurogenic neurosteroid, allopregnanolone, in the restoration of the components of the nigrostriatal pathway in MPTP-lesioned mice by measuring striatal dopamine levels, total and tyrosine hydroxylase immunoreactive neuron numbers and BrdU-positive cells in the SNpc. An acute treatment (once/week for two weeks) with allopregnanolone restored the number of tyrosine hydroxylase-positive and total cell numbers in the SNpc of MPTP-lesioned mice, even though this did not increase striatal dopamine. It was also noted that MPTP treated mice to which allopregnanolone was administered had an increase in BrdU-positive cells in the SNpc. The effects of allopregnanolone in MPTP-lesioned mice were more apparent in mice that underwent behavioral tests. Interestingly, mice treated with allopregnanolone after MPTP lesion were able to perform at levels similar to that of non-lesioned control mice in a rotarod test. These data demonstrate that allopregnanolone promotes the restoration of tyrosine hydroxylase immunoreactive neurons and total cells in the nigrostriatal tract, improves the motor performance in MPTP-treated mice, and may serve as a therapeutic strategy for Parkinson's disease. |
Audience | Academic |
Author | Farley, Jerry M Hill, Rosanne Mosley, Thomas Adeosun, Samuel O Bigler, Steven Zheng, Baoying Paul, Ian Kyle, Patrick Smeyne, Richard Hou, Xu Brinton, Roberta Diaz Jiao, Yun Pani, Amar Stockmeier, Craig He, Zhi Henry, Sherry Ou, Xiaoming Wang, Jun Ming |
AuthorAffiliation | 6 Department of Developmental Neurobiology, St. Jude Children's Hospital, Memphis, Tennessee, United States of America 2 Department of Psychiatry and Human Behavior, University of Mississippi Medical Center, Jackson, Mississippi, United States of America 4 Program in Neuroscience, University of Mississippi Medical Center, Jackson, Mississippi, United States of America 7 Department of Pharmacology and Pharmaceutical Sciences, University of Southern California, Los Angeles, California, United States of America 5 The Memory Impairment Neurodegenerative Dementia Research Center, University of Mississippi Medical Center, Jackson, Mississippi, United States of America 1 Department of Pathology, University of Mississippi Medical Center, Jackson, Mississippi, United States of America Emory University, United States of America 3 Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi, United States of America |
AuthorAffiliation_xml | – name: 1 Department of Pathology, University of Mississippi Medical Center, Jackson, Mississippi, United States of America – name: 3 Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi, United States of America – name: 5 The Memory Impairment Neurodegenerative Dementia Research Center, University of Mississippi Medical Center, Jackson, Mississippi, United States of America – name: 7 Department of Pharmacology and Pharmaceutical Sciences, University of Southern California, Los Angeles, California, United States of America – name: Emory University, United States of America – name: 6 Department of Developmental Neurobiology, St. Jude Children's Hospital, Memphis, Tennessee, United States of America – name: 2 Department of Psychiatry and Human Behavior, University of Mississippi Medical Center, Jackson, Mississippi, United States of America – name: 4 Program in Neuroscience, University of Mississippi Medical Center, Jackson, Mississippi, United States of America |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23209637$$D View this record in MEDLINE/PubMed |
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Copyright | COPYRIGHT 2012 Public Library of Science 2012 Adeosun et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2012 Adeosun et al 2012 Adeosun et al |
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Notes | Competing Interests: The authors have declared that no competing interests exist. Conceived and designed the experiments: JMW JMF CS IP SB RS. Performed the experiments: SA XH YJ BZ SH RH ZH AP PK RS JMW. Analyzed the data: SA XH YJ BZ AP PK XO TM JMF CS IP SB RDB RS JMW. Contributed reagents/materials/analysis tools: RS PK IP. Wrote the paper: SA XH JMF CS IP XO RS RDB JMW. |
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Snippet | Restorative/protective therapies to restore dopamine neurons in the substantia nigra pars compacta (SNpc) are greatly needed to effectively change the... |
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SubjectTerms | Acids Alzheimer's disease Alzheimers disease Animals Apoptosis Biology Brain research Burglary Children & youth Dementia Disease Models, Animal Dopamine Dopamine - metabolism Health aspects Hospitals Hydroxylase Hydroxylases Male Medicine Memory Mesencephalon - drug effects Mesencephalon - metabolism Metabolites Mice Motor task performance Movement disorders MPTP MPTP Poisoning - metabolism MPTP Poisoning - physiopathology Neostriatum Neurobiology Neurodegenerative diseases Neurons Neurons - drug effects Neurons - metabolism Neurosciences Norepinephrine - metabolism Parkinson's disease Parkinsons disease Pathology Pharmacology Phenols (Class of compounds) Pregnanolone Pregnanolone - pharmacology Psychiatry Psychomotor Performance - drug effects Restoration Rodents Substantia nigra Substantia Nigra - drug effects Substantia Nigra - metabolism Toxicology Traumatic brain injury Tyrosine Tyrosine 3-monooxygenase Tyrosine 3-Monooxygenase - metabolism |
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Title | Allopregnanolone reinstates tyrosine hydroxylase immunoreactive neurons and motor performance in an MPTP-lesioned mouse model of Parkinson's disease |
URI | https://www.ncbi.nlm.nih.gov/pubmed/23209637 https://www.proquest.com/docview/1350911457/abstract/ https://pubmed.ncbi.nlm.nih.gov/PMC3510204 https://doaj.org/article/59d821c9f03f4717ba7f657db3177b07 http://dx.doi.org/10.1371/journal.pone.0050040 |
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