Acyl-Ghrelin Attenuates Neurochemical and Motor Deficits in the 6-OHDA Model of Parkinson’s Disease

The feeding-related hormone, acyl-ghrelin, protects dopamine neurones in murine 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-based models of experimental Parkinson’s disease (PD). However, the potential protective effect of acyl-ghrelin on substantia nigra pars compacta (SNpc) dopaminergic...

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Autores principales: Rees, Daniel, Beynon, Amy L., Lelos, Mariah J., Smith, Gaynor A., Roberts, Luke D., Phelps, Lyndsey, Dunnett, Stephen B., Morgan, Alwena H., Brown, Rowan M., Wells, Timothy, Davies, Jeffrey S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2022
Materias:
Brief Communication
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10287784/
https://www.ncbi.nlm.nih.gov/pubmed/36107359
http://dx.doi.org/10.1007/s10571-022-01282-9
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author Rees, Daniel
Beynon, Amy L.
Lelos, Mariah J.
Smith, Gaynor A.
Roberts, Luke D.
Phelps, Lyndsey
Dunnett, Stephen B.
Morgan, Alwena H.
Brown, Rowan M.
Wells, Timothy
Davies, Jeffrey S.
author_facet Rees, Daniel
Beynon, Amy L.
Lelos, Mariah J.
Smith, Gaynor A.
Roberts, Luke D.
Phelps, Lyndsey
Dunnett, Stephen B.
Morgan, Alwena H.
Brown, Rowan M.
Wells, Timothy
Davies, Jeffrey S.
author_sort Rees, Daniel
collection PubMed
description The feeding-related hormone, acyl-ghrelin, protects dopamine neurones in murine 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-based models of experimental Parkinson’s disease (PD). However, the potential protective effect of acyl-ghrelin on substantia nigra pars compacta (SNpc) dopaminergic neurones and consequent behavioural correlates in the more widely used 6-hydroxydopamine (6-OHDA) rat medial forebrain bundle (MFB) lesion model of PD are unknown. To address this question, acyl-ghrelin levels were raised directly by mini-pump infusion for 7 days prior to unilateral injection of 6-OHDA into the MFB with assessment of amphetamine-induced rotations on days 27 and 35, and immunohistochemical analysis of dopaminergic neurone survival. Whilst acyl-ghrelin treatment was insufficient to elevate food intake or body weight, it attenuated amphetamine-induced circling behaviour and SNpc dopamine neurone loss induced by 6-OHDA. These data support the notion that elevating circulating acyl-ghrelin may be a valuable approach to slow or impair progression of neurone loss in PD. GRAPHICAL ABSTRACT: [Image: see text]
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spelling pubmed-102877842023-06-24 Acyl-Ghrelin Attenuates Neurochemical and Motor Deficits in the 6-OHDA Model of Parkinson’s Disease Rees, Daniel Beynon, Amy L. Lelos, Mariah J. Smith, Gaynor A. Roberts, Luke D. Phelps, Lyndsey Dunnett, Stephen B. Morgan, Alwena H. Brown, Rowan M. Wells, Timothy Davies, Jeffrey S. Cell Mol Neurobiol Brief Communication The feeding-related hormone, acyl-ghrelin, protects dopamine neurones in murine 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-based models of experimental Parkinson’s disease (PD). However, the potential protective effect of acyl-ghrelin on substantia nigra pars compacta (SNpc) dopaminergic neurones and consequent behavioural correlates in the more widely used 6-hydroxydopamine (6-OHDA) rat medial forebrain bundle (MFB) lesion model of PD are unknown. To address this question, acyl-ghrelin levels were raised directly by mini-pump infusion for 7 days prior to unilateral injection of 6-OHDA into the MFB with assessment of amphetamine-induced rotations on days 27 and 35, and immunohistochemical analysis of dopaminergic neurone survival. Whilst acyl-ghrelin treatment was insufficient to elevate food intake or body weight, it attenuated amphetamine-induced circling behaviour and SNpc dopamine neurone loss induced by 6-OHDA. These data support the notion that elevating circulating acyl-ghrelin may be a valuable approach to slow or impair progression of neurone loss in PD. GRAPHICAL ABSTRACT: [Image: see text] Springer US 2022-09-15 2023 /pmc/articles/PMC10287784/ /pubmed/36107359 http://dx.doi.org/10.1007/s10571-022-01282-9 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Brief Communication
Rees, Daniel
Beynon, Amy L.
Lelos, Mariah J.
Smith, Gaynor A.
Roberts, Luke D.
Phelps, Lyndsey
Dunnett, Stephen B.
Morgan, Alwena H.
Brown, Rowan M.
Wells, Timothy
Davies, Jeffrey S.
Acyl-Ghrelin Attenuates Neurochemical and Motor Deficits in the 6-OHDA Model of Parkinson’s Disease
title Acyl-Ghrelin Attenuates Neurochemical and Motor Deficits in the 6-OHDA Model of Parkinson’s Disease
title_full Acyl-Ghrelin Attenuates Neurochemical and Motor Deficits in the 6-OHDA Model of Parkinson’s Disease
title_fullStr Acyl-Ghrelin Attenuates Neurochemical and Motor Deficits in the 6-OHDA Model of Parkinson’s Disease
title_full_unstemmed Acyl-Ghrelin Attenuates Neurochemical and Motor Deficits in the 6-OHDA Model of Parkinson’s Disease
title_short Acyl-Ghrelin Attenuates Neurochemical and Motor Deficits in the 6-OHDA Model of Parkinson’s Disease
title_sort acyl-ghrelin attenuates neurochemical and motor deficits in the 6-ohda model of parkinson’s disease
topic Brief Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10287784/
https://www.ncbi.nlm.nih.gov/pubmed/36107359
http://dx.doi.org/10.1007/s10571-022-01282-9
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