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Int. J. Mol. Sci. 2017, 18(3), 558; doi:10.3390/ijms18030558

Caloric Restriction Protects against Lactacystin-Induced Degeneration of Dopamine Neurons Independent of the Ghrelin Receptor

1
Research Group Experimental Pharmacology (EFAR/FASC), Center for Neurosciences (C4N), Vrije Universiteit Brussel (VUB), Laarbeeklaan 103, 1090 Brussel, Belgium
2
Research Group Pharmaceutical Biotechnology and Molecular Biology (MICH), Center for Neurosciences (C4N), Vrije Universiteit Brussel (VUB), Laarbeeklaan 103, 1090 Brussel, Belgium
3
Department of Physiology, School of Biomedical and Psychological Sciences, Monash University, Clayton, Melbourne 3800, Australia
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Academic Editor: Suzanne L. Dickson
Received: 21 December 2016 / Revised: 14 February 2017 / Accepted: 20 February 2017 / Published: 4 March 2017
(This article belongs to the Special Issue Neurobiological Perspectives on Ghrelin)
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Abstract

Parkinson’s disease (PD) is a neurodegenerative disorder, characterized by a loss of dopamine (DA) neurons in the substantia nigra pars compacta (SNc). Caloric restriction (CR) has been shown to exert ghrelin-dependent neuroprotective effects in the 1-methyl-4-phenyl-1,2,3,6-tetrathydropyridine (MPTP)-based animal model for PD. We here investigated whether CR is neuroprotective in the lactacystin (LAC) mouse model for PD, in which proteasome disruption leads to the destruction of the DA neurons of the SNc, and whether this effect is mediated via the ghrelin receptor. Adult male ghrelin receptor wildtype (WT) and knockout (KO) mice were maintained on an ad libitum (AL) diet or on a 30% CR regimen. After 3 weeks, LAC was injected unilaterally into the SNc, and the degree of DA neuron degeneration was evaluated 1 week later. In AL mice, LAC injection significanty reduced the number of DA neurons and striatal DA concentrations. CR protected against DA neuron degeneration following LAC injection. However, no differences were observed between ghrelin receptor WT and KO mice. These results indicate that CR can protect the nigral DA neurons from toxicity related to proteasome disruption; however, the ghrelin receptor is not involved in this effect. View Full-Text
Keywords: Parkinson’s disease; caloric restriction; lactacystin; ghrelin receptor Parkinson’s disease; caloric restriction; lactacystin; ghrelin receptor
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Coppens, J.; Bentea, E.; Bayliss, J.A.; Demuyser, T.; Walrave, L.; Albertini, G.; Van Liefferinge, J.; Deneyer, L.; Aourz, N.; Van Eeckhaut, A.; Portelli, J.; Andrews, Z.B.; Massie, A.; De Bundel, D.; Smolders, I. Caloric Restriction Protects against Lactacystin-Induced Degeneration of Dopamine Neurons Independent of the Ghrelin Receptor. Int. J. Mol. Sci. 2017, 18, 558.

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