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

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...

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Published in:International journal of molecular sciences 2017-03, Vol.18 (3), p.558-558
Main Authors: Coppens, Jessica, Bentea, Eduard, Bayliss, Jacqueline A, Demuyser, Thomas, Walrave, Laura, Albertini, Giulia, Van Liefferinge, Joeri, Deneyer, Lauren, Aourz, Najat, Van Eeckhaut, Ann, Portelli, Jeanelle, Andrews, Zane B, Massie, Ann, De Bundel, Dimitri, Smolders, Ilse
Format: Article
Language:English
Subjects:
Acetylcysteine - administration & dosage
Acetylcysteine - analogs & derivatives
Acetylcysteine - pharmacology
Age Factors
Animals
Caloric Restriction
Cell Count
Dopaminergic Neurons - drug effects
Dopaminergic Neurons - metabolism
Male
Mice
Mice, Knockout
Neuroprotective Agents
Receptors, Ghrelin - genetics
Receptors, Ghrelin - metabolism
Substantia Nigra - drug effects
Substantia Nigra - metabolism
Substantia Nigra - pathology
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Summary: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.
ISSN:1422-0067
1422-0067
DOI:10.3390/ijms18030558