Foliglurax, a positive allosteric modulator of the metabotrophic glutamate receptor 4, protects dopaminergic neurons in MPTP-lesioned male mice.


Journal

Brain research
ISSN: 1872-6240
Titre abrégé: Brain Res
Pays: Netherlands
ID NLM: 0045503

Informations de publication

Date de publication:
15 06 2023
Historique:
received: 31 01 2023
revised: 20 03 2023
accepted: 24 03 2023
medline: 8 5 2023
pubmed: 28 3 2023
entrez: 27 3 2023
Statut: ppublish

Résumé

Overactivity of the corticostriatal glutamatergic pathway is documented in Parkinson's disease (PD) and stimulation of presynaptic metabotropic glutamate (mGlu) receptors 4 on these striatal afferents inhibits glutamate release normalizing neuronal activity in the basal ganglia. Moreover, mGlu4 receptors are also expressed in glial cells and are able to modulate glial function making this receptor a potential target for neuroprotection. Hence, we investigated whether foliglurax, a positive allosteric modulator of mGlu4 receptors with high brain exposure after oral administration, has neuroprotective effects in MPTP mice to model early PD. Male mice were treated daily from day 1 to 10 with 1, 3 or 10 mg/kg of foliglurax and administered MPTP on the 5th day then euthanized on the 11th day. Dopamine neuron integrity was assessed with measures of striatal dopamine and its metabolites levels, striatal and nigral dopamine transporter (DAT) binding and inflammation with markers of striatal astrocytes (GFAP) and microglia (Iba1). MPTP lesion produced a decrease in dopamine, its metabolites and striatal DAT specific binding that was prevented by treatment with 3 mg/kg of foliglurax, whereas 1 and 10 mg/kg had no beneficial effect. MPTP mice had increased levels of GFAP; foliglurax treatment (3 mg/kg) prevented this increase. Iba1 levels were unchanged in MPTP mice compared to control mice. There was a negative correlation between dopamine content and GFAP levels. Our results show that positive allosteric modulation of mGlu4 receptors with foliglurax provided neuroprotective effects in the MPTP mouse model of PD.

Identifiants

pubmed: 36972837
pii: S0006-8993(23)00120-8
doi: 10.1016/j.brainres.2023.148349
pii:
doi:

Substances chimiques

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 9P21XSP91P
Antiparkinson Agents 0
Dopamine VTD58H1Z2X
glial fibrillary astrocytic protein, mouse 0
metabotropic glutamate receptor 4 YZN9W7P1BX
Neuroprotective Agents 0
Receptors, Metabotropic Glutamate 0
Aif1 protein, mouse 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

148349

Informations de copyright

Copyright © 2023 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. Dr. Di Paolo received a contract from Prexton Therapeutics for this study that was performed by Drs. M. Bourque and M. Morissette. Drs. D. Charvin and F. Conquet were employed by Prexton Therapeutics now Lundbeck.

Auteurs

Mélanie Bourque (M)

Centre de Recherche du CHU de Québec, Axe Neurosciences, Québec, QC G1V4G2, Canada.

Marc Morissette (M)

Centre de Recherche du CHU de Québec, Axe Neurosciences, Québec, QC G1V4G2, Canada.

François Conquet (F)

H. Lundbeck A/S, 2500 Valby, Denmark.

Delphine Charvin (D)

H. Lundbeck A/S, 2500 Valby, Denmark.

Thérèse Di Paolo (T)

Centre de Recherche du CHU de Québec, Axe Neurosciences, Québec, QC G1V4G2, Canada; Faculté de Pharmacie, Pavillon Ferdinand-Vandry, Université Laval, Québec, QC G1V 0A6, Canada. Electronic address: therese.dipaolo@crchudequebec.ulaval.ca.

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Classifications MeSH