Venerdì 19 dicembre - ore 14:00
Aula seminari, NICO
GluN2A-containing NMDA receptors as synaptic trait of levodopa-induced dyskinesias: from experimental models to patients
Dipartimento di Scienze Farmacologiche e Biomolecolari, Università di Milano
Levodopa (L-DOPA)-induced dyskinesias (LIDs) are a major complication in the pharmacological management of Parkinson's Disease (PD). Abnormal glutamatergic transmission in striatum is considered a key factor in the development of LIDs.
Here we show that an altered ratio of synaptic GluN2A/GluN2B-containing NMDA receptors (NMDARs) in striatum represents a common trait in L-DOPA-treated dyskinetic animals (6-OHDA rats and MPTP monkeys) and in post-mortem tissue from dyskinetic PD patients. The modulation of synaptic NMDAR composition by cell-permeable peptides interfering with GluN2A subunit clustering at postsynaptic sites leads to a reduction in the dyskinetic motor behavior in the two animal models of LIDs.
Our results indicate that targeting synaptic NMDAR subunit composition may represent an intriguing therapeutic approach aimed at ameliorating L-DOPA motor side effects.
Host: Alessandro Vercelli
Since 2001, this meeting represented an important event for basic and clinical researchers working on this emerging scientific topic. We will address state-of-the-art approaches in the field of steroids and nervous system, including behavior, epigenetics, genomic and non-genomic actions, the vitamin D, neurodegenerative and psychiatric disorders, and the interference among endocrine disruptors and steroid signaling.
Un malfunzionamento dei mitocondri, le centrali energetiche delle cellule, causa lo sviluppo della SCA28, una forma ereditaria di atassia. Dopo 10 anni di studi e grazie al sostegno di Fondazione Telethon, la scoperta del team di ricerca guidato dai proff. Alfredo Brusco e Filippo Tempia dell’Università di Torino e NICO. Lo studio pubblicato sulla prestigiosa rivista Neurobiology of Disease.