Thursday, 22nd March – h. 14:30
Seminars Room, NICO
Molecular mechanisms of neural circuit development
The midbrain dopamine system is involved in the control of cognitive and motor behavior. Midbrain dopamine neurons (mDA) are grossly divided into two anatomically and functionally distinct subpopulations: substantia nigra pars compacta (SNc) and ventral tegmental area (VTA) neurons. SNc neurons make precise connections with dorsal striatum (nigrostriatal projections), while VTA neurons target ventral striatum and cortex (mesocorticolimbic projections). Both pathways collectively run in the medial forebrain bundle (MFB) towards the forebrain. However, how mDA neurons establish their complex connections remains poorly understood. Therefore, we use the mDA system to examine how axons find their way during development, how neurons migrate and how ultimately synaptic connections are established.
In this lecture, I’ll cover two topics. First, novel axon-dependent mechanisms for mDA axon pathfinding that rely on specific cell adhesion molecules, and 2) recently developed mouse genetics tools to distinguish between different subsets of dopaminergic projections in vivo (called Pitx3-ITC mice).
The subtractive genetic strategy we have developed relies on the expression of different fluorescent proteins in different subsets of mDA neurons in a single mouse. Pitx3-ITC mice display labeling of SNc neurons and selective visualization of nigrostriatal projections in the MFB and in striatum, from early embryonic development onwards. Combination of Pitx3-ITC mice with 3D-imaging of solvent cleared organs (3DISCO) technology and light sheet imaging allows for 3D analysis of neuronal migration and axonal/dendritic development of SNc neurons.
Host: Silvia De Marchis
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.