Thursday, 2nd July - h 14:00
Seminar room, NICO
Expression and functional characterisation of transient receptor potential vanilloid-related channel 4 (TRPV4) in hippocampal astrocytes after ischemia/reperfusion
Olena Butenko, Department of Cellular Neurophysiology Institute of Experimental Medicine ASCR, v.v.i. Videnska - Czech Republic
During cerebral ischemia a rapid increase of intracellular calcium ([Ca2+]i) initiates dramatic changes in the nervous tissue leading to apoptotic and necrotic cell death and reactive gliosis. Propagating [Ca2+]i waves evoked by ischemia can spread through the astroglial syncytium for a long distance and cause damage in distal CNS regions.
It has been suggested that in astrocytes the massive and uncontrolled plasmalemal Ca2+ entry after hypoxia/ischemia could be mediated by the activation of diverse Ca2+-permeable cation channels and potentially by transient receptor potential vanilloid-related channel 4 (TRPV4).
However, to the best of our knowledge, the role of astrocytic TRPV4 channels during in vivo ischemic injury has not yet been defined. In the first part of the seminar we will discuss pathological changes in the CA1 region of the adult rat hippocampus during the reperfusion after cerebral hypoxia/ischemia (H/I).
The second part of the seminar will be dedicated to the pathophysiological role of TRPV4 channels in adult rat astrocytes – we will talk about the functional expression of TRPV4 channels 1 hour (acute phase of reperfusion) and 7 days (late phase of reperfusion) after H/I in situ as well as in vitro.
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.