Carles Solsona Sancho

Pathology and Experimental Therapeutics
University of Barcelona
Spain

Professor Pathology
Biography

Carles Solsona Sancho is Associate Professor from Department of Pathology and Experimental Therapeutics at University of Barcelona. Current Projects SAF 2005-00736. CONNEXINS AND ATP RELEASE. ROLE IN THE PATHOGENESIS OF X-LINKED CHARCOT MARIE TOOTH DISEASE. Ministry of Science and Education. Spanish Government.

Research Intrest

The main goal of my research is to find cellular and molecular mechanisms underlying the neurodegenerative diseases, especially those related with the communication between neurons and their targets. Because ATP is present inside synaptic vesicles and it is exocyted during synaptic transmission I have found the interaction of ATP into the luminal synaptic vesicle matrix. However, other alternative cellular pathways may be activated to allow the release of intracellular ATP release. We have found that at least two molecules: NTPDases and connexins, are implicated in making the plasma membrane permeable to ATP. Because it has been demonstrated that Connexin 32 is implicated in the development of Charcot Marie Tooth disease linked to chromosome X, at present my major focus of interest is how connexins form the so called hemichannels or connexons and their physiological role controlling ATP release and its putative role in the pathogenis of CMTX. I’m also investigating about the possible implication of purinergic signaling in the Amyotrophic Lateral Sclerosis. I also collaborate with Professor Antonio Felipe, Department of Biochemistry and Molecular Biology, looking for the activity of potassium channels in the immune response.

List of Publications
Pattern of Kv beta subunit expression in macrophages depends upon proliferation and the mode of activation.
Effect of galantamine on the human alpha7 neuronal nicotinic acetylcholine receptor, the Torpedo nicotinic acetylcholine receptor and spontaneous cholinergic synaptic activity.
Endogenous hemichannels play a role in the release of ATP from Xenopus oocytes.