Education and training


Born: Padova, Italy, May, 14, 1962 Italian Citizenship


1981 - High School degree: Liceo Classico "T.Livio", Padova
1988 - Doctor in Medicine and Surgery, magna cum laude - University of Padova 1988 - Minister of Health licensure for medical practice
1992 - Specialization in Neurology, magna cum laude - University of Padova


Research Assistant, Institute of Human Physiology and Institute of Neurology, University of Padova 1988-1992 Adjunct Professor, Molecular Biology Institute, Dep of Biology, SDSU, California, USA 1996-1997
Assistant Professor, tenure position, Istitute of Human Physiology, University of Padova, 1992-2010
Associate Professor, tenure position, Departmet of Human Anatomy and Physiology, University of Padova, 2010-

Head of the Neurobiology and Electrophysiology Lab, Department of Human Anatomy and Physiology, University of Padova, 1997-

Actual Teaching activity

Professor of Human Physiology, Human Physiology Course, Faculty of Medicine and Surgery, 2003-

Professor of Physiology, Physiology Course, Faculty of Pharmacy, University of Padova 2007-

Past scientific activity

  • Neuromotor and neurotrophic regulation of mammalian skeletal muscle contractile proteins. Using different experimental protocols (denervation, denervation without fibrillation, nerve activity block, nerve transport block, muscle regeneration) it was shown that slow contractile proteins expression is linked to neuromotor activity, while fast type contractile proteins are differently regulated by neuromotor and/or neurotrophic factors.
  • Electrophysiological and mechanical properties of mammalian skeletal muscle during ageing. During ageing mammalian skeletal muscle undergoes to a slow-to-fast shift in both contractile and electrophysiological properties.
  • Neurophysiological activity in Drosophila melanogaster null mutants of circadian pacemaker genes tim and per. The neurophysiological response and synaptic plasticity phenomena of a specified neuronal circuit (giant fiber pathway of adult flies) are changed in flies with no circadian rithm behaviour.
  • Neurophysiological analysis of D.melanogaster genes mutations involving visual behaviour. Specific promoter regions of NonA are differently affecting optomotor behaviour and eye electrophysiological responses to light stimuli. N
  • Regulatory role upon neurotransmitter release, of MAGUK presynaptic protein CASK. Null mutation of D.melanogaster caki , homolog of human gene CASK, is associated to an increase in spontaneous synaptic release and a decrease in evoked synaptic release.
  • Postsynaptic NFkB and IkB mobilization related to synaptic activity. In this study it was demonstrated that: a) D.melanogaster NFkB and IkB are localized at the postsynaptic membrane of neuromuscular junction in third instar larvae; b) they are mobilized following high frequency synaptic activity.



Actual scientific activity

  • Morphological, neurophysiological and behavioural characterisation of null mutations or functional KDs(by RNAi) of D.melanogaster homologs of human genes linked to inherited mitochondrial encephalo(-myo)pathies. Surf1 is D.melanogaster homolog of the human gene linked to Leigh disease, the most commun mitochondrial encephalomyopathy. Surf1 tissue selective functinal silencing using RNAi and UAS/Gal4 binary system in is associated to nervous system behavioural and functional alterations, as well as muscle functional and ultrastructural changes. DLETM1 is D.melanogaster homolog of human LETM1, which is linked to Wolf-Hirschorn syndrome, a disease associated to mental and growth retardation, malformations and epilepsy. Its tissue selective functional silencing using RNAi and UAS/Gal4 binary system, causes the appearance of behavioural, functional and morphological alterations at the level of nervous system and compound eye.
  • Functional role of membrane lipid composition in regulating neurotransmitter vesicle fusion with presynaptic membrane during exocytosis at the D.melanogaster neuromuscular junction. Artificial (adding artificial lipids to the experimental bath) or genetical (using null mutants for key enzymes of sphingolipid metabolic pathway) alterations of synaptic membranes lipid composition are associated to an increase or a decrease in vesicle release, according to the energetic profile favouring or interferring the biophysical fusion between vesicle and presynaptic membrane.
  • Analysis of SNARE complexes aggregation in mediating synaptic vesicle exocytosis at the D.melanogaster neuromuscular junction. Point mutation of SNAP25 residue involved in SNARE complexes aggregation into a rosette supercomplex around the fusion point of synaptic vesicle with presynaptic membrane, is associated to a decreased spontaneous and evoked synaptic release.