Associate Professor in neuroscience. Dr Valentino obtained his Ph.D in 2001 with distinction through a scholarship awarded by the Max Planck Institute for Neurological Research, Cologne, Germany following a brief training period as Research Guest Fellow. His study involved the investigation of the haemodynamic and cellular mechanisms of ischemic brain damage caused by strokes. Subsequently, he was awarded a 3-year post-doctoral fellowship in the Dept. of Neurology, Washington University, St.Louis, MO and the Hope Centre For Neurological Disorders, USA, to study the neurobiology of white matter damage in the context of ischemia and hypoglycemia using advanced imaging techniques. In Malta he has established the Laboratory for the Study of Neurological Disorders at the University of Malta that is centred around the study of mechanisms of injury and recovery after Stroke with special emphasis towards combined optical in vivo imaging techniques and electrophysiology. He is currently an active member of The Society of Neuroscience, International Brain Research Organization, Federation of Neuroscience Society and the New York Academy of Science. Prof. Valentino serves as ad hoc reviewer for the editorial boards of the journals: Stroke, J. of Neuroscience Methods, J. of Visualized Experiments, Glia, Neuroscience, Frontiers in Cellular Neuroscience, Neuroscience Research, CNS Neuroscience and Therapeutics, Future Neurology and J. of Cerebral Blood Flow and Metabolism and supervised several student doctoral and masters projects in his field. He has published extensively in high impact journals and book chapters and serves as a reviewer for the World Stroke Conference for the term 2015-2018. He is also Review Editor for Frontiers in Cellular Neuroscience, American Journal of Biomedical Research, International J. Biological Studies, CNS Neuroscience and Therapeutics and Neurology and Neurotherapy.
Vesicular glutamate release from central axons contributes to myelin damage. Nature Communications, 2018; 9 (1) DOI: 10.1038/s41467-018-03427-1
Early Loss of Blood-Brain Barrier Integrity Precedes NOX2 Elevation in the Prefrontal Cortex of an Animal Model of Psychosis (2016). Mol.Neurobiology; DOI 10.1007/s12035-016-9791-8.
Acute nicotine induces anxiety and disrupts temporal pattern organization of rat exploratory behavior in hole-board: A potential role for the lateral habenula (2015). Frontiers in Cellular Neuroscience, Vol 9, 1-17.
Hsp60 response in experimental and human temporal lobe epilepsy (2015). Scientific Reports 5: 9434, DOI: 10.1038/srep09434.
The central role of Aquaporins in the Pathophysiology of Ischemic Stroke (2015). Frontiers in Cellular Neuroscience. http://dx.doi.org/10.3389/fncel.2015.00108.
Cerebral White Matter Injury following a Hypoxic/Ischemic Insult during the Perinatal Period: Pathophysiology, Prognostic Factors, and Future Strategy of Treatment Approach (2015). Current Pharmaceutical Design. DOI:10.2174/1381612821666150105122008.
Oligodendrocyte pathophysiology and treatment strategies in cerebral ischemia (2014). CNSNeuroscience and Therapeutics. 20(7):603-12.
Î²2-adrenergic receptors protect axons during energetic stress but do not influence basal glio-axonal lactate shuttling in mouse white matter (2014). Neuroscience, 26;277:367-74. The spectrum of ischaemia-induced white matter injury varies with age (2013). Xjenza online (1), 1-11.
High dose of 8-OH-DPAT decreases maximal dentate gyrus activation and facilitates granular cell plasticity in vivo (2013). Exp Brain Res.230(4):441-51.
Dysfunction of voltage-gated K+ Channels Kv1.1 in sciatic nerve causes spontaneous and stress- induced neuromuscular hyperexcitability (2012). Neurobiology of Disease, 47, 310-321.
Central axons preparing for myelination are highly sensitivity to ischemic injury due to the transient expression of Ca2+ channels (2012). Ann. Neurology 72:936â€“951.
Serotonin-Dopamine interaction in Nicotine Addiction: Focus on 5-HT2C Receptors (2012). In:Nicotine Addiction: Prevention, Health Effects and Treatment Options, Nova Publisher, NY ,ISBN:978-1- 62081,25-52.
NO modulation of the basal ganglia circuitry:Therapeutic implication for parkinson's disease (2011). CNS & Neurological Disorders. Drug Targets, 10 (7):777-79.