Professore Ordinario

Since the very beginning, the scientific career of Maurizio Taglialatela has concentrated on the study of various aspects of ion channel physiology and pharmacology and, more recently, of human genetic diseases caused by ion channel pathogenic variants (genetic channelopathies).

During his early training as a medical and PhD student, he focused on learning the neurochemical tools used to investigate the role of calcium transport systems in dopamine release from hypothalamic tuberoinfundibular neuron. These studies provided pharmacological evidence for both a minor role for dihydropyridine-sensitive L-type on presynaptic nerve terminals (Annunziato et al., Neuropharmacology 1986), and for a novel role of the sodium-calcium exchanger (Taglialatela et al., J Pharm Exp Ther 1988; Taglialatela et al., Mol Pharmacol. 1990).
After a training period with patch-clamp, the gold-standard technique for electrophysiological investigation of ion channel function, his work contributed significantly to the emerging field of the structure-function of ion channels. In fact, it was during his early post- doctoral years at Baylor College of Medicine, immediately after the cloning of the first ion channel genes in the mid-80’s, that he used pharmacological tools to investigate the location of the ion-conduction pore in voltage- and non-voltage-gated potassium channels. Overall, these studies provided seminal contributions to the understanding of the molecular mechanism of ion permeation, conduction, and block.

His current research efforts continue to concentrate on these rare channelopathies, which lack effective therapies. The results achieved thus far have had a direct impact on patients and their families, since they helped to define the natural history of these diseases, reveal genotype-phenotype correlations, and improve patient stratification. As understanding of the molecular pathogenesis of these rare diseases grows, his research hopes to lead to clinical trials based on the underlying molecular etiology, thus accelerating the identification of new therapies for these severe neurodevelopmental disorders (Zanello et al., EMBO Mol Med 2023).