Lia Forti
Lia Forti
affiliation: Università dell'Insubria
research area(s): Neuroscience, Cell Biology
Course: Neurobiology
University/Istitution: Università dell'Insubria
Educational and Scientific Profile:

Graduated in Physics, University of Milan, 1987.

PhD in Biophysics, International School for Advanced Studies (SISSA-ISAS), Trieste, 1992. Supervisor: D. Pietrobon (University of Padua).

1991-1993. PhD student: patch-clamp study of voltage-operated Ca2+ channels in cerebellar neurons, lab of D. Pietrobon (Univ of Padua)

1993-1997. Post-doc: patch-clamp study of the quantal properties of excitatory neurotransmission, lab of A.Malgaroli (Dibit, Scientific Institute San Raffaele, Milano)

1997-1999. Post-doc: patch-clamp and Ca2+ imaging in cerebellar slices, lab of A. Marty e I. Llano (Max-Planck Institut fur biophysikalische Chemie, Göttingen, Germany)

1999-2007. Research Associate: patch-clamp studies of the excitability and synaptic properties of cerebellar interneurons, lab. of E. D’Angelo (University of Pavia)

2008 – present. University Researcher, Univ of Insubria. PI of the Cellular Neurophysiology Laboratory: patch-clamp and microelectrode array (MEA) recordings from brain slices.

Member of the Italian Neuroscience Society (SINS) and the american Society for Neuroscience (SfN).

1999-2004: Membrane Biophysics Course, Physics Degree, Univ of Milano;
2005-2006: Biophysics Course, Biotechnology Degree, Univ of Insubria
2003-2011: Applied Physics Laboratory, Biotechnology, Biology and Biomedicine Degrees, Univ of Insubria.
2012-present: Physics Course, Biological Sciences and Technologies Degree, Univ of Insubria
Lia Forti has an expertise of cellular neurophysiologist, using patch-clamp electrophysiology, calcium imaging and multi-electrode array (MEA) recordings in brain slices and cell cultures.

Current research interests:

1) MEA STUDY OF NEOCORTICAL EXCITABILITY IN AN ANIMAL MODEL OF FAMILIAL MIGRAINE (in collaboration with D. Pietrobon, Univ of Padua, and with R. Fesce, Univ of Insubria).

Alterations of neocortical excitability in an animal model of familial migraine. The goal is the study of the neurobiological basis in the pathogenesis of migraine. Using a transgenic murine migraine model (familial hemiplegic migraine type 1, FHM1), available in the collaborating laboratory of dr. Pietrobon (University of Padua), and MEA extracellular recordings in slices from the mouse barrel cortex, we aim at identifying possible alterations in the balance of excitation and inhibition in neocortical circuits. These alterations may favor the start of cortical spreading depression (CSD), which is a wave of neuronal over-excitation followed by depression, typical of some migraine patients, and triggered by specific sensory inputs. In the framework of this project, our lab is involved in the characterization, in wild type (wt)and mutant (KI) animals, of the functional and pharmacological properties of local field potential (LFP) responses to layer IV and thalamic stimulation. We are also analyzing, in collaboration with R. Fesce, the strain-related differences in the spatio-temporal dynamics of neocortical spontaneous population activity (up-states).


The synaptic inputs and intrinsic excitability of cerebellar inhibitory interneurons is studied in Golgi cells. We have recently described, using patch-clamp, Ca2+-imaging and immuncytochemical techniques, a novel class of excitatory synaptic inputs from granule cells to Golgi cells in the granular layer (Cesana et al., submitted), which has relevance for the organization of the cerebellar inhibitory system and the elaboration of cerebellar output. We now proceed with the study of neuromodulation of the inhibitory network by serotonin (5-HT). In the cerebellum, 5-HT regulates the generation of synchronous firing in neuronal sub-populations, with implications for motion control and motion learning. 5-HT-activated mechanisms and targets in cerebellar neurons are largely ignored. In Golgi cells, 5-HT regulates intrinsic excitability by controlling a depolarizing basal current. The molecular identity of this current is under study (Polenghi & Forti, “Serotonergic modulation of excitability in a cerebellar interneuron“, 8th IBRO World Congress of Neuroscience, Florence, 2011). The 5-HT modulation of synaptic inputs to Golgi cells should also be studied in the near future.
(submitted): Cesana E, Pietrajtis K, Bidoret C, Isope P, D'Angelo E, Dieudonné S, Forti L. “Granule cell ascending axon excitatory synapses onto Golgi cells implement a potent feedback circuit in the cerebellar granular layer”.

Fesce R, Forti L, Polenghi A, Locarno A, Canella R, Sacchi O, Rossi ML. (2011). Can selectivity be functionally modulated in ion channels? J Gen Physiol. 138(3):367-70.

Solinas SM, Forti L, Cesana E, Mapelli J, De Schutter E, D`Angelo E [2007]. ”Computational reconstruction of pacemaking and intrinsic electroresponsiveness in cerebellar Golgi cells”. Front. Cell. Neurosci. 1:2. doi:10.3389/neuro.03.002.2007

Solinas SM, Forti L, Cesana E, Mapelli J, De Schutter E, D`Angelo E [2007]. ”Fast-reset of pacemaking and theta-frequency resonance patterns in cerebellar Golgi cells: simulations of their impact in vivo”. Front. Cell. Neurosci. 1:4. doi:10.3389/neuro.03.004.2007

Forti L, Cesana E, Mapelli J, D'Angelo E (2006). "Ionic mechanisms of autorhythmic firing in cerebellar Golgi cells". J. Physiology, 574(3):711-729.

Gall D, Prestori F, D’Errico A, Roussel C, Sola E, Forti L, Rossi P,D’Angelo E (2005). "Intracellular calcium regulates bidirectional long-term synaptic plasticity at the mossy fiber-cerebellar granule cell synapse". Journal of Neuroscience, 25(19):4813-22.

Abenavoli A, Forti L, Bossi M, Bergamaschi A, Villa A, Malgaroli A (2002). "Multimodal Quantal Release at individual hippocampal synapses: evidence for lack of lateral inhibition". Journal of Neuroscience, 22(15):6336-46.

Forti L, Pouzat C, Llano I (2000). "Action potential-evoked Ca2+ signals and calcium channels in axons of developing rat cerebellar interneurons", Journal of Physiology, 527(1):33-48.

Forti L, Bossi M, Bergamaschi A, Villa A, Malgaroli A (1997). "Loose-patch recordings of single quanta at individual hippocampal synapses". Nature, 388:874-878.

Forti A, Tottene A, Moretti A, Pietrobon D (1994). "Three novel types of voltage-dependent calcium channels in rat cerebellar neurons", Journal of Neuroscience, 14: 5243-5256.

Forti L, Pietrobon D (1993). "Functional diversity of L-type calcium channels in rat cerebellar neurons", Neuron, 10: 437-450.

Galgani L, Angaroni C, Forti L, Giorgilli A, Guerra F (1989). "Classical Electrodynamics as a nonlinear dynamical system", Physics Letters A, 139:221-230.
Project Title:
MEA STUDY OF NEOCORTICAL EXCITABILITY IN AN ANIMAL MODEL OF FAMILIAL MIGRAINE: origin and properties of spontaneous and thalamically-evoked up-states
The goal of this project is the study of the neurobiological basis in the pathogenesis of migraine. The underlying hypothesis is that migraine results from a cascade of events originating from an unbalance in the activity of excitatory and inhibitory networks in the neocortex and/or subcortical structures (Vecchia and Pietrobon, Trends Neurosci. 2012 Aug;35(8):507-20). To validate this hypothesis, in this project we will perform electrophysiological recordings of up-states in brain slices from the somato-sensory cortex of a transgenic murine migraine model (familial hemiplegic migraine type 1, FHM1, studied in collaboration with D. Pietrobon, Univ of Padua), and compare them to up-states in wild-type animals, using multi-electrode array (MEA) recordings and analytical procedures implemented in MatLab.
Up-states are episodes of depolarization and increased excitability occurring simultaneously in assemblies of connected neurons, observed in various cortical and subcortical areas in awake and sleeping animals, as well as in in-vitro slice preparations (Wilson, 2010, Scholarpedia; In the course of the project, we want to describe how the properties of up-states are changed in transgenic migraine animals, and relate this to specific alteration in the synaptic properties of excitatory and inhibitory neurons.