Massimo Avoli, MD, PhD
Massimo Avoli is Professor at À¦°óSMÉçÇø in the Departments of Neurology & Neurosurgery and of Physiology. He received his Medical Degree (1975) and Neurology training (1979) from the Sapienza University of Rome, and his PhD (1982) from À¦°óSMÉçÇø. In 1983, he worked in Dr. Per Andersen’s laboratory at University of Oslo analyzing the mechanisms underlying long-term potentiation of synaptic transmission. Dr. Avoli’s laboratory employs electrophysiological, pharmacological and molecular approaches to analyze the excitability of the rodent forebrain in experimental preparations both in vivo and in vitro. These studies focus on the interplay of inhibitory and excitatory mechanisms, especially as they relate to the genesis of synchronicity in neuronal networks. These neuronal processes are fundamental for understanding the mechanisms causing the generation of seizures in epileptic patients thus leading to develop new antiepileptic strategies. Dr. Avoli is particularly interested in the pathophysiology of mesial temporal lobe epilepsy, one of the most common forms of focal epilepsy in adulthood. Ongoing studies center on the role of GABAA receptor signaling in epileptogenesis and ictogenesis in this focal epileptic disorder. Dr. Avoli also employs optogenetic protocols to test the hypothesis that activation of specific cell types causes Ìýspecific seizure onset patterns in in vitro and in vivo preparations; such Ìýexperimental procedures seek to identify whether and how these processes influence and halt epileptogenesis. Several of Dr. Avoli's studies originate from collaborations with colleagues at the Neuro (Drs. S. Baillet, J. Gotman, T. Kennedy, P. McPherson, and Y. Zhou), À¦°óSMÉçÇø (Drs. N. Sonenberg and S. Williams), and Université de Montréal (Dr.G. Di Cristo, , and) as well as in Germany (Dr. R. Köhling), Italy (Drs. G. Biagini, and M. de Curtis), and USA (Drs. M. Bazhenov, M. Rogawski and S. Vicini).Ìý
Wang S, Lévesque M, Fisher TAJ, Kennedy TE, Avoli M. (2023) CA3 principal cell activation triggers hypersynchronous-onset seizures in a mouse model of mesial temporal lobe epilepsy. J Neurophysiol. 130: 1041-1052.Ìý
Avoli M, Chen LY, Di Cristo G, Librizzi L, Scalmani P, Shiri Z, Uva L, de Curtis M, Lévesque M. (2023) Ìý
Neurobiol Dis. 180:106097.Ìý
J Neurosci. 43: 1987-2001.Ìý
Sharma V, Sood R, Lou D, Hung TY, Lévesque M, Han Y, Levett JY, Wang P, Murthy S, Tansley S, Wang S, Siddiqui N, Tahmasebi S, Rosenblum K, Avoli M, Lacaille JC, Sonenberg N, Khoutorsky A. (2021) 4E-BP2-dependent translation in parvalbumin neurons controls epileptic seizure threshold. Proc Natl Acad Sci U S A. 118: e2025522118.ÌýÌý
Lévesque M, Chen LY, Etter G, Shiri Z, Wang S, Williams S, Avoli M. (2019) Paradoxical effects of optogenetic stimulation in mesial temporal lobe epilepsy. Ann Neurol. 86: 714-728.ÌýÌý
Shiri Z, Lévesque M, Etter G, Manseau F, Williams S, Avoli M. (2017) Optogenetic low-frequency stimulation of specific neuronal populations abates ictogenesis. J Neurosci. 37: 2999-3008.Ìý
Shiri Z, Manseau F, Lévesque M, Williams S, Avoli M. (2016) Activation of specific neuronal networks leads to different seizure onset types. Ann Neurol. 79: 354-65.Ìý
Avoli M, de Curtis M, Gnatkovsky V, Gotman J, Köhling R, Lévesque M, Manseau F, Shiri Z, Williams S. (2016) Specific imbalance of excitatory/inhibitory signaling establishes seizure onset pattern in temporal lobe epilepsy. J Neurophysiol. 115: 3229-3237.Ìý