ISSN: 2329-6895

Journal of Neurological Disorders
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Lucas Pozzo-Miller
Lucas Pozzo-Miller

Lucas Pozzo-Miller, PhD
Department of Neurobiology
The University of Alabama


Professor Lucas Pozzo Miller completed his undergraduate studies in Biology (M.Sc., 1986) and earned his graduate degree in Neurobiology from the Universidad Nacional de Córdoba, Argentina (Ph.D., 1989). He trained as postdoctoral fellow at Case Western Reserve University, Cleveland OH, with Dr. Dennis Landis (1990-­â€1992), and at the former Roche Institute of Molecular Biology, Nutley NJ, with Dr. John Connor (1992-­â€ 1995). He performed research at the Marine Biological Laboratory, Woods Hole MA, with Dr. Rodolfo Llinás (1994 Grass Foundation Fellow, and 1995 Lakian Foundation Fellow). He held a Senior Staff Fellow position at the National Institutes of Health, Bethesda MD, in the laboratory of Dr. Thomas Reese (1995-­â€1998), and joined the faculty of the Department of Neurobiology at The University of Alabama at Birmingham in 1998. He is presently Professor of Neurobiology.

Research Interest

The long-­â€term interest of the Pozzo-­â€Miller lab is to characterize the functional role of structurally defined neuronal compartments such as dendritic spines and presynaptic terminals, and how they participate in synaptic development, function and plasticity as they relate to learning and memory. We focus on the hippocampus due to its well-­â€known role in learning and memory. Neurotrophins such as brain-­â€derived neurotrophic factor (BDNF) are secretory proteins that regulate neuronal survival and differentiation, as well as synapse development, function and plasticity.

Neurotrophic factors are strong candidates to provide the molecular signaling pathways mediating complex interactions leading to appropriate dendritic maturation and synapse development. We focus on the actions of neurotrophins in the hippocampus to characterize the regulation of synaptic transmission and plasticity by slow-­â€acting non-­â€classical neuromodulators. Currently, we are investigating the "BDNF hypothesis" of Rett syndrome, a neurodevelopmental disorder associated with autistic features and intellectual disabilities that is caused by mutations in MECP2, a transcriptional regulator of many genes, including Bdnf. In our studies, we apply several functional and structural approaches to acute and cultured slices of hippocampus, including intracellular whole-­â€cell recordings, Ca2+ and voltage-­â€dye imaging, confocal microscopy, synaptic vesicle recycling with FM dyes, multiphoton excitation microscopy, as well as conventional and rapid-­â€freezing electron microscopy


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