Dr. Liliana Minichiello, is a Reader in Cellular and Molecular Neuroscience, and has joined the Department of Pharmacology in October 2012. She received a Laurea in Biological Sciences from the University of Naples, Federico II, Italy and then went on for her graduate studies in Molecular Biology first at the University of Naples, Federico II, Italy (group of Prof Arturo Leone), and then at The National Cancer Institute, NIH, Bethesda, (MD) USA (group of Dr Pier Paolo Di Fiore). This was followed by a few years spent at the European Molecular Biology Laboratory (EMBL) in Heidelberg, Germany, for her postdoctoral training (group of Dr Rüdiger Klein), where she worked on the biological functions of neurotrophin receptor tyrosine kinases (Trks) in the mouse nervous system by generation and analysis of genetic mouse models. She then became the leader of a group at the EMBL Mouse Biology Unit in Monterotondo, Rome, Italy (2000-09). She was then appointed as Reader and Deputy Director of the Centre for Neuroregeneration at the University of Edinburgh, Scotland, moving to Oxford in 2012.
Dr Minichiello is presently a visiting scientist at the Mouse Biology Unit, EMBL-Monterotondo, Rome, Italy. She has held a visiting professorship at the Lund Stem Cell Center, Lund University, Lund, Sweden (2005-2010). She has been awarded prestigious fellowship for her postdoctoral studies such as EMBO long-term fellowship, and has organized and taught on many EMBO courses in the past few years.
Therefore, our main research interest has long been to define molecular and cellular mechanisms underlying synaptic plasticity, learning and memory. Key achievements include the genetic demonstration that the neurotrophin receptor TrkB is a potent regulator of hippocampal synaptic plasticity via activation of pathway/s through its PLCγ-site; that the molecular pathways required for learning are also those generating long-term potentiation (LTP, which is considered to be the mechanism for acquisition and storage of information by synapses in the brain) when measured directly on the relevant circuit of a learning animal; that TrkB modulates specific phases of fear learning and amygdalar synaptic plasticity by specific docking sites.
In order to improve our understanding of the basic mechanisms underlying age-related cognitive decline one current main aim is the molecular dissection of cellular pathway/s involved in age-dependent neurodegeneration process via a combination of state of the art technologies including spatially restricted genetic manipulation, gene expression analysis, ChIP-sequencing, and intracellular signalling and protein chemistry integrated with physiological readouts such as behaviour, histology and imaging.
Moreover, very little has been achieved so far regarding the specific functions of different inhibitory neuronal subtypes in the living animal. Therefore, we aim to determine the role of distinct subtypes of inhibitory neurons in functional brain circuits by using combinatorial approaches and defined genetic mouse models.
We believe that by understanding how specific neuronal subtypes and specific molecules contribute to normal animal behavior and diseased neurological conditions will help to develop better therapies and treatments
NGF-TrkA signaling in sensory nerves is required for skeletal adaptation to mechanical loads in mice.
Tomlinson RE. et al, (2017), Proc Natl Acad Sci U S A, 114, E3632 - E3641
Retinol Dehydrogenase-10 Regulates Pancreas Organogenesis and Endocrine Cell Differentiation via Paracrine Retinoic Acid Signaling.
Arregi I. et al, (2016), Endocrinology, 157, 4615 - 4631
Neurotrophin Signaling Is Required for Glucose-Induced Insulin Secretion.
Houtz J. et al, (2016), Dev Cell, 39, 329 - 345
NGF-TrkA Signaling by Sensory Nerves Coordinates the Vascularization and Ossification of Developing Endochondral Bone.
Tomlinson RE. et al, (2016), Cell Rep, 16, 2723 - 2735
Synaptic mechanisms of adenosine A2A receptor-mediated hyperexcitability in the hippocampus.
Rombo DM. et al, (2015), Hippocampus, 25, 566 - 580