My scientific training spans biology and neuroscience, with a focus on synaptic development. My research has spanned topics such as neuron/glia interaction at synapses during the period of synaptic formation and refinement, to exploring how neonatal seizures change molecular and cellular pathways at the synapse to contribute to the development of autistic behavior and epilepsy. In my current work, I focus largely on the development of excitatory synapses, and the mechanisms by which the responsive capacity of synaptic structures can be altered during brain development. A long-term goal of my research is not only to uncover the mechanisms underlying normal brain development, but also to provide a new line of research on which to base therapies for multiple neurodevelopmental deficits.
In addition to research, I have taught and assisted in multiple Neuroscience courses at Brown University, Harvard University, and Bryn Mawr College. I also have a passion for science writing, and have contributed content a range of publications and companies.
Throughout my research career, I have been dedicated to uncovering mechanisms of synaptic development, maintenance, and plasticity. I am interested in how early-life events can disrupt these mechanisms, often with long-term consequences. I focus largely on excitatory synapses, particularly those located on synaptic structures called dendritic spines, small protrusions off of dendrites that are the sites of 90% of the excitatory contacts in the brain. Specifically, I aim to elucidate mechanisms by which the responsive capacity of synaptic structures, known as structural plasticity, can be altered during brain development. Although structural plasticity is a major component of the process of synaptic plasticity, which is involved in everything from learning and memory to addiction, it is still poorly understood. Changes indicative of altered structural plasticity of dendritic spines have been observed in epilepsy, autism, chronic stress, and depression models, signifying its importance in a broad range of neurological and psychiatric disorders. As such, a long-term goal of my research is not only to uncover the mechanisms underlying normal brain development, but also to provide a new line of research on which to base therapies for multiple neurodevelopmental deficits.
Sun H, Takesian AE, Wang TT, Lippman‐Bell JJ, Hensch T, Jensen FE. (2018) Early seizures prematurely unsilence auditory synapses to disrupt thalamocortical critical period plasticity. Cell Rep. 23(9):2533-40.
Rosenberg EC, Lippman-Bell JJ*, Handy M, Soldan SS, Rakhade S, Hilario-Gomez C, Folweiler K, Jacobs L, Jensen FE. (2018) Regulation of seizure-induced MeCP2 Ser421 phosphorylation in the developing brain. Neurobiol Dis. pii: S0969-9961(18)30139-6. *co-first author
Lippman-Bell JJ, Zhou C, Sun H, Feske JS, Jensen FE. (2016) Early-life seizures alter synaptic calcium-permeable AMPA receptor function and plasticity. Mol. Cell. Neurosci. 76: 11-20.
Lippman-Bell JJ, Rakhade S, Klein PM, Obeid M, Jackson MC, Joseph A, Jensen FE. (2013) AMPA Receptor antagonist NBQX attenuates later-life epileptic seizures and autism-like behavioral deficits following neonatal seizures. Epilepsia. 54(11):1922-32.
Zhou C, Lippman Bell JJ, Sun H, Jensen FE. (2011) Hypoxia-induced neonatal seizures diminish silent synapses and long-term potentiation in hippocampal CA1 neurons. J. Neurosci. 31(50): 18211-18222.
Lippman Bell JJ, Lordkipanidze T, Cobb N, Dunaevsky A. (2010) Bergmann glial ensheathment of dendritic spines regulates synapse number without affecting spine motility. Neuron Glia Biology. 6(3): 193-200.
Lippman JJ, Lordkipanidze T, Buell ME, Yoon SO, Dunaevsky A. (2008) Morphogenesis and regulation of Bergmann glial processes during Purkinje cell dendritic spine ensheathment and synaptogenesis. Glia. 56: 1463-77.
Lippman JJ, Dunaevsky A. (2005) Dendritic Spine Morphogenesis and Plasticity. J. Neurobiol. 64(1): 47-57.
Sanchez RM, Dai W, Leveda R, Lippman JJ, Jensen FE. (2005) AMPA/kainate receptor-mediated downregulation of GABAergic synaptic transmission by calcineurin following seizures in the developing rat brain. J. Neurosci. 25: 3442-51.