David C. Martinelli, Ph.D.Assistant Professor of Neuroscience
|B.S.||University of Rochester||Molecular Genetics|
|Ph.D.||Johns Hopkins University and Carnegie Institution for Science||Developmental Biology; Thesis Advisor: Dr. Chen-Ming Fan|
|Postdoctoral||Stanford University||Advisor: Dr. Thomas Südhof, 2013 Nobel laureate. Research Focuses: Neuroscience, Mouse Behavior, Virus Vectors, Genetics, Cellular Biology and Biochemistry|
|Name of Award/Honor||Awarding Organization|
|Ruth L. Kirschstein-NRSA postdoctoral fellowship (2012-2015)||National Institute on Drug Abuse|
|Dean’s Postdoctoral Fellowship (2010-2011)||Stanford University|
|First Prize in Poster Competition (2007)||Society for Development Biology Annual Meeting|
|First Prize in Poster Competition, Biology Department Annual Retreat (2007)||Johns Hopkins University|
|Phi Beta Kappa, Member (2003)||Phi Beta Kappa Society|
|Donald R.Charles Memorial Award for Promise in Scientific Career (2003)||University of Rochester|
|Undergraduate Writing Colloquium Winner (2002)||University of Rochester|
|Rush Rhees Scholarship Recipient for Academic Achievement (1999-2003)||University of Rochester|
A synapse is the fundamental structural unit by which neurons communicate. The importance of synapses cannot be overstated as their collective activities impact every moment of our subconscious and conscious mind. Furthermore, synapses are formed and continuously restructured throughout life based on different experiences, which ultimately shapes us as individuals with unique memories, thoughts, skills, and personalities. How the trillions of synapses in a brain are wired into functional neural networks and the mechanisms of experience-dependent synaptic plasticity are important outstanding questions.
I am particularly fascinated by synaptic adhesion proteins, which bind across the synaptic cleft to form a molecular interface between pre- and post-synaptic membranes and also initiate intercellular trans-synaptic signaling. These proteins are at the junction of our genes and experiences and are critical for initiating and stabilizing synaptic changes in a multitude of ways. My research goal is to understand the molecular logic of how synaptic adhesion proteins, in a defined brain circuit, orchestrate synaptic formation, modification, and function, and to ultimately provide an explanation for how these events influence behaviors, in particular the aberrant behaviors associated with neuropsychiatric diseases.
The immediate focus of my research is on the neuronally secreted C1q-like family of proteins. The lab will study the biochemical interactions with their pre- and post-synaptic protein binding partners, their synaptic signaling activities, and their eventual behavioral consequences. A priori, their localization in the synaptic cleft almost predestines them to have neuropsychiatric disease relevance. Genetic analyses of C1q-like mutant mice revealed behavioral abnormalities potentially resembling several neuropsychiatric diseases, including ADHD, schizophrenia, and addiction predisposition. How C1q-like proteins and their binding partners influence synapses and ultimately behaviors is unknown. The techniques used in the lab to answer these questions encompass biochemistry, genetics, cell biology, circuit analysis using viral vectors, and mouse behavioral assays.
I am currently accepting applications from graduate students, postdocs, and technicians.
Accepting students for Lab Rotations: Summer '17, Fall '17, Spring '18
Potential rotation projects:
1) Biochemistry of synaptic adhesion proteins. This project would be tailored to a student with an interest in the biochemistry of proteins relevant to neuropsychiatric diseases. The project involves the production and purification of proteins from eukaryotic cells, and then biochemical analysis of their binding properties.
2) Synaptic cell biology. This project would be tailored to a student interested in modeling neuronal systems in vitro and would involve learning to culture primary neurons and analyzing intracellular signaling events in response to C1q-like protein manipulation.
3) Behavioral study of addiction phenotype of C1q-like mutant mice. This project would be tailored to a student interested in behavioral neuroscience and a clear link to translational research. This project will involve learning to set up a cocaine self-administration paradigm and testing mutant mice for potential phenotypes.