The goal of our laboratory is to understand the mechanisms that underlie synaptic and circuit plasticity in the developing and mature mammalian central nervous system. We use a combination of tools, including electrophysiological, in vitro and in vivo optical imaging methods, along with genetically altered mouse strains, optogenetics and pharmacogenetics to examine the regulation of synaptic circuits in the visual system.
One area of our research focuses on the establishment and refinement of synaptic circuits during development. We have characterized, using electrophysiological techniques, the convergence of the retinogeniculate synapse during development as multiple inputs are eliminated and remaining synaptic inputs strengthened. In addition, we have uncovered an experience-dependent critical period at this synapse during which connections can be re-wired late in development. Our recent studies show that cortical feedback regulates plasticity of this feedforward pathway. To identify and characterize the factors that mediate the different phases of remodeling of the retinogeniculate synapse, we are taking advantage of mouse mutants and viral-mediated circuit manipulations to elucidate the roles of specific molecular cues and plasticity mechanisms. These approaches are also used to advance our understanding of how disruption of proper synaptic circuit development can lead to neurodevelopmental disorders such as autism spectrum disorders, intellectual disabilities and epilepsy.
In another line of research, we are interested in understanding the mechanisms that regulate how firing patterns of retinal cells are decoded into the output of the thalamocortical neurons. These mechanisms are especially important during development, in the face of dramatic changes in strength and connectivity. We are addressing several questions: (1) how do specific retinal firing patterns influence synaptic strength through presynaptic and postsynaptic mechanisms, (2) how do ascending neurotransmitter systems from the brainstem and feedback circuits from the cortex and thalamic reticular nucleus alter the strength of the retinogeniculate synapse and sensory processing, and (3) how do long-term changes in presynaptic activity alter the properties of the retinogeniculate synapse.
About Chinfei Chen
Chinfei Chen received an MD/PhD from the Harvard/MIT Division of Health Sciences and Technology. She trained in adult neurology at Massachusetts General Hospital and as a postdoctoral fellow in the Neurobiology Department at Harvard Medical School before joining the faculty at Boston Children's Hospital . Chen was a 2001 Pew Scholar in the Biomedical Sciences.
Hooks BM, Chen C. Vision triggers an experience-dependent sensitive period at the retinogeniculate synapse. J Neurosci 2008 Apr 30; 28(18):4807-17.
Liu X, Chen C. Differential Roles for AMPA and NMDA Receptors in at the Immature Retinogeniculate Synapse. J Neurophysiology 2008; 99:629-43.
Hooks BM, Chen C. Critical periods in the visual system: changing views for a model of experience-dependent plasticity. Neuron 2007 Oct 25; 56(2):312-26.
Paradis S, Harrar DB, Lin Y, Koon AC, Hauser JL, Griffith EC, Zhu L, Brass LF, Chen C, Greenberg ME. An RNAi-based approach identifies molecules required for glutamatergic and GABAergic synapse development. Neuron 2007 Jan 18; 53(2):217-32.
Hooks BM, Chen C. Distinct roles for spontaneous and visual activity in remodeling of the retinogeniculate synapse. Neuron 2006 Oct 19; 52(2):281-91.
Hooks BM and Chen C. A model for synaptic refinement in visual thalamus. In: Erzurumlu R et al, eds. Development and Plasticity in Sensory Thalamus and Cortex. 2006. Springer Science+ Business Media, LL.
Seeburg DP, Liu X, Chen C. Frequency-dependent modulation of retinogeniculate transmission by serotonin. J Neurosci 2004; 24:10950-62.
For a list of Chinfei Chen's publications on PubMed, click here.