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During postnatal development, mammals, including humans, acquire vast amounts of information by interacting with their environments. In contrast to creatures having nervous systems that are fully pre-wired at birth, mammals benefit from an enormous flexibility in behavior due to the driving force of experience on their brain development. This flexibility comes at a potential cost, however, because interaction with noxious or otherwise abnormal
environments can cause lasting and often deleterious changes in brain circuitry. Our
working hypothesis is that environmental insults during development can result in impaired human cognition during adulthood. One way this might happen is through an increased susceptibility to diseases thought to have environmental components as risk factors (schizophrenia and Alzheimer's disease, for example). The research done in the Synaptic and Developmental Plasticity Group focuses on determining how the connections in the brain (synapses) change in response to activity, how synaptic plasticity during early postnatal development is different from plasticity in the adult, and why some brain regions are more plastic than others. This research should bring us a better understanding of how environmental factors play a role in brain development so that we may begin to address the associated problems of brain disease caused by toxicant exposure.
We are working on three main projects in the lab:
- Synapse elimination in the cerebral cortex during development (how experience shapes brain circuitry)
- Circuitry in a layer of the cerebral cortex (layer IV) noted for its lack of plasticity, and incidentally, resistance to damage by Alzheimer's disease
- Long-lasting changes in the strength of synapses, specifically how neuronal activity changes gene expression in neurons
Relevant Publications
Dudek, S.M. and Fields, R.D. Somatic action potentials are sufficient for late-phase LTP-related cell signaling. Proc Natl Acad Sci U S A. 99(6): 3962-3967, 2002.
Dudek, S.M. and Fields, R.D. MAP-Kinase/ERK phosphorylation in somato-dendritic compartments: roles of action potentials, frequency, and mode of calcium entry. J. Neurosci. 21: RC122, 2001.
Dudek, S.M. and Fields, R.D. Gene expression in hippocampal long-term potentiation. The Neuroscientist 5: 275-279, 1999.
Dudek, S.M. and Friedlander, M.J. Developmental down-regulation of LTD in cortical layer IV and its independence of modulation by inhibition. Neuron 16: 1097-1106, 1996.
Dudek, S.M. and Bear, M.F. Bidirectional long-term modification of synaptic effectiveness in the adult and immature hippocampus. J. Neurosci. 13: 2910-2918, 1993.
Dudek, S.M. and Bear, M.F. Homosynaptic long-term depression in area CA1 of hippocampus and the effects of NMDA receptor blockade. Proc. Natl. Acad. Sci. USA, 89: 4363-4367, 1992.
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Last updated May 2003
