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Neuroscience Graduate Program at UCSF
Synapse Formation, Growth and Plasticity
Neurons are organized into intricate circuits through synaptic connections. Synapses form, retract, strengthen and weaken during the early wiring of neural circuits, and throughout life as a basis for phenomena such as learning and memory. We are taking a genetic approach in Drosophila to elucidate the molecular mechanisms that specify the formation, development and plasticity of synaptic connections. My laboratory brings together molecular, genetic and electrophysiological techniques to address these questions.
One focus is to identify trans-synaptic signaling molecules that control synaptic growth and plasticity. Of particular interest are target derived molecules that influence presynaptic structure and function. First generation genetic screens have identified several mutations, expressed in muscle, that regulate various aspects of presynaptic growth and function. We are in the process of cloning and characterizing these genetic loci, as well as continuing to screen for new mutations in these retrograde signaling systems.
A second focus is to investigate the mechanisms of activity-dependent synaptic plasticity. Long-term changes in synaptic function require parallel changes in the expression levels of cell adhesion molecules at the synapse, and CREB mediated transcription in the cell nucleus. We are investigating how activity-dependent changes in cell adhesion regulates synaptic structure. We are also searching for the key regulatory molecules downstream of the transcription factor CREB that are necessary for activity-dependent strengthening of synaptic connections.Link to Publications via PubMed
Schuster, C.M., Davis, G.W. and Goodman, C.S. (1996) Genetic analysis of structural and function components of synaptic plasticity II. Fasciclin II controls presynaptic structural plasticity. Neuron 17, 655-667.
Davis, G.W., Schuster, C.M. and Goodman, C.S. (1996) Genetic analysis of structural and functional components of synaptic plasticity III. CREB is necessary for presynaptic functional plasticity. Neuron 17, 669-679.
Davis, G.W., Schuster, C.M. and Goodman, C.S. (1997) Genetic analysis of the molecular mechanisms controlling target selection: target-derived Fasciclin II regulates the pattern of synapse formation. Neuron 19, 516-517.
Davis, G.W., DiAntonio, A., Petersen, S.A., and Goodman, C.S. (1998) PKA controls quantal size and reveals a retrograde signal that regulates presynaptic release in Drosophila. Neuron 20, 305-315.
Davis, G.W., and Goodman, C.S. (1998) Synapse-specific control of synaptic efficacy at the terminals of a single neuron. Nature 392, 82-86.Graeme Davis, Ph.D.
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