Garner Lab Research Areas
Human neural development is an amazingly complex process. It begins with the birth of neural cells in the developing neural tube and is followed by the migration of these cells to specific layers within the developing brain. Near the end of their migration, nerve cells undergo a phase of differentiation during which they form both axons and dendrites that traverse large distances forming synaptic contacts with specific subpopulations of target nerve cells throughout the central and peripheral nervous system.
Mechanistically, these early phases of neuronal differentiation and synaptogenesis appear to be largely genetically encoded. However, once axons reach their appropriate targets, the refinement, maintenance and elimination of synaptic contacts becomes strongly influenced by neural activity and sensory input. These activity-dependent events are tightly coupled to a phenomenon known as synaptic plasticity—a process wherein synapses can modify the strength with which they transmit information. For example, strong correlated signaling tends to strengthen synaptic contacts, while weak asynchronous neurotransmission leads to the weakening or loss of synapses or both. Synaptic plasticity is also critically important for the encoding and processing of information in our mature brain and is ultimately responsible for our ability to learn, retain and access memories.
Of the many phases of neural development, we are most interested in understanding the molecular mechanisms underlying the formation and plasticity of synapses. These events are critical to the proper wiring of the nervous system and for information processing in the developing and mature brain.
Research in the Garner lab is focused on three areas. The first research area is aimed at understanding the molecular mechanisms that guide synapse formation. The second is designed to define the principles that regulate synaptic strength or synaptic plasticity. The third research area aims to understand how changes in synaptic function in individuals with neurodevelopmental disabilities alter their behavior and capacity to learn. In this regard, we are focusing our efforts on Down syndrome and autism spectrum disorders. Experiments designed to address each of these questions have begun to lay the foundation for both an understanding of how specific genetic lesions can cause intellectual disabilities and possible treatment strategies.
See also
The work described here was supported by grants from the National Institutes of Health, the Nancy Pritzker Foundation, the Hillblom Foundation, the Down syndrome research and treatment foundation (dsrtf.org), the Deutsche Forschungsgemeinschaft (DFG) and US-Israel Binational Science Foundation (BSF) .
