2015 Seed Grant
Matthew Kennedy, Ph.D.
University of Colorado
Synaptic plasticity is thought to be essential for normal cognition and is impaired in numerous neuropsychiatric disorders and diseases, including schizophrenia, autism, and Alzheimer’s. While plasticity defects likely underlie many symptoms of these disorders, little is known about why plasticity is impaired. On a molecular level, plasticity dependent synaptic changes are governed by molecular signaling and trafficking events that occur at synapses. A major difficulty in studying these molecular events is the lack of suitable tools to study processes on fast time scales in localized regions of neurons. Furthermore, there remains an unmet need for tools to acutely, reversibly and locally control these events in vivo. Such tools would help resolve longstanding questions concerning where, when and whether intensely investigated forms of synaptic plasticity, mostly studied in brain slices or dissociated neurons, are relevant for behavior in normal and disease models.
