When I think back to what inspired me to a lifelong dedication to neuroscience the answer is clear: a captivating undergraduate lecture on bat echolocation. The professor had the ability to weave scientific findings into a historical narrative and ignited my fascination with scientific controversy. This professor subsequently became my undergraduate advisor. I began my research career in the invertebrate nervous system doing extracellular recordings from the giant nerve fibers of the earthworm and sharp electrode recordings from crayfish ganglia.
I joined New York University’s Center for Neural Science for my doctorate where I worked on the following question: how is synaptic activity transformed into spiking output? The dendritic trees of most neurons in the brain have voltage and time-dependent conductances (ion channels), and I focused on how these impact the transformation of input to output in layer 5 pyramidal neurons. How these neurons perform this operation is of great interest because their dendritic tree is a hot point of integration in the cerebral cortex and they are they main output neurons of cortical circuits. Layer 5 pyramidal neurons receive tens of thousands of excitatory synapses arising from most cortical layers and distant brain areas.
During my postdoctoral work at Cold Spring Harbor Laboratory I extended my expertise of single cell computations to circuits. I began by studying temporal integration in the auditory cortex. I found a variety of temporal response patterns to simple auditory stimuli, and realized quickly that more information about the underlying circuitry was needed to interpret them. Thus began my quest to link structure and function in the auditory cortex.
My most fascinating discovery was to find that the fine-scale organization of the primary auditory cortex is specialized to the unique anisotropic and one-dimensional functional representation of sound frequency in the auditory cortex. This is another blow to lumpers in science who hold on to the notion that all cortical areas are wired according to the same general schema, regardless of what computation is performed in each area.
My most recent postdoctoral endeavor has been to link mouse models of human mental disorders with specific deficits in functional circuitry. Many mental disorders are genetically complex, but their ultimate effect on neuronal circuits may present a more constrained set of alternations. I have characterized circuit deficits in a wide range of autism spectrum disorder (ASD) candidate gene mouse models. From models with severe clinical phenotypes (MeCP2 and PTEN knockouts) to the milder Neuroligin 3 knockout.
At this very moment I am neglecting 2-3 new projects…