The general theme of the work in the lab is a desire to understand the mechanisms underlying neural network function from both the perspective of an individual cell as well as the coordinated activity of the network as a whole.

Our model systems are the crustacean stomatogastric ganglion (STG) and cardiac ganglion (CG), as well as the mouse spinal cord and lower urinary tract. The STG has been at the forefront of electrophysiological questions of neural network function for over 3 decades. Our approach seeks to take this well characterized network to the molecular level to ask detailed questions about the interaction between the genome and the electrophysiogical output of individual cells and the network as a whole.

Our goal is to use these model systems to shed light on both the endogenous mechanisms of neural network function, but also responses of these networks in response to injury and other perturbations that challenge the system.

MouseWorkSpinal Cord Function and Changes in Spinal Motor Networks and Bladder Control Networks Associated with Spinal Cord Injury

The newest direction in our lab is using mammalian models to examine the physiological and molecular underpinnings of motor network function in mammalian spinal cord (mouse models). We are interested in how coordinated patterns of channel and receptor gene expression are established during development of the postnatal spinal cord, and how these relationships may be altered by spinal cord injury. By combining molecular and electrophysiological approaches we hope to gain a more complete picture of how the spinal cord functions normally, as well as is changed following injury.

LPcellbarsaHomeostatic Plasticity and Compensatory Mechanisms that Stabilize Neuronal Output

To maintain this distinct functional output, neurons must adapt to changing patterns of synaptic excitation. These adaptations are essential to prevent neurons from either falling silent as synaptic excitation falls or becoming saturated as excitation increases. In the absence of stabilizing mechanisms, activity-dependent plasticity could drive neural activity to saturation or quiescence. Furthermore, as cells adapt to changing patterns of synaptic input, presumably the overall balance of intrinsic conductances of the cell must be maintained so that reliable output is achieved. Although these regulatory phenomena have been well documented, the molecular and physiological mechanisms involved are poorly understood.

crabLPtrace1The Cellular and Molecular Basis of Functional Neuronal Identity

The intrinsic properties of a neuron determine the translation of synaptic input to axonal output. As such, the overall regulation of intrinsic excitability of a neuron directly determines the output of that neuron at a given point in time, giving the cell a unique “functional identity.” Our research is designed to further our understanding of the regulation of neuronal excitability and thus functional identity using molecular and electrophysiological techniques. This “molecular neurophysiology” approach has revealed that the same neuron in different animals may achieve its conserved output by highly variable underlying mechanisms. Thus there is not a single “solution” to neuronal identity, but parameters vary from cell to cell.