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About Robert W. Putnam

Dr. Putnam's research focused on the cellular neuroscience of respiratory control. He studied the neurons from the brainstem of neonatal rats and their response to elevated levels of CO2. It is believed that these neurons play a major role in controlling ventilation and our work is thus of relevance to disorders that involve altered respiratory drive, such as sudden infant death syndrome (SIDS) and sleep apnea. There were two main thrusts of his work:
Cellular Signals and Targets in CO2-sensitive Neurons: He looked at the cellular signaling pathways and the ion channel targets involved in the sensing of elevated CO2 by central chemosensitive neurons. This work involves pH and calcium sensitive fluorescent dyes to study changes of intracellular pH and intracellular calcium and their role in CO2-induced increased firing rate of these neurons. We also employ electrophysiological techniques to study the change in electrophysiological properties of these neurons as well as using immunohistochemical and voltage clamp techniques to characterize the ion channel targets of the chemosensitive signals. He began studies to alter central chemosensitivity in rats to determine the cellular alterations that correlate with the altered central chemosensitivity. He also developed a mathematical model of excitability in central chemosensitive neurons to determine the channels, signals and properties that make a neuron chemosensitive.
Development of Central Chemosensitivity: He did some of the first studies to fully characterize the development of the CO2 responsiveness of ventilation in neonatal rats. The studies suggested a triphasic pattern of development, with an early neonatal form of chemosensitivity that gives way after 2 weeks to an adult form of chemosensitivity, and a critical window of minimal chemosenstivity at week 1. He also studied the development of chemosensitivity in individual neurons within various chemosensitive regions. Finally, he examined which brainstem regions are responsible for each type of chemosensitivity and the effects of chronic exposures to hypercapnia or hypoxia on these developmental patterns.

Positions

July 1986 - April 2017 Professor, Wright State University Neuroscience, Cell Biology & Physiology
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