Denis Baylor

After completing his Postdoctoral Fellow, Baylor worked as a lab associate at the National Institute of Neurological Disorders and Stroke from 1968 to 1970. Baylor was an Associate professor of Physiology at the University of Colorado Medical School.[1] He then moved to Stanford University where he was an Associate Professor of Physiology up to 1975.[1]. Baylor was then an Associate Professor of Neurobiology between 1975 and 1978. In 1978, he became a Professor of Neurobiology at Stanford until 2001, when he became a Professor Emeritus of Neurobiology at Stanford.[1] Throughout his career, Baylor has served on the visiting committee at Harvard Medical School, the editorial board for The Journal of Physiology, Neuron, Journal of Neurophysiology, Visual Neuroscience, and The Journal of Neuroscience. He has also been on multiple medical and scientific advisory boards, along with being a Trustee for multiple foundations.[1][5]

One of Baylor's first large works was published in 1985 by the National Academy of Science in an article titled “Interaction of Hydrolysis-Resistant Analogs of Cyclic

For reference: a structural diagram of the human eye

GMP with the Phosphodiesterase and Light-Sensitive Channel of Retinal Rod Outer Segments.” Throughout this study, a series of nonhydrolyzable versions of cGMP were used to test the light sensitive gating mechanism of the rods.[6] The hydrolysis of the cGMP allows for the normal light response of the rods, opening channels for the entrance of light and closing in its absence. The study monitored the electrodes that were flowing throughout the cell with different nonhydrolyzable analogs. It was found that when the channel receptor was bound to the homologue of cGMP there was an increase in the dark current and a much slower overall response to light.[6] The study also found that whether a cGMP or its homologue was used, an increased concentration present could cause the rods to have slower responses as there was less control on the ability to open the gate quickly. Overall, this study provided insight into how light travels to the rods, and is used and processed by the rods within the eye.[6]

In 1991, Baylor published “Synchronous bursts of action potentials in ganglion cells of the developing mammalian retina” where he studied the visual systems of mammals.[7] The study used stimulus recordings to measure the action potential of the optic nerve fiber, and measured electrical movement of the neurons into the different eye specific layers of the retina[7]. The recorded electrical activity from the neurons excited many ganglion cells. This study illustrated that the fired neurons created the connection between the retina and the geniculate nucleus. Overall, this study was a breakthrough in proving how light can move through the eye and be received by the brain so that images and the environment can be perceived rapidly.[7]

Baylor's study on “Multi-neuronal signals from the retina: acquisition and analysis” utilized a new method to observe the many electrical activities of all the neurons in a section of the retina of the eye.[8] This study focused on how the eye processes information it receives despite having so many overlapping nerve fibers and networks. The extracellular action potentials are measured giving an idea as to the arrangement of the ganglion cells, which was followed by the measure of the voltage of the signals.[8] In addition, this study utilized visual methods to characterize a neuron's response to stimuli. The results from these two methods were combined and correlations were created between the electrical activity and visual responses to determine the different functions of the ganglion cells when prompted with a stimulus. Overall the new methods used in this study could help future studies publish detailed information about how optic nerve fibers work.[8]

In 1996, Baylor's article “How photons start vision” was published in the Proceedings of the National Academy of Sciences of the United States of America. This paper addressed the process of shutting down the transduction pathway that occurs in the response to light stimuli.[9] When a photon enters the eye, it is sent to the back of the eye and is absorbed by rods and cones. These cells are excited by the photon and as a response hydrolyze the GTP and cGMP. This finding proved to be the rate limiting step.[9] This causes gated channels to close and create a polarity. The signal can then be sent through the nerve cells to the brain where the image is processed. The study utilized lab controlled cells that could easily show the presence and concentration of nucleotides and calcium.[9] It showed that to end this signal amplification there has to be a drop in Ca²⁺ concentrations, which results in a negative feedback to return the cell back to its original state with GTP and cGMP, unhydrolyzed.[9]

His more recent publications focus on genetically targeting cells and observing what happens to their function with a deletion, over-expression, or insertion.[9] This information can give more detail into the job of individual cells, and their roles in processing images.

Baylor has received many awards and honors throughout his career in neurobiology and cellular biology. He was awarded the Sinsheimer Foundation Award for Medical Research in 1975. He received the Mathilde Solowey Award in NeuroSciences in 1978.[1] He also received the Proctor medal from the Association for Research in Vision and Ophthalmology in 1986. In 1988, Dr. Baylor received the Kayser International Award from the Retina Research Foundation. Along with these awards, he has received appointments to the Royal Society of London (2003), the National Academy of Science (1993), and became a fellow of American Academy of Arts and Sciences (1992).[1][2][4]