PhD: University of California, Davis, 1990
Phone: (225) 578-1748
Lab Phone: (225) 578-9115
Office: A241 Life Sciences Annex
Lab: A249/261 Life Sciences Building
Area of Interest
Perhaps the most important feature of a neuron is its ability to communicate with other cells at synapses. Research in my lab focuses on synaptic transmission in the vertebrate retina. Retinal neurons have distinctive anatomical and physiological properties that suggest they employ unique synaptic mechanisms. The long term objective of our research is to understand how retinal synapses are specialized to transmit visual information. The intact retina is complex and it is therefore difficult to study the mechanisms of synaptic transmission between retinal neurons. To circumvent this difficulty, we use a simplified culture system containing isolated pairs of retinal neurons. This preparation permits high resolution electrophysiological recording that allows us to directly study the ionic currents involved in synaptic transmission. In addition, we are using immunocytochemistry, calcium imaging, and molecular techniques to study several aspects of synaptic function. At synapses, calcium ions act as the presynaptic trigger for initiation of a cascade of events that culminate in the fusion of synaptic vesicles with the plasma membrane and release of neurotransmitter. Because calcium plays such a critical role in synaptic transmission we are interested in the ways in which calcium is regulated in the presynaptic terminal during synaptic transmission. We are currently examining novel Ca2+ influx pathways as well as the role of mitochondria in shaping local Ca2+ signals. On the postsynaptic side, we are also investigating the role that nitric oxide plays in regulating the sign (inhibitory or excitatory) of synapses between amacrine cells.
W. Maddox and E. Gleason (2017) Nitric oxide promotes GABA release by activating a voltage-independent Ca2+ influx pathway in retinal amacrine cells. Journal of Neurophysiology DOI: 10.1152/jn.00803.2016.
V. Krishnan and E. Gleason (2015) Nitric oxide releases Cl- from acidic organelles in retinal amacrine cells. Frontiers in Cellular Neuroscience. 9:213. doi:10.3389/fncel.2015.00213.
M. Tekmen and E. Gleason (2013) Nitric oxide production and the expression of two nitric oxide synthases in the avian retina. Visual Neuroscience. 30: 91-103.
E. Gleason. (2012) The influences of metabotropic receptor activation on cellular signaling and synaptic function in amacrine cells. Visual Neuroscience 29:31-39.
E. McMains and E. Gleason. (2011) The role of pH in a nitric oxide-dependent increase in cytosolic chloride in retinal amacrine cells. Journal of Neurophysiology. 106: 641-651.
E. McMains, V. Krishnan, S. Prasad and E. Gleason. (2011) Expression and Localization of CLC Chloride Transport Proteins in the Avian Retina. PLoS ONE 6(3): e17647. doi:10.1371/journal.pone.0017647.
M. Tekmen and E. Gleason. (2010) Multiple Ca2+-dependent mechanisms regulate L-type Ca2+ current in retinal amacrine cells. Journal of Neurophysiology, 104: 1849-1866.
S. Crousillac, J. Colonna, E. McMains, J.S. Dewey and E. Gleason. (2009) Sphingosine-1-phosphate elicits receptor-dependent calcium signaling in retinal amacrine cells. Journal of Neurophysiology 102, 3295-3309. PMC2804436
M. Sen, E. McMains and E. Gleason. (2007) Local influence of mitochondrial Ca2+ transport in retinal amacrine cells. Visual Neuroscience 24, 663-678.
B. Hoffpauir, E. McMains, and E. Gleason. (2006) Nitric Oxide transiently converts synaptic inhibition to excitation in retinal amacrine cells. Journal of Neurophysiology 95: 2866-2877.