Evanna Gleason

George C. Kent Professor #2
CDIB Division

PhD: University of California, Davis, 1990

Chair Phone: 225-578-2601
Chair Office: 202 Life Sciences Building

Phone: 225-578-1748
Lab Phone: 225-578-9115
Office: A241 Life Sciences Annex
Lab: A247/249 Life Sciences Annex
E-mail: egleaso@lsu.edu 

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.

Selected Publications

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.

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 117: 1185-1999. DOI: 10.1152/jn.00803.2016.

V. Krishnan, W. Maddox, T. Rodriguez and E. Gleason. (2017) A role for CFTR in the​NO-dependent release of Cl- from acidic organelles in amacrine cells. Journal of ​​Neurophysiology 118: 2842-2852.doi:0.1152/jn.00511.2017.

W. Maddox N. Khorsandi and E. Gleason (2018) TRPC5 is required for the NO-dependent increase in dendritic Ca2+ and GABA release from chick retinal amacrine cells. Journal of Neurophysiology 119: 262-273. doi:10.1152/jn.00500.2017.

V. Dunn and E. Gleason (2018) Inhibition of endocytosis suppresses the NO-dependent release of Cl- from retinal amacrine cells. PLoS One 13:doi: 10.1371/ pone. 0201184.2018.

L. Zhong and E. Gleason (2021) Adenylate cyclase 1 links calcium signaling to CFTR-​dependent cytosolic chloride elevations in chick amacrine cells. Frontiers in ​Cellular Neuroscience 15: doi: 10.3389/fncel.2021.726605.