VISION RESEARCH CENTER FACULTY

Salvatore Stella, Jr., PhD

Assistant Professor of Ophthalmology
and Basic Medical Sciences
M5-307
Office : 816-235-6445
Fax: 816-235-6517

Education:
University of Nebraska Medical Center, Omaha, NE
Ph.D. ( Pharmacology, 2000)
San Diego State University, San Diego, CA
B.S. (Biology, 1992)

Research Interest:
Our laboratory is interested in synaptic signaling and plasticity in the visual system. These fundamental processes have challenged neuroscientists since the age of Cajal. The visual system is constantly adapting to varying levels of illumination. I am interested in understanding how the visual system adjusts to these conditions through synaptic signaling in the retina. We study questions relating to synaptic Ca2+ signaling and plasticity at the level of neural networks and their components, in particular the retina provides a way to study synaptic modulation with a normal physiological stimulus, light. Our lab’s major interests are centered on four critical areas:

1) To understand how adaptation, contrast, and conditions of illumination are regulated within retinal circuits. In particular, how L-glutamate release is regulated from the first synapse in visual processing, and what role purines like adenosine have in modulating this synapse and regulating the retinas ability to adapt to conditions of light and darkness.

2) To understand how horizontal cells contribute to center surround antagonistic properties in the outer retina. Specifically, in what ways are feed forward signaling regulated at the first synapse in visual processing, and how is GABA released from horizontal cells to regulate excitability of ON and OFF cone bipolar cells?

3)To understand how synaptic regulation of Ca2+ signaling by internal Ca2+ stores at first and second order synapses alter the synaptic release of L-glutamate from these neurons and influence retinal processing.

4) Develop novel strategies and therapies to treat retinal diseases like age related macular degeneration, and glaucoma, using purinergic drug targets and hybrid biophotonic sensors and nano-based prosthetic devices.

To address these questions I study the retinas of both lower vertebrates and mammals. I use optical, electrophysiological, cell biological and molecular tools to probe the dynamics of retinal circuits from single synapses to integrated functional signaling. Experiments are performed in intact retinal whole mounts and slices as well as in reduced preparations, examining isolated single cell function.

Selected publications:
Stella, S. L., Jr., Vila, A., Hung, A.Y., Rome, M., Kreienkamp, HJ, Huynh, U, Sheng, M., and Brecha, N. C. Shank 1 is expressed at cone but not rod synaptic terminals in mammalian retina, submitted, Journal of Comparative Neurology, 2010.

Guo, C., Hirano, A. A., Stella, S. L., Jr., Bitzer, M., and Brecha, N. C.. Guinea pig horizontal cells express GABA, the GABA synthesizing enzyme, GAD65 and the GABA vesicular transporter, Journal of Comparative Neurology, 518:1647-69,2010.

Stella, S. L., Jr., Hu, W. D., Brecha, N. C. Adenosine suppress exocytosis from cone terminals of the salamander retina, HYPERLINK "javascript:AL_get(this,%20'jour',%20'Neuroreport.');" \o "Neuroreport." Neuroreport 20:923-9, 2009.

Guo, C., Stella, S. L., Jr., Hirano, A. A., and Brecha, N. C. Plasmalemmal and vesicular GABA transporter expression in the developing mouse retina., Journal of Comparative Neurology, 512:6-26, 2008.
Stella, S. L., Jr., Li, S., Sabatini, A., Vila, A., and Brecha, N. C. Comparison of the ontogeny of the vesicular glutamate transporter 3 (VGLUT3) with VGLUT1 and VGLUT2 in the rat retina., Brain Res., 1215:20-29, 2008.

Stella, S. L., Jr., Hu, W. D., Brecha, N. C. Adenosine inhibits voltage-dependent Ca2+ influx in cone photoreceptor terminals of the tiger salamander retina., Journal of Neuroscience Research, 85:1126-1137, 2007.

Stella, S. L., Jr., Bryson, E.J., Dale, N., and Thoreson, W. B. Adenosine transport blockers suppress synaptic transmission from rods through direct inhibition of voltage-dependent Ca2+ channels., Submitted, J. of Neurophysiol., 2010.