UCLA Neuroscience Program Ph.D. Admissions Neuroscience Faculty UCLA and Beyond  



Gordon Fain
Cellular Physiology of Vertebrate Retina

Email Address:  gfain@lifesci.ucla.edu

Work Address:
LSB
LSB


Phone Numbers:
(310) 206-4281 Office
(310) 825-8330 Laboratory


Selected Publications:

Fain GL Why photoreceptors die (and why they don't).. BioEssays 2006; 28: 344-354.
Tsang SH, Woodruff ML, Chen CK, Yamashita CY, Cilluffo MC, Rao AL, Farber DB, Fain GL GAP-independent termination of photoreceptor light response by excess gamma subunit of the cGMP-phosphodiesterase.. Journal of Neuroscience 2006; 26: 4472-4480.
Fan J, Woodruff ML, Cilluffo MC, Crouch RK, Fain GL Opsin activation of transduction in the rods of dark-reared Rpe65 knockout mice.. The Journal of Physiology 2005; 568: 83-95.
Lem J & Fain GL Constitutive opsin signalling: congenital night blindness or retinal degeneration?. Trends in Molecular Medicine 2004; 10: 150-157.
Woodruff, ML Wang, Z Chung, HY Redmond, TM Fain, GL Lem, J Spontaneous activity of opsin apoprotein is a cause of Leber congenital amaurosis.. Nature genetics. . 2003; 35(2): 158-64.
Matthews, HR Fain, GL The effect of light on outer segment calcium in salamander rods.. The Journal of physiology. . 2003; 552(Pt 3): 763-76.
Fain GL Sensory Transduction. . 2003; .
Fain GL, Matthews HR, Cornwall MC & Koutalos Y Adaptation in vertebrate photoreceptors.. Physiological Reviews. 2001; 81: 117-151.
Research Interest:

Light falling on the retina excites a photopigment (rhodopsin), which then triggers an enzymatic cascade in the rod and cone photoreceptors . This cascade reduces the intracellular cGMP concentration and decreases the conductance of the photoreceptor plasma membrane. We use a variety of techniques, including intracellular and extracellular recording, patch-clamp, and fluorescent dye laser spot Ca2+ measurement, in order to understand how visual transduction is modulated by Ca2+ to produce adaptation to light and to darkness. We are also interested in mechanisms of photoreceptor degeneration during inherited retinal dystrophy in diseases like retinitis pigmentosa and Leber's amaurosis. Our work has shown that continuous activation of the visual cascade is the cause of apoptosis in some of these disorders, and that cell death is probably triggered by a prolonged decrease in Ca2+ concentration. Increases in Ca2+ can also trigger apoptosis--the photoreceptor regulates its Ca2+ concentration within a narrow range and uses a variety of protective mechanisms to prevent damage from constant light. Our studies are helping to define mechanisms of Ca2+ regulation that, for rods and cones, are literally a matter of life or death.