Andrew Ishida
Professor
atishida (at) ucdavis (dot) edu

Neurobiology, Physiology and Behavior
Opthalmology - Medicine

Office
1133 Life Sciences
(530) 752-3569

Lab
(530) 752-8507



 
Degrees:
1981 PhD University of California, Los Angeles (Biology)
Research Interests:

Vertebrate retinas use fast neurotransmitters to signal moment-to-moment changes in the distribution of incident light. Retinas contain an additional set of neurotransmitters which operate on slower time scales to modulate signal flow and processing. My lab studies how action potentials and voltage-gated ion currents are modulated by such slow neurotransmitters, in retinal ganglion cells. The transmitter that interests us is dopamine, because light augments intraretinal dopamine release and because dopamine produces several effects that help retinas function, during daylight, as the most distal cells of the visual system. Our goal is to understand how dopamine alters ganglion cell excitability. We started this work by examining effects of dopamine on goldfish ganglion cells, because previous studies of this species identified the cells that release dopamine, some of the cells that respond to dopamine, conditions that release dopamine, and some consequences of depleting intraretinal dopamine. In ganglion cells of freshly isolated retinas, we found evidence that light-stimulated release of dopamine activates D1-type receptors and elevates cAMP (adenosine 3',5' cyclic monophosphate) levels. We then dissociated retinas and found that dopamine and 8-bromo-cAMP (a membrane-permeable cAMP analog) inhibit ganglion cell spike firing, that this inhibition entails cAMP-dependent protein kinase activation, and that this inhibition resembles effects of background light in at least two ways (Vaquero et al 2001). We are now working on a number of projects stemming from these initial results. First, we are using mammalian retinas to test whether dopamine generally serves as a 'light switch' at the level of ganglion cells. Secondly, we are analyzing a number of effects of dopamine and related ligands on isolated voltage-gated currents. Thirdly, we are identifying signalling cascade components that mediate ganglion cell responses to dopamine.
CBS Graduate Group Affiliations:
Neuroscience  
Molecular, Cellular, and Integrative Physiology  
Publications: Last updated 11/17/2009
  • Hayashida Y, Varela Rodríguez C, Ogata G, Partida GJ, Oi H, Stradleigh TW, Lee SC, Felipe Colado A, Ishida AT (2009). Inhibition of adult rat retinal ganglion cells by D1-type dopamine receptor activation. Journal of Neuroscience 29: 15001-15016.
  • Oi H, GJ Partida, SC Lee, AT Ishida (2008). HCN4-like immunoreactivity in rat retinal ganglion cells. Visual Neuroscience 25: 95-102.
  • Lee SC, AT Ishida (2007). I(h) without K(ir) in adult rat retinal ganglion cells. Journal of Neurophysiology 97: 3790-3799
  • Partida GJ, SC Lee, L Haft-Candell, GS Nichols, AT Ishida (2004). DARPP-32-like immunoreactivity in AII amacrine cells of rat retina. Journal of Comparative Neurology 480: 251-263
  • Hayashida Y, AT Ishida (2004). Dopamine receptor activation can reduce voltage-gated Na+ current by modulating both entry into and recovery from inactivation. Journal of Neurophysiology 92: 3134-3141
  • Ishida AT (2004). Retinal ganglion cell excitability. In: LM Chalupa and JS Werner (Eds.) The Visual Neurosciences. Cambridge, MA. MIT Press. pp 422-450
  • Lee SC, Y Hayashida, AT Ishida (2003). Availability of low-threshold Ca2+ current in retinal ganglion cells. Journal of Neurophysiology 90: 3888-3901
  • Vaquero CF, A Pignatelli, GJ Partida, AT Ishida (2001). A dopamine- and protein kinase A-dependent mechanism for network adaptation in retinal ganglion cells. Journal of Neuroscience 21:8624-8635
Laboratory Personnel:
Ishida Lab

Iv Godzdanker, Kalen Krempely, Aaron Lemieux, Bryan Lemieux, Genki Ogata, Gloria Partida, Tyler Stradleigh, Monique Vaughn, Andrew Ishida

Teaching Interests:
Neurobiology and Physiology
Courses:
NPB 101 Systemic Physiology
NSC 261A Topics in Vision