May 2005
Volume 46, Issue 13
ARVO Annual Meeting Abstract  |   May 2005
Effects of Dopamine on Glutamate Responses in Horizontal and Bipolar Cells Isolated From Zebrafish Retina
Author Affiliations & Notes
  • M.N. Asare
    Biology, American University, Washington, DC
  • R. Nelson
    Basic Neurosciences Program, NINDS, NIH, Rockville, MD
  • V.P. Connaughton
    Biology, American University, Washington, DC
  • Footnotes
    Commercial Relationships  M.N. Asare, None; R. Nelson, None; V.P. Connaughton, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 605. doi:
  • Views
  • Share
  • Tools
    • Alerts
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      M.N. Asare, R. Nelson, V.P. Connaughton; Effects of Dopamine on Glutamate Responses in Horizontal and Bipolar Cells Isolated From Zebrafish Retina . Invest. Ophthalmol. Vis. Sci. 2005;46(13):605.

      Download citation file:

      © ARVO (1962-2015); The Authors (2016-present)

  • Supplements

Abstract: : Purpose: The purpose of this study is to determine the effects of dopamine on isolated zebrafish retina cell responses to glutamate. Methods: Glutamate responses of papain dissociated horizontal and bipolar cells were studied with the voltage probe oxonol, DiBaC4(5). Such responses were then recorded in the presence of selective dopamine agonists and antagonists. Results: In general glutamate voltage responses were found to increase in the presence of dopamine, the D1 agonist SKF 38393, or the D2 agonist quinpirole. Effects of dopamine antagonists were both consistent and prominent, but presented a more complex picture. In the presence of dopamine, the D2 antagonist sulpiride and the D1 antagonist SCH 23390 further increased glutamate voltage responses. In the presence of glutamate and SKF 38393, SCH 23390 potentiated the glutamate response, however, the glutamate–quinpirole potentiation was inhibited by sulpiride. Application of tetraethylammonium potentiated the glutamate response with dopamine, D1 or D2 agonists. Conclusions: These results suggest two opposing dopamine receptor mechanisms, each activated by D1 or D2 receptors. In the excitatory mechanism, dopamine or its agonists potentiate the glutamate response. Only the D2 antagonist acting at the D2 receptor can be seen to suppress this effect. In the inhibitory mechanism, the D1 receptor has a D2 antagonist binding site. One possibility for an inhibitory second site of action is stimulation of outwardly rectifying potassium currents by dopamine (Fan and Yazulla, 1999). These currents tend to reduce the voltage amplitude of glutamate responses. Blockade of potassium channel enhancement by selective dopamine antagonists might then further augment glutamate voltage responses.

Keywords: excitatory neurotransmitters • retina: distal (photoreceptors, horizontal cells, bipolar cells) • dopamine 

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.