ZFIN ID: ZDB-PUB-051101-7
Olfactoretinal centrifugal input modulates zebrafish retinal ganglion cell activity: A possible role for dopamine-mediated Ca2+ signaling pathways
Huang, L., Maaswinkel, H., and Li, L.
Date: 2005
Source: The Journal of physiology   569(3): 939-948 (Journal)
Registered Authors: Li, Lei, Maaswinkel, Hans
Keywords: none
MeSH Terms:
  • Amino Acids/pharmacology
  • Animals
  • Benzazepines/pharmacology
  • Calcium Signaling/drug effects
  • Calcium Signaling/physiology*
  • Dopamine/metabolism*
  • Dopamine/pharmacology
  • Dopamine Antagonists/pharmacology
  • Evoked Potentials/drug effects
  • Methionine/pharmacology
  • Models, Animal
  • Neural Inhibition
  • Olfactory Pathways/drug effects
  • Olfactory Pathways/metabolism
  • Photic Stimulation
  • Receptors, Dopamine D1/drug effects
  • Receptors, Dopamine D1/metabolism
  • Retinal Ganglion Cells/drug effects
  • Retinal Ganglion Cells/metabolism*
  • Sensory Thresholds/drug effects
  • Synaptic Transmission/drug effects
  • Synaptic Transmission/physiology
  • Zebrafish
PubMed: 16239263 Full text @ J. Physiol.
ABSTRACT
The vertebrate retina receives centrifugal input from the brain. In zebrafish, the major centrifugal input originates in the terminal nerve (TN). TN cell bodies are located in the olfactory bulb and/or ventral telencephalon. The TN projects axons to the retina where they branch in the inner plexiform layer (IPL) and synapse onto several inner retinal cell types, including dopaminergic interplexiform cells (DA-IPCs). This olfactoretinal centrifugal input plays a role in modulating retinal ganglion cell (RGC) activity, likely via dopamine-mediated Ca2+ signaling pathways. Normally, dopamine inhibits RGC firing by decreasing the inward Ca2+ current. Olfactory stimulation with amino acids decreases dopamine release in the retina, thereby reducing dopaminergic inhibition of RGCs. This model of olfacto-visual integration was directly tested by recording single-unit RGC activity in response to olfactory stimulation in the presence or absence of dopamine receptor blockers. Stimulation of the olfactory neurons increased RGC activity. However, this effect diminished when the dopamine D1 receptors were pharmacologically blocked. In isolated RGCs, the application of dopamine or dopamine D1 receptor agonist decreased voltage-activated Ca2+ current and lowered Ca2+ influx. Together, the data suggest that olfactory input has a modulatory effect on RGC firing, and that this effect is likely mediated by dopamine D1 receptor-coupled Ca2+ signaling pathways.
ADDITIONAL INFORMATION No data available