Pharmacological properties of motion vision in goldfish measured with the optomotor response.
In goldfish, the retinal pathways involved in motion coding have been demonstrated to have an L-cone dominated action spectrum (S. Schaerer, C. Neumeyer, Motion detection in goldfish investigated with the optomotor response is "color blind", Vision Res. 36 (1996) 4025-4034). The neurotransmitters involved in retinal motion coding mechanisms, and the relevance of these retinal motion coding mechanisms for motion perception, are little investigated in fish. In this study, the optomotor response was used to investigate the effect of antagonists on different receptor types for acetylcholine (ACh), GABA, for the dopamine D2-receptor (D2-R) - which is known to modulate the action spectrum in motion coding (C. Mora-Ferrer, K. Behrend, Dopaminergic modulation of photopic temporal transfer properties in goldfish retina investigated with the ERG, Vision Res. 44 (2004) 2067-2081) - and of an agonist for against the mGluR6-receptor (mGluR6) on goldfish motion vision in the photopic range. Blockade of nicotinic ACh-R, GABAa-R and both GABAa- and GABAc-R eliminated the optomotor response completely. Neither a muscarinic ACH-R antagonist, a D2-R antagonist or a mGluR6-agonist affected goldfish motion vision. The pharmacological profile of the goldfish optomotor response resembles the pharmacological profile of direction-selective ganglion cells (DS-GC) described for vertebrate retinas in electrophysiological experiments, e.g. (S. Weng, W. Sun, S. He, Identification of ON-OFF direction-selective ganglion cells in the mouse retina, J. Physiol. 562 (2005) 915-923). This indicates that cells with direction-selective receptive field properties exist in the goldfish retina. It is proposed that these cells provide the input for the full field motion perception in goldfish.
Mora-Ferrer
Carlos
C
Institute Zoology III, J Gutenberg University Mainz, 55099 Mainz, Germany. carlos.mora-ferrer@uni-mainz.de
Hausselt
Susanne
S
Schmidt Hoffmann
Ruth
R
Ebisch
Boris
B
Schick
Susanne
S
Wollenberg
Katharina
K
Schneider
Cora
C
Teege
Patrick
P
Jürgens
Karin
K
D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D004298:Dopamine / Q000378:metabolism; D005133:Eye Movements / Q000187:drug effects / Q000502:physiology; D018756:GABA Antagonists / Q000494:pharmacology; D006054:Goldfish; D009039:Motion Perception / Q000187:drug effects / Q000502:physiology*; D018733:Nicotinic Antagonists / Q000494:pharmacology; D011597:Psychomotor Performance / Q000187:drug effects / Q000502:physiology*; D017448:Receptors, Dopamine D2 / Q000187:drug effects / Q000378:metabolism; D018079:Receptors, GABA / Q000187:drug effects / Q000378:metabolism; D011963:Receptors, GABA-A / Q000187:drug effects / Q000378:metabolism; D011978:Receptors, Nicotinic / Q000187:drug effects / Q000378:metabolism; D012160:Retina / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D012165:Retinal Ganglion Cells / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D014785:Vision, Ocular / Q000187:drug effects / Q000502:physiology*; D014794:Visual Fields / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D018756:GABA Antagonists; C087200:GABA-C receptor; D018733:Nicotinic Antagonists; D017448:Receptors, Dopamine D2; D018079:Receptors, GABA; D011963:Receptors, GABA-A; D011978:Receptors, Nicotinic; D005680:gamma-Aminobutyric Acid; D000109:Acetylcholine; D004298:Dopamine