The Journal of Neuroscience, March 1, 2000, 20(5):1883-1892
Disruption of the Olfactoretinal Centrifugal Pathway May
Relate to the Visual System Defect in night blindness b
Mutant Zebrafish
Lei
Li and
John E.
Dowling
Department of Molecular and Cellular Biology, Harvard University,
Cambridge, Massachusetts 02138
We describe here a dominant mutation, night blindness
b (nbb), which causes an age-related visual
system defect in zebrafish. At 4-5 months of age, dark-adapted
nbb+/
mutants show abnormal visual threshold fluctuations when measured behaviorally. Light sensitizes the animals; thus early dark adaptation of
nbb+/
fish is normal. After 2 hr of dark adaptation, however, visual thresholds of
nbb+/
mutants are raised on average 2-3 log units, and rod system function is not detectable. Electroretinograms recorded from
nbb+/
mutants are normal, but ganglion cell thresholds are raised in prolonged darkness, suggesting an inner retinal defect. The visual defect of
nbb+/
mutants may be likely caused by an abnormal olfactoretinal centrifugal innervation; in
nbb+/
mutants, the olfactoretinal centrifugal projection to the retina is
disrupted, and the number of retinal dopaminergic interplexiform cells
is reduced. A similar visual defect as shown by
nbb+/
mutants is observed in zebrafish in which the olfactory epithelium and
olfactory bulb have been excised. Homozygous nbb fish
display an early onset neural degeneration throughout the CNS and die by 7-8 d of age.
Key words:
dark adaptation; dopamine; escape response; mutation; neuronal degeneration; olfactory bulb; olfactoretinal centrifugal
pathway; terminal nerve neuron; visual sensitivity; zebrafish
Copyright © 2000 Society for Neuroscience 0270-6474/00/2051883-10$05.00/0
Previous Article | Next Article
