Linked Life Data

20484654

Source:http://linkedlifedata.com/resource/pubmed/id/20484654

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
20
pubmed:dateCreated
2010-5-20
pubmed:abstractText
The optokinetic response (OKR) to a visual stimulus moving at constant velocity consists of a series of two alternating components, a slow phase, during which the eyes follow the stimulus, and a quick phase, which resets the eyes to begin a new response cycle. The quick phases of the OKR resemble the saccades observed during free viewing. It is unclear to what extent the premotor circuitry underlying these two types of jerky, conjugate eye movements is conserved among vertebrates. Zebrafish (Danio rerio) larvae, broadly expressing halorhodopsin (NpHR) or channelrhodopsin-2 (ChR2) in most neurons, were used to map the location of neurons involved in this behavior. By blocking activity in localized groups of NpHR-expressing neurons with an optic fiber positioned above the head of the fish and by systematically varying the site of photostimulation, we discovered that activity in a small hindbrain area in rhombomere 5 was necessary for saccades to occur. Unilateral block of activity at this site affected behavior in a direction-specific manner. Inhibition of the right side suppressed rightward saccades of both eyes, while leaving leftward saccades unaffected, and vice versa. Photostimulation of this area in ChR2-transgenic fish was sufficient to trigger saccades that were precisely locked to the light pulses. These extra saccades could be induced both during free viewing and during the OKR, and were distinct in their kinetics from eye movements elicited by stimulating the abducens motor neurons. Zebrafish double indemnity (didy) mutants were identified in a chemical mutagenesis screen based on a defect in sustaining saccades during OKR. Positional cloning, molecular analysis, and electrophysiology revealed that the didy mutation disrupts the voltage-gated sodium channel Scn1lab (Nav1.lb). ChR2 photostimulation of the putative hindbrain saccade generator was able to fully reconstitute saccades in the didy mutant. Our studies demonstrate that an optogenetic approach is useful for targeted loss-of-function and gain-of-function manipulations of neural circuitry underlying eye movements in zebrafish and that the saccade-generating circuit in this species shares many of its properties with that in mammals.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
19
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
7111-20
pubmed:dateRevised
2010-8-16
pubmed:meshHeading
pubmed-meshheading:20484654-Animals, pubmed-meshheading:20484654-Animals, Genetically Modified, pubmed-meshheading:20484654-Bacterial Proteins, pubmed-meshheading:20484654-Carrier Proteins, pubmed-meshheading:20484654-Halorhodopsins, pubmed-meshheading:20484654-Kinetics, pubmed-meshheading:20484654-Larva, pubmed-meshheading:20484654-Luminescent Proteins, pubmed-meshheading:20484654-Microinjections, pubmed-meshheading:20484654-Mutagenesis, Site-Directed, pubmed-meshheading:20484654-Mutation, pubmed-meshheading:20484654-Neurons, pubmed-meshheading:20484654-Nystagmus, Optokinetic, pubmed-meshheading:20484654-Oocytes, pubmed-meshheading:20484654-Photic Stimulation, pubmed-meshheading:20484654-Reaction Time, pubmed-meshheading:20484654-Rhombencephalon, pubmed-meshheading:20484654-Saccades, pubmed-meshheading:20484654-Sodium Channels, pubmed-meshheading:20484654-Xenopus, pubmed-meshheading:20484654-Zebrafish, pubmed-meshheading:20484654-Zebrafish Proteins
pubmed:year
2010
pubmed:articleTitle
Optogenetic localization and genetic perturbation of saccade-generating neurons in zebrafish.
pubmed:affiliation
Department of Physiology, Programs in Neuroscience, Genetics and Developmental Biology, University of California, San Francisco, San Francisco, California 94158-2324, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural