Click here to close
Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly.
We suggest using a current version of Chrome,
FireFox, or Safari.
J Neurosci
2010 May 19;3020:7111-20. doi: 10.1523/JNEUROSCI.5193-09.2010.
Show Gene links
Show Anatomy links
Optogenetic localization and genetic perturbation of saccade-generating neurons in zebrafish.
Schoonheim PJ
,
Arrenberg AB
,
Del Bene F
,
Baier H
.
???displayArticle.abstract???
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.
Aksay,
Functional dissection of circuitry in a neural integrator.
2007, Pubmed
Aksay,
Functional dissection of circuitry in a neural integrator.
2007,
Pubmed
Aksay,
Anatomy and discharge properties of pre-motor neurons in the goldfish medulla that have eye-position signals during fixations.
2000,
Pubmed
Aksay,
In vivo intracellular recording and perturbation of persistent activity in a neural integrator.
2001,
Pubmed
Arrenberg,
Optical control of zebrafish behavior with halorhodopsin.
2009,
Pubmed
Beck,
Quantifying the ontogeny of optokinetic and vestibuloocular behaviors in zebrafish, medaka, and goldfish.
2004,
Pubmed
Beck,
Precerebellar hindbrain neurons encoding eye velocity during vestibular and optokinetic behavior in the goldfish.
2006,
Pubmed
Brainard,
The Psychophysics Toolbox.
1997,
Pubmed
Brockerhoff,
A behavioral screen for isolating zebrafish mutants with visual system defects.
1995,
Pubmed
Carr,
Transmitter modulation of slow, activity-dependent alterations in sodium channel availability endows neurons with a novel form of cellular plasticity.
2003,
Pubmed
Catterall,
A 3D view of sodium channels.
2001,
Pubmed
Easter,
The development of vision in the zebrafish (Danio rerio).
1996,
Pubmed
Glimcher,
The neurobiology of visual-saccadic decision making.
2003,
Pubmed
Goldin,
Mechanisms of sodium channel inactivation.
2003,
Pubmed
Goldin,
Expression of ion channels by injection of mRNA into Xenopus oocytes.
1991,
Pubmed
,
Xenbase
Granato,
Genes controlling and mediating locomotion behavior of the zebrafish embryo and larva.
1996,
Pubmed
Ilg,
Responses of neurons of the nucleus of the optic tract and the dorsal terminal nucleus of the accessory optic tract in the awake monkey.
1996,
Pubmed
Ilg,
Responses of monkey nucleus of the optic tract neurons during pursuit and fixation.
1991,
Pubmed
Jung,
Prolonged sodium channel inactivation contributes to dendritic action potential attenuation in hippocampal pyramidal neurons.
1997,
Pubmed
Kamogawa,
Inhibitory input to pause neurons from pontine burst neuron area in the cat.
1996,
Pubmed
Kanda,
Glycinergic inputs cause the pause of pontine omnipause neurons during saccades.
2007,
Pubmed
Kearney,
A gain-of-function mutation in the sodium channel gene Scn2a results in seizures and behavioral abnormalities.
2001,
Pubmed
,
Xenbase
Lopez-Barneo,
Neuronal activity in prepositus nucleus correlated with eye movement in the alert cat.
1982,
Pubmed
Major,
Plasticity and tuning by visual feedback of the stability of a neural integrator.
2004,
Pubmed
Marsh,
Normal and adapted visuooculomotor reflexes in goldfish.
1997,
Pubmed
Masseck,
Comparative neurobiology of the optokinetic reflex.
2009,
Pubmed
Mickus,
Slow sodium channel inactivation in CA1 pyramidal cells.
1999,
Pubmed
Muto,
Forward genetic analysis of visual behavior in zebrafish.
2005,
Pubmed
Neuhauss,
Genetic disorders of vision revealed by a behavioral screen of 400 essential loci in zebrafish.
1999,
Pubmed
Novak,
Embryonic and larval expression of zebrafish voltage-gated sodium channel alpha-subunit genes.
2006,
Pubmed
Ogiwara,
Nav1.1 localizes to axons of parvalbumin-positive inhibitory interneurons: a circuit basis for epileptic seizures in mice carrying an Scn1a gene mutation.
2007,
Pubmed
Pastor,
Eye position and eye velocity integrators reside in separate brainstem nuclei.
1994,
Pubmed
Pelli,
The VideoToolbox software for visual psychophysics: transforming numbers into movies.
1997,
Pubmed
Quandt,
Modification of slow inactivation of single sodium channels by phenytoin in neuroblastoma cells.
1988,
Pubmed
Ragsdale,
How do mutant Nav1.1 sodium channels cause epilepsy?
2008,
Pubmed
Rudy,
Slow inactivation of the sodium conductance in squid giant axons. Pronase resistance.
1978,
Pubmed
Scott,
Targeting neural circuitry in zebrafish using GAL4 enhancer trapping.
2007,
Pubmed
Scott,
The cellular architecture of the larval zebrafish tectum, as revealed by gal4 enhancer trap lines.
2009,
Pubmed
Scudder,
The brainstem burst generator for saccadic eye movements: a modern synthesis.
2002,
Pubmed
Shimoda,
Zebrafish genetic map with 2000 microsatellite markers.
1999,
Pubmed
Smear,
Vesicular glutamate transport at a central synapse limits the acuity of visual perception in zebrafish.
2007,
Pubmed
Straka,
Morphology and physiology of the cerebellar vestibulolateral lobe pathways linked to oculomotor function in the goldfish.
2006,
Pubmed
Strassman,
Anatomy and physiology of saccadic burst neurons in the alert squirrel monkey. I. Excitatory burst neurons.
1986,
Pubmed
Strassman,
Anatomy and physiology of saccadic burst neurons in the alert squirrel monkey. II. Inhibitory burst neurons.
1986,
Pubmed
Toib,
Interaction between duration of activity and time course of recovery from slow inactivation in mammalian brain Na+ channels.
1998,
Pubmed
,
Xenbase
Tomlinson,
Signals in vestibular nucleus mediating vertical eye movements in the monkey.
1984,
Pubmed
Wyart,
Optogenetic dissection of a behavioural module in the vertebrate spinal cord.
2009,
Pubmed
Yoshida,
Morphological and physiological characteristics of inhibitory burst neurons controlling horizontal rapid eye movements in the alert cat.
1982,
Pubmed
Zannino,
Olig2+ precursors produce abducens motor neurons and oligodendrocytes in the zebrafish hindbrain.
2009,
Pubmed
