Source 1primary paper2021Neuron
Toolkit/eOPN3
eOPN3
Also known as: targeting-enhanced mosquito homolog of the vertebrate encephalopsin
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
eOPN3 is a targeting-enhanced mosquito homolog of vertebrate encephalopsin developed as an optogenetic silencing construct for presynaptic terminals. Brief illumination activates eOPN3 to suppress neurotransmitter release and synaptic transmission through the G_i/o signaling pathway, with spontaneous recovery within minutes in vitro and in vivo.
Usefulness & Problems
Why this is useful
eOPN3 is useful for selective silencing of defined neuronal projection pathways at presynaptic terminals with optical control. The source positions it as an alternative to prior inhibitory optogenetic tools with poor presynaptic efficacy and off-target effects, and to chemogenetic approaches with weaker spatial and temporal control.
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eOPN3 is an optogenetic silencing tool that suppresses synaptic transmission and neurotransmitter release from presynaptic terminals upon brief illumination. The abstract describes it as a targeting-enhanced mosquito rhodopsin homolog.
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selective suppression of neurotransmitter release at presynaptic terminals
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functional interrogation of long-range neuronal circuits in vivo
Problem solved
This tool addresses the problem of achieving effective, reversible suppression of neurotransmitter release specifically at presynaptic terminals. It is presented as enabling manipulation of synaptic output from defined afferents with high spatiotemporal precision.
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It is presented as a way to manipulate defined neuronal projection pathways with high spatiotemporal precision. The paper positions it as overcoming poor efficacy and off-target effects of prior inhibitory optogenetic tools at presynaptic terminals.
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provides temporally precise manipulation of defined neuronal projection pathways
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addresses low efficacy and off-target effects of existing inhibitory optogenetic tools at presynaptic terminals
Problem links
addresses low efficacy and off-target effects of existing inhibitory optogenetic tools at presynaptic terminals
LiteratureIt is presented as a way to manipulate defined neuronal projection pathways with high spatiotemporal precision. The paper positions it as overcoming poor efficacy and off-target effects of prior inhibitory optogenetic tools at presynaptic terminals.
Source:
It is presented as a way to manipulate defined neuronal projection pathways with high spatiotemporal precision. The paper positions it as overcoming poor efficacy and off-target effects of prior inhibitory optogenetic tools at presynaptic terminals.
provides temporally precise manipulation of defined neuronal projection pathways
LiteratureIt is presented as a way to manipulate defined neuronal projection pathways with high spatiotemporal precision. The paper positions it as overcoming poor efficacy and off-target effects of prior inhibitory optogenetic tools at presynaptic terminals.
Source:
It is presented as a way to manipulate defined neuronal projection pathways with high spatiotemporal precision. The paper positions it as overcoming poor efficacy and off-target effects of prior inhibitory optogenetic tools at presynaptic terminals.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Architecture: A reusable architecture pattern for arranging parts into an engineered system.
Mechanisms
g i/o signalingoptogenetic activation by illuminationsuppression of neurotransmitter releasesuppression of synaptic transmissionTechniques
No technique tags yet.
Target processes
signalingImplementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationoperating role: regulator
Use requires heterologous expression of the eOPN3 opsin construct in presynaptic terminals and optical illumination. The construct is described as a targeting-enhanced mosquito rhodopsin homolog, and its effect is mediated through the G_i/o signaling pathway; the provided evidence does not specify additional cofactors, wavelengths, or delivery formats.
The supplied evidence supports presynaptic silencing through G_i/o signaling, but does not provide quantitative performance metrics, spectral parameters, or direct comparisons to other tools. Validation in the provided evidence is centered on synaptic suppression and one behavioral application, so broader generality across cell types and preparations is not established here.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Observations
successMouseapplication demomouse
Inferred from claim cl3 during normalization. In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias. Derived from claim cl3. Quoted text: In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
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successMouseapplication demomouse
Inferred from claim cl3 during normalization. In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias. Derived from claim cl3. Quoted text: In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
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successMouseapplication demomouse
Inferred from claim cl3 during normalization. In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias. Derived from claim cl3. Quoted text: In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
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successMouseapplication demomouse
Inferred from claim cl3 during normalization. In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias. Derived from claim cl3. Quoted text: In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
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successMouseapplication demomouse
Inferred from claim cl3 during normalization. In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias. Derived from claim cl3. Quoted text: In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
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successMouseapplication demomouse
Inferred from claim cl3 during normalization. In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias. Derived from claim cl3. Quoted text: In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
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successMouseapplication demomouse
Inferred from claim cl3 during normalization. In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias. Derived from claim cl3. Quoted text: In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
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successMouseapplication demomouse
Inferred from claim cl3 during normalization. In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias. Derived from claim cl3. Quoted text: In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
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successMouseapplication demomouse
Inferred from claim cl3 during normalization. In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias. Derived from claim cl3. Quoted text: In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
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Supporting Sources
Ranked Claims
In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
Brief illumination of presynaptic terminals expressing eOPN3 triggers lasting suppression of synaptic output that recovers spontaneously within minutes in vitro and in vivo.
Brief illumination of presynaptic terminals expressing eOPN3 triggers a lasting suppression of synaptic output that recovers spontaneously within minutes in vitro and in vivo.
recovery time within minutes
Brief illumination of presynaptic terminals expressing eOPN3 triggers lasting suppression of synaptic output that recovers spontaneously within minutes in vitro and in vivo.
Brief illumination of presynaptic terminals expressing eOPN3 triggers a lasting suppression of synaptic output that recovers spontaneously within minutes in vitro and in vivo.
recovery time within minutes
Brief illumination of presynaptic terminals expressing eOPN3 triggers lasting suppression of synaptic output that recovers spontaneously within minutes in vitro and in vivo.
Brief illumination of presynaptic terminals expressing eOPN3 triggers a lasting suppression of synaptic output that recovers spontaneously within minutes in vitro and in vivo.
recovery time within minutes
Brief illumination of presynaptic terminals expressing eOPN3 triggers lasting suppression of synaptic output that recovers spontaneously within minutes in vitro and in vivo.
Brief illumination of presynaptic terminals expressing eOPN3 triggers a lasting suppression of synaptic output that recovers spontaneously within minutes in vitro and in vivo.
recovery time within minutes
Brief illumination of presynaptic terminals expressing eOPN3 triggers lasting suppression of synaptic output that recovers spontaneously within minutes in vitro and in vivo.
Brief illumination of presynaptic terminals expressing eOPN3 triggers a lasting suppression of synaptic output that recovers spontaneously within minutes in vitro and in vivo.
recovery time within minutes
Brief illumination of presynaptic terminals expressing eOPN3 triggers lasting suppression of synaptic output that recovers spontaneously within minutes in vitro and in vivo.
Brief illumination of presynaptic terminals expressing eOPN3 triggers a lasting suppression of synaptic output that recovers spontaneously within minutes in vitro and in vivo.
recovery time within minutes
Brief illumination of presynaptic terminals expressing eOPN3 triggers lasting suppression of synaptic output that recovers spontaneously within minutes in vitro and in vivo.
Brief illumination of presynaptic terminals expressing eOPN3 triggers a lasting suppression of synaptic output that recovers spontaneously within minutes in vitro and in vivo.
recovery time within minutes
Brief illumination of presynaptic terminals expressing eOPN3 triggers lasting suppression of synaptic output that recovers spontaneously within minutes in vitro and in vivo.
Brief illumination of presynaptic terminals expressing eOPN3 triggers a lasting suppression of synaptic output that recovers spontaneously within minutes in vitro and in vivo.
recovery time within minutes
Brief illumination of presynaptic terminals expressing eOPN3 triggers lasting suppression of synaptic output that recovers spontaneously within minutes in vitro and in vivo.
Brief illumination of presynaptic terminals expressing eOPN3 triggers a lasting suppression of synaptic output that recovers spontaneously within minutes in vitro and in vivo.
recovery time within minutes
eOPN3 effectively suppresses synaptic transmission through the G_i/o signaling pathway.
Here, we show that a targeting-enhanced mosquito homolog of the vertebrate encephalopsin (eOPN3) can effectively suppress synaptic transmission through the G_i/o signaling pathway.
eOPN3 effectively suppresses synaptic transmission through the G_i/o signaling pathway.
Here, we show that a targeting-enhanced mosquito homolog of the vertebrate encephalopsin (eOPN3) can effectively suppress synaptic transmission through the G_i/o signaling pathway.
eOPN3 effectively suppresses synaptic transmission through the G_i/o signaling pathway.
Here, we show that a targeting-enhanced mosquito homolog of the vertebrate encephalopsin (eOPN3) can effectively suppress synaptic transmission through the G_i/o signaling pathway.
eOPN3 effectively suppresses synaptic transmission through the G_i/o signaling pathway.
Here, we show that a targeting-enhanced mosquito homolog of the vertebrate encephalopsin (eOPN3) can effectively suppress synaptic transmission through the G_i/o signaling pathway.
eOPN3 effectively suppresses synaptic transmission through the G_i/o signaling pathway.
Here, we show that a targeting-enhanced mosquito homolog of the vertebrate encephalopsin (eOPN3) can effectively suppress synaptic transmission through the G_i/o signaling pathway.
eOPN3 effectively suppresses synaptic transmission through the G_i/o signaling pathway.
Here, we show that a targeting-enhanced mosquito homolog of the vertebrate encephalopsin (eOPN3) can effectively suppress synaptic transmission through the G_i/o signaling pathway.
eOPN3 effectively suppresses synaptic transmission through the G_i/o signaling pathway.
Here, we show that a targeting-enhanced mosquito homolog of the vertebrate encephalopsin (eOPN3) can effectively suppress synaptic transmission through the G_i/o signaling pathway.
eOPN3 effectively suppresses synaptic transmission through the G_i/o signaling pathway.
Here, we show that a targeting-enhanced mosquito homolog of the vertebrate encephalopsin (eOPN3) can effectively suppress synaptic transmission through the G_i/o signaling pathway.
eOPN3 effectively suppresses synaptic transmission through the G_i/o signaling pathway.
Here, we show that a targeting-enhanced mosquito homolog of the vertebrate encephalopsin (eOPN3) can effectively suppress synaptic transmission through the G_i/o signaling pathway.
eOPN3 can be used to selectively suppress neurotransmitter release at presynaptic terminals with high spatiotemporal precision.
We conclude that eOPN3 can be used to selectively suppress neurotransmitter release at presynaptic terminals with high spatiotemporal precision
eOPN3 can be used to selectively suppress neurotransmitter release at presynaptic terminals with high spatiotemporal precision.
We conclude that eOPN3 can be used to selectively suppress neurotransmitter release at presynaptic terminals with high spatiotemporal precision
eOPN3 can be used to selectively suppress neurotransmitter release at presynaptic terminals with high spatiotemporal precision.
We conclude that eOPN3 can be used to selectively suppress neurotransmitter release at presynaptic terminals with high spatiotemporal precision
eOPN3 can be used to selectively suppress neurotransmitter release at presynaptic terminals with high spatiotemporal precision.
We conclude that eOPN3 can be used to selectively suppress neurotransmitter release at presynaptic terminals with high spatiotemporal precision
eOPN3 can be used to selectively suppress neurotransmitter release at presynaptic terminals with high spatiotemporal precision.
We conclude that eOPN3 can be used to selectively suppress neurotransmitter release at presynaptic terminals with high spatiotemporal precision
eOPN3 can be used to selectively suppress neurotransmitter release at presynaptic terminals with high spatiotemporal precision.
We conclude that eOPN3 can be used to selectively suppress neurotransmitter release at presynaptic terminals with high spatiotemporal precision
eOPN3 can be used to selectively suppress neurotransmitter release at presynaptic terminals with high spatiotemporal precision.
We conclude that eOPN3 can be used to selectively suppress neurotransmitter release at presynaptic terminals with high spatiotemporal precision
eOPN3 can be used to selectively suppress neurotransmitter release at presynaptic terminals with high spatiotemporal precision.
We conclude that eOPN3 can be used to selectively suppress neurotransmitter release at presynaptic terminals with high spatiotemporal precision
eOPN3 can be used to selectively suppress neurotransmitter release at presynaptic terminals with high spatiotemporal precision.
We conclude that eOPN3 can be used to selectively suppress neurotransmitter release at presynaptic terminals with high spatiotemporal precision
Approval Evidence
1 source4 linked approval claimsfirst-pass slug eopn3
Here, we show that a targeting-enhanced mosquito homolog of the vertebrate encephalopsin (eOPN3) can effectively suppress synaptic transmission through the G_i/o signaling pathway.
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behavioral applicationsupports
In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents induces a reversible ipsiversive rotational bias.
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functional effectsupports
Brief illumination of presynaptic terminals expressing eOPN3 triggers lasting suppression of synaptic output that recovers spontaneously within minutes in vitro and in vivo.
Brief illumination of presynaptic terminals expressing eOPN3 triggers a lasting suppression of synaptic output that recovers spontaneously within minutes in vitro and in vivo.
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mechanism of actionsupports
eOPN3 effectively suppresses synaptic transmission through the G_i/o signaling pathway.
Here, we show that a targeting-enhanced mosquito homolog of the vertebrate encephalopsin (eOPN3) can effectively suppress synaptic transmission through the G_i/o signaling pathway.
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use casesupports
eOPN3 can be used to selectively suppress neurotransmitter release at presynaptic terminals with high spatiotemporal precision.
We conclude that eOPN3 can be used to selectively suppress neurotransmitter release at presynaptic terminals with high spatiotemporal precision
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Comparisons
Source-stated alternatives
The abstract contrasts eOPN3 with existing inhibitory optogenetic tools and chemogenetic tools. Existing inhibitory optogenetic tools are said to have low efficacy and off-target effects at presynaptic terminals, while chemogenetic tools are described as difficult to control in space and time.
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The abstract contrasts eOPN3 with existing inhibitory optogenetic tools and chemogenetic tools. Existing inhibitory optogenetic tools are said to have low efficacy and off-target effects at presynaptic terminals, while chemogenetic tools are described as difficult to control in space and time.
Source-backed strengths
The reported functional effect is lasting suppression of synaptic output after brief illumination, followed by spontaneous recovery within minutes in vitro and in vivo. In freely moving mice, eOPN3-mediated suppression of dopaminergic nigrostriatal afferents produced a reversible ipsiversive rotational bias, supporting behavioral efficacy in an intact circuit.
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effective suppression of synaptic transmission
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high spatiotemporal precision
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lasting suppression after brief illumination with spontaneous recovery within minutes
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works in vitro and in vivo
Compared with chemogenetic circuit manipulation
The abstract contrasts eOPN3 with existing inhibitory optogenetic tools and chemogenetic tools. Existing inhibitory optogenetic tools are said to have low efficacy and off-target effects at presynaptic terminals, while chemogenetic tools are described as difficult to control in space and time.
Shared frame: source-stated alternative in extracted literature
Strengths here: effective suppression of synaptic transmission; high spatiotemporal precision; lasting suppression after brief illumination with spontaneous recovery within minutes.
Source:
The abstract contrasts eOPN3 with existing inhibitory optogenetic tools and chemogenetic tools. Existing inhibitory optogenetic tools are said to have low efficacy and off-target effects at presynaptic terminals, while chemogenetic tools are described as difficult to control in space and time.
Compared with chemogenetics
The abstract contrasts eOPN3 with existing inhibitory optogenetic tools and chemogenetic tools. Existing inhibitory optogenetic tools are said to have low efficacy and off-target effects at presynaptic terminals, while chemogenetic tools are described as difficult to control in space and time.
Shared frame: source-stated alternative in extracted literature
Strengths here: effective suppression of synaptic transmission; high spatiotemporal precision; lasting suppression after brief illumination with spontaneous recovery within minutes.
Source:
The abstract contrasts eOPN3 with existing inhibitory optogenetic tools and chemogenetic tools. Existing inhibitory optogenetic tools are said to have low efficacy and off-target effects at presynaptic terminals, while chemogenetic tools are described as difficult to control in space and time.
Compared with optogenetic
The abstract contrasts eOPN3 with existing inhibitory optogenetic tools and chemogenetic tools. Existing inhibitory optogenetic tools are said to have low efficacy and off-target effects at presynaptic terminals, while chemogenetic tools are described as difficult to control in space and time.
Shared frame: source-stated alternative in extracted literature
Strengths here: effective suppression of synaptic transmission; high spatiotemporal precision; lasting suppression after brief illumination with spontaneous recovery within minutes.
Source:
The abstract contrasts eOPN3 with existing inhibitory optogenetic tools and chemogenetic tools. Existing inhibitory optogenetic tools are said to have low efficacy and off-target effects at presynaptic terminals, while chemogenetic tools are described as difficult to control in space and time.
Ranked Citations
- 1.