Source 1review2014Progress in Neurobiology
Toolkit/cell-specific receptor subtype gene deletion mouse models
cell-specific receptor subtype gene deletion mouse models
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
the development of mouse models characterised by cell-specific deletions of receptor subtype genes ... has greatly increased our understanding of the molecular mechanisms and neural substrates of nicotine addiction
Usefulness & Problems
Why this is useful
These mouse models remove receptor subtype genes in specific cell populations to study their contribution to nicotine addiction mechanisms.; testing cell-specific roles of receptor subtype genes in nicotine addiction; dissecting molecular and neural substrates of nicotine dependence
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These mouse models remove receptor subtype genes in specific cell populations to study their contribution to nicotine addiction mechanisms.
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testing cell-specific roles of receptor subtype genes in nicotine addiction
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dissecting molecular and neural substrates of nicotine dependence
Problem solved
They help assign mechanistic roles to defined receptor subtypes and cell populations within mesocorticolimbic circuitry.; enables cell-specific genetic dissection of receptor subtype contributions to nicotine-related mechanisms
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They help assign mechanistic roles to defined receptor subtypes and cell populations within mesocorticolimbic circuitry.
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enables cell-specific genetic dissection of receptor subtype contributions to nicotine-related mechanisms
Problem links
enables cell-specific genetic dissection of receptor subtype contributions to nicotine-related mechanisms
LiteratureThey help assign mechanistic roles to defined receptor subtypes and cell populations within mesocorticolimbic circuitry.
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They help assign mechanistic roles to defined receptor subtypes and cell populations within mesocorticolimbic circuitry.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Architecture: A reusable architecture pattern for arranging parts into an engineered system.
Techniques
No technique tags yet.
Target processes
recombinationInput: Light
Implementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationimplementation constraint: spectral hardware requirementoperating role: sensor
They require genetically engineered mouse lines with cell-specific deletions of receptor subtype genes.; requires mouse models with cell-specific receptor subtype gene deletions
The abstract does not indicate that these models alone capture all acute and chronic effects of nicotine or all behavioural dimensions of dependence.; the abstract does not identify specific receptor subtype genes, mouse lines, or phenotypic readouts
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Ranked Claims
Various aspects of nicotine dependence are mediated by close interactions of glutamatergic, dopaminergic, and GABAergic systems in the mesocorticolimbic system.
It is now becoming clear that various aspects of nicotine dependence are mediated by close interactions of the glutamatergic, dopaminergic and γ-aminobutyric acidergic systems in the mesocorticolimbic system.
New technologies including optogenetics and mouse genetic models with cell-specific receptor subtype deletions or gain-of-function nAChR subunits have greatly increased understanding of the molecular mechanisms and neural substrates of nicotine addiction.
The use of new technologies (including optogenetics) and the development of mouse models characterised by cell-specific deletions of receptor subtype genes or the expression of gain-of-function nAChR subunits has greatly increased our understanding of the molecular mechanisms and neural substrates of nicotine addiction
Approval Evidence
1 source2 linked approval claimsfirst-pass slug cell-specific-receptor-subtype-gene-deletion-mouse-models
the development of mouse models characterised by cell-specific deletions of receptor subtype genes ... has greatly increased our understanding of the molecular mechanisms and neural substrates of nicotine addiction
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mechanistic summarysupports
Various aspects of nicotine dependence are mediated by close interactions of glutamatergic, dopaminergic, and GABAergic systems in the mesocorticolimbic system.
It is now becoming clear that various aspects of nicotine dependence are mediated by close interactions of the glutamatergic, dopaminergic and γ-aminobutyric acidergic systems in the mesocorticolimbic system.
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review summarysupports
New technologies including optogenetics and mouse genetic models with cell-specific receptor subtype deletions or gain-of-function nAChR subunits have greatly increased understanding of the molecular mechanisms and neural substrates of nicotine addiction.
The use of new technologies (including optogenetics) and the development of mouse models characterised by cell-specific deletions of receptor subtype genes or the expression of gain-of-function nAChR subunits has greatly increased our understanding of the molecular mechanisms and neural substrates of nicotine addiction
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Comparisons
Source-stated alternatives
The abstract mentions optogenetics and classic electrophysiological, neurochemical and behavioural approaches as complementary or alternative strategies.
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The abstract mentions optogenetics and classic electrophysiological, neurochemical and behavioural approaches as complementary or alternative strategies.
Source-backed strengths
presented as having greatly increased understanding of nicotine addiction mechanisms
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presented as having greatly increased understanding of nicotine addiction mechanisms
Compared with optogenetic functional interrogation
The abstract mentions optogenetics and classic electrophysiological, neurochemical and behavioural approaches as complementary or alternative strategies.
Shared frame: source-stated alternative in extracted literature
Strengths here: presented as having greatly increased understanding of nicotine addiction mechanisms.
Relative tradeoffs: the abstract does not identify specific receptor subtype genes, mouse lines, or phenotypic readouts.
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The abstract mentions optogenetics and classic electrophysiological, neurochemical and behavioural approaches as complementary or alternative strategies.
Compared with optogenetic membrane potential perturbation
The abstract mentions optogenetics and classic electrophysiological, neurochemical and behavioural approaches as complementary or alternative strategies.
Shared frame: source-stated alternative in extracted literature
Strengths here: presented as having greatly increased understanding of nicotine addiction mechanisms.
Relative tradeoffs: the abstract does not identify specific receptor subtype genes, mouse lines, or phenotypic readouts.
Source:
The abstract mentions optogenetics and classic electrophysiological, neurochemical and behavioural approaches as complementary or alternative strategies.
Ranked Citations
- 1.