Source 1primary paper2025MED
Toolkit/chemogenetic activation of glutamatergic lateral habenula neurons
chemogenetic activation of glutamatergic lateral habenula neurons
Also known as: chemogenetic activation, temporary excitation of glutamatergic neurons in the mouse LHb
Taxonomy: Mechanism Branch / Architecture. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
Towards this goal, we used chemogenetic activation to temporarily excite glutamatergic neurons in the mouse LHb and assessed impacts on associative memory.
Usefulness & Problems
Why this is useful
This approach temporarily excites glutamatergic neurons in the mouse lateral habenula using chemogenetic activation. In this paper it is used to test how acute LHb activation affects associative memory.; transient excitation of a defined neuronal population in mouse lateral habenula; testing causal effects of LHb glutamatergic neuron activity on memory-related behavior
Source:
This approach temporarily excites glutamatergic neurons in the mouse lateral habenula using chemogenetic activation. In this paper it is used to test how acute LHb activation affects associative memory.
Source:
transient excitation of a defined neuronal population in mouse lateral habenula
Source:
testing causal effects of LHb glutamatergic neuron activity on memory-related behavior
Problem solved
It provides a way to causally perturb LHb glutamatergic neuron activity during a defined post-training interval. This helps test whether LHb activity contributes to memory consolidation.; enables temporally controlled perturbation of LHb glutamatergic neurons during behavioral experiments
Source:
It provides a way to causally perturb LHb glutamatergic neuron activity during a defined post-training interval. This helps test whether LHb activity contributes to memory consolidation.
Source:
enables temporally controlled perturbation of LHb glutamatergic neurons during behavioral experiments
Problem links
enables temporally controlled perturbation of LHb glutamatergic neurons during behavioral experiments
LiteratureIt provides a way to causally perturb LHb glutamatergic neuron activity during a defined post-training interval. This helps test whether LHb activity contributes to memory consolidation.
Source:
It provides a way to causally perturb LHb glutamatergic neuron activity during a defined post-training interval. This helps test whether LHb activity contributes to memory consolidation.
Published Workflows
Objective: Test whether transient activation of glutamatergic neurons in the mouse lateral habenula affects associative memory and identify the memory stage and pharmacological sensitivity of that effect.
Why it works: The workflow perturbs LHb glutamatergic neurons transiently after training, then compares behavioral memory outcomes across tasks and timing conditions, with ketamine rescue used to probe mechanism.
modulation of memory consolidation by LHb glutamatergic neuronsNMDA-mediated mechanismchemogenetic activationbehavioral memory testingsystemic ketamine rescue
Stages
- 1.Chemogenetic perturbation and broad associative memory testing(broad_screen)
This stage establishes whether transient LHb glutamatergic neuron activation has any measurable impact on associative memory.
Selection: Assess whether transient activation of mouse LHb glutamatergic neurons alters associative memory outcomes.
- 2.Task-specific secondary characterization(secondary_characterization)
This stage determines whether the observed impairment generalizes across memory modalities or is selective.
Selection: Compare effects across object recognition, reward-based associative memory, and fear-associated memory.
- 3.Temporal-window characterization of the memory effect(functional_characterization)
This stage localizes the behavioral effect to a specific memory-processing window.
Selection: Test whether impairment is limited to a post-training or post-conditioning interval corresponding to consolidation.
- 4.Ketamine rescue as confirmatory mechanistic validation(confirmatory_validation)
This stage tests whether the induced memory deficit is sensitive to ketamine, supporting an NMDA-mediated interpretation.
Selection: Determine whether systemic ketamine rescues the long-term memory deficits caused by LHb activation.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Architecture: A reusable architecture pattern for arranging parts into an engineered system.
Mechanisms
chemogenetic neuronal activationtemporal perturbation during memory consolidationtransient excitation of glutamatergic lhb neuronsTechniques
No technique tags yet.
Target processes
No target processes tagged yet.
Implementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationoperating role: actuator
The abstract supports a mouse experiment with LHb-targeted chemogenetic activation and behavioral memory assays. It does not specify the exact actuator, vector, or driver line.; requires mouse LHb targeting and a chemogenetic activation setup; requires behavioral timing relative to training or conditioning
The abstract does not show that this method by itself identifies the exact molecular or circuit pathway downstream of LHb activation. It also does not specify the construct details needed for implementation.; exact chemogenetic actuator, vector, and genetic targeting strategy are not stated in the abstract
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Ranked Claims
Chemogenetic activation of glutamatergic lateral habenula neurons in mice impaired long-term associative memory.
we used chemogenetic activation to temporarily excite glutamatergic neurons in the mouse LHb and assessed impacts on associative memory. Surprisingly, we found that transient activation of LHb impaired long-term memory
Systemic ketamine rescued the long-term memory deficits caused by LHb glutamatergic neuronal activation.
pairing LHb glutamatergic neuronal activation with systemic ketamine administration rescued the long-term memory deficits
Post-training activation of LHb glutamatergic neurons disrupted object recognition and reward-based associative long-term memory while sparing fear-associated long-term memory.
post-training activation of LHb glutamatergic neurons disrupted object recognition and reward-based associative long-term memory, while sparing fear associated long-term memory
The memory impairment caused by LHb glutamatergic neuron activation was restricted to a critical post-training or post-conditioning temporal window corresponding to long-term memory consolidation.
The memory impairment was restricted to a critical temporal window post-training/conditioning that corresponded with the consolidation stage of long-term memory.
Approval Evidence
1 source4 linked approval claimsfirst-pass slug chemogenetic-activation-of-glutamatergic-lateral-habenula-neurons
Towards this goal, we used chemogenetic activation to temporarily excite glutamatergic neurons in the mouse LHb and assessed impacts on associative memory.
Source:
functional effectsupports
Chemogenetic activation of glutamatergic lateral habenula neurons in mice impaired long-term associative memory.
we used chemogenetic activation to temporarily excite glutamatergic neurons in the mouse LHb and assessed impacts on associative memory. Surprisingly, we found that transient activation of LHb impaired long-term memory
Source:
pharmacologic rescuesupports
Systemic ketamine rescued the long-term memory deficits caused by LHb glutamatergic neuronal activation.
pairing LHb glutamatergic neuronal activation with systemic ketamine administration rescued the long-term memory deficits
Source:
task specific effectsupports
Post-training activation of LHb glutamatergic neurons disrupted object recognition and reward-based associative long-term memory while sparing fear-associated long-term memory.
post-training activation of LHb glutamatergic neurons disrupted object recognition and reward-based associative long-term memory, while sparing fear associated long-term memory
Source:
temporal windowsupports
The memory impairment caused by LHb glutamatergic neuron activation was restricted to a critical post-training or post-conditioning temporal window corresponding to long-term memory consolidation.
The memory impairment was restricted to a critical temporal window post-training/conditioning that corresponded with the consolidation stage of long-term memory.
Source:
Comparisons
Source-stated alternatives
The abstract does not name a direct alternative perturbation method. It does mention systemic ketamine as a pharmacological manipulation that modifies the observed memory phenotype.
Source:
The abstract does not name a direct alternative perturbation method. It does mention systemic ketamine as a pharmacological manipulation that modifies the observed memory phenotype.
Source-backed strengths
supports transient post-training manipulation aligned to a memory consolidation window
Source:
supports transient post-training manipulation aligned to a memory consolidation window
Ranked Citations
- 1.