chemogenetic activation of glutamatergic lateral habenula neurons
Construct PatternTowards this goal, we used chemogenetic activation to temporarily excite glutamatergic neurons in the mouse LHb and assessed impacts on associative memory.
Browse the toolkit beneath workflows. The mechanism branch runs mechanism -> architecture -> component, while the technique branch runs from high-level approaches down to concrete methods.
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Mechanism Branch
Layer 1
Mechanisms
Top-level concepts: biophysical action modes such as heterodimerization, photocleavage, or RNA binding.
Layer 2
Architectures
Arrangements that realize or deploy mechanisms, including switches, construct patterns, and delivery strategies.
Layer 3
Components
Low-level parts and sequence-defined elements used inside architectures, including protein domains and RNA elements.
Technique Branch
Layer 1
Approaches
High-level engineering practices such as computational design, directed evolution, sequence verification, and functional assay.
Layer 2
Methods
Concrete methods used to design, build, verify, or characterize engineered systems.
Showing 1-12 of 12
Towards this goal, we used chemogenetic activation to temporarily excite glutamatergic neurons in the mouse LHb and assessed impacts on associative memory.
This study uses middle cerebral artery occlusion mouse model and chemogenetic techniques to study the underlying mechanisms of neuronal excitotoxicity and severe neuroinflammation after ischemic stroke. Chemogenetic inhibition of neuronal activity in ipsilesional M1 alleviates infarct area and neuroinflammation, and improves motor recovery in ischemia mice.
Chemogenetic methods of transmembrane receptors are a set of approaches for cell-specific regulation of receptor signaling. A 2022 review describes them as methods to control receptor functions in cells, with some strategies applied in living animals to reveal signaling in target cells.
Fetal neuroblasts are transplanted donor cells used to replace neurons in damaged basal ganglia circuits. The review describes their use in early rodent studies of circuitry repair.
Recent progress in the generation of striatal and nigral progenitors from pluripotent stem cells have provided compelling evidence that they can survive and mature in the lesioned brain and re-establish afferent and efferent axonal connectivity with a remarkable degree of specificity.
Recent progress in the generation of striatal and nigral progenitors from pluripotent stem cells have provided compelling evidence that they can survive and mature in the lesioned brain and re-establish afferent and efferent axonal connectivity with a remarkable degree of specificity.
AAV5, oral administration of deschloroclozapine, and clozapine-N-oxide were also effective but with slightly less potency.
Chemogenetic tools allow the expression of designer receptors exclusively activated by designer drugs (DREADDs) specifically in microglia.
Unexpectedly, in response to the administration of deschloroclozapine, we observed inhibitory effects with pan-neuronal hM3D(Gq) stimulation.
Here, we express the Gi-DREADD hM4Di in glutamatergic telencephalic neurons... activation of hM4Di leads to a complete arrest of spontaneous synchrony in CA1 in vitro.
The sequential activation of hM3D(Gq) and KORD DREADDs within the same neuronal population validated the role of the VTA-AcbSh circuit in reinforced responding for concurrently available natural and drug rewards.
Self-localizing ligand-induced protein translocation (SLIPT) is an emerging technique that we developed to control protein localization in living cells using synthetic self-localizing ligands (SLs).