Remote control of neuronal activity in transgenic mice expressing evolved G protein-coupled receptors.
By G. M. Alexander, Sarah C. Rogan, Atheir I. Abbas, Blaine N. Armbruster, Ying Pei, John A. Allen, Randal J. Nonneman, J. Hartmann, S. Moy, Miguel A. L. Nicolelis and 2 more. Neuron, 2009
944 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/79a55ad3b89b063ba95f92a4a2b0060285e380be
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In Cellular and Molecular Neuroscience
- Bryan L. Roth
- Y. Dudai
- E. Kandel
- M. Mayford
- M. Krashes
- E. Maratos-Flier
- S. Siegelbaum
- Bradford B. Lowell
In Molecular Biology
Citations in the corpus
- DREADDs for Neuroscientists (2016, methodology): “, 2013), mice (Alexander et al., 2009), rats (Ferguson et al.”
- Synapses and memory storage. (2012, background): “Also effective for turning neurons on or off are ligand-gated proteins with customized binding sites, such as the G-protein-coupled designer receptor (Alexander et al. 2009) and a chimeric ligand-gated ion channel, which are activated by an inert ligand (Magnus et al.”
- The molecular and systems biology of memory. (2014, positive): “One such designer receptor (hM3Dq) is a Gq coupled human muscarinic receptor that has been mutated so that it no longer responds to acetylcholine but instead responds to the synthetic ligand clozapine-N-oxide (CNO) (Alexander et al., 2009).”
- A New DREADD Facilitates the Multiplexed Chemogenetic Interrogation of Behavior (2015, positive): “The kinetics of CNO on neuronal activation via hM3Dq have been demonstrated thoroughly by a large number of independent studies, with in vivo DREADD mediated responses beginning 5–10 min after IP injection, and peak electrophysiological response occurring 45– 50 min after injection (Alexander et al.”
- Rapid, reversible activation of AgRP neurons drives feeding behavior in mice. (2011, methodology): “Results and Discussion One way to accomplish this is via designer receptors exclusively activated by designer drugs (DREADD) technology, in which muscarinic GPCRs are mutated so that their ability to bind natural ligands is lost, while nanomolar potency is gained for the otherwise pharmacologically ”