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Behavioral Effect of Chemogenetic Inhibition Is Directly Related to Receptor Transduction Levels in Rhesus Monkeys.
We used inhibitory DREADDs (designer receptors exclusively activated by designer drugs) to reversibly disrupt dorsolateral prefrontal cortex (dlPFC) function in male rhesus monkeys. Monkeys were tested on a spatial delayed response task to assess working memory function after intramuscular injection of either clozapine--oxide (CNO) or vehicle. CNO injections given before DREADD transduction were without effect on behavior. rAAV5/hSyn-hM4Di-mCherry was injected bilaterally into the dlPFC of five male rhesus monkeys, to produce neuronal expression of the inhibitory (Gi-coupled) DREADD receptor. We quantified the percentage of DREADD-transduced cells using stereological analysis of mCherry-immunolabeled neurons. We found a greater number of immunolabeled neurons in monkeys that displayed CNO-induced behavioral impairment after DREADD transduction compared with monkeys that showed no behavioral effect after CNO. Even in monkeys that showed reliable effects of CNO on behavior after DREADD transduction, the number of prefrontal neurons transduced with DREADD receptor was on the order of 3% of total prefrontal neurons counted. This level of histological analysis facilitates our understanding of behavioral effects, or lack thereof, after DREADD vector injection in monkeys. It also implies that a functional silencing of a relatively small fraction of dlPFC neurons, albeit in a widely distributed area, is sufficient to disrupt spatial working memory. Cognitive domains such as working memory and executive function are mediated by the dorsolateral prefrontal cortex (dlPFC). Impairments in these domains are common in neurodegenerative diseases as well as normal aging. The present study sought to measure deficits in a spatial delayed response task following activation of viral-vector transduced inhibitory DREADD (designer receptor exclusively activated by designer drug) receptors in rhesus macaques and compare this to the level of transduction in dlPFC using stereology. We found a significant relationship between the extent of DREADD transduction and the magnitude of behavioral deficit following administration of the DREADD actuator compound clozapine--oxide (CNO). These results demonstrate it will be critical to validate transduction to ensure DREADDs remain a powerful tool for neuronal disruption.
Authors : Upright Nicholas A , Brookshire Stephen W , Schnebelen Wendy , Damatac Christienne G , Hof Patrick R , Browning Philip G F , Croxson Paula L , Rudebeck Peter H , Baxter Mark G ,
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WP1963: The effect of Glucocorticoids on target gene expression
WP1965: VEGF-receptor Signal Transduction
WP2272: Pathogenic Escherichia coli infection
WP26: Signal Transduction of S1P Receptor
WP57: Signal Transduction of S1P Receptor
WP1004: Kit Receptor Signaling Pathway
WP1011: T Cell Receptor Signaling Pathway
WP1014: Androgen receptor signaling pathway
WP1025: B Cell Receptor Signaling Pathway
WP1045: TGF-beta Receptor Signaling Pathway
WP1046: Signaling of Hepatocyte Growth Factor Receptor
WP1067: Toll-like receptor signaling pathway
WP1081: Signal Transduction of S1P
WP1112: EPO Receptor Signaling
WP1121: Kit Receptor Signaling Pathway
WP1130: T Cell Receptor Signaling Pathway
WP1133: Androgen receptor signaling pathway
WP1144: B Cell Receptor Signaling Pathway
WP1161: TGF-beta Receptor Signaling Pathway
WP1162: Signaling of Hepatocyte Growth Factor Receptor
WP1183: Toll-like receptor signaling pathway
WP1198: Signal Transduction of S1P
WP1206: Signaling of Hepatocyte Growth Factor Receptor
WP1235: Signaling of Hepatocyte Growth Factor Receptor
WP1249: EPO Receptor Signaling
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Bibliography :
[30082415] Behavioral Effect of Chemogenetic Inhibition Is Directly Related to Receptor Transduction Levels in Rhesus Monkeys.
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