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Circumventing neural damage in a C. elegans chemosensory circuit using genetically engineered synapses.


ABSTRACT: Neuronal loss can considerably diminish neural circuit function, impairing normal behavior by disrupting information flow in the circuit. Here, we use genetically engineered electrical synapses to reroute the flow of information in a C. elegans damaged chemosensory circuit in order to restore organism behavior. We impaired chemotaxis by removing one pair of interneurons from the circuit then artificially coupled two other adjacent neuron pairs by ectopically expressing the gap junction protein, connexin, in them. This restored chemotaxis in the animals. We expected to observe linear and direct information flow between the connexin-coupled neurons in the recovered circuit but also revealed the formation of new potent left-right lateral electrical connections within the connexin-expressing neuron pairs. Our analysis suggests that these additional electrical synapses help restore circuit function by amplifying weakened neuronal signals in the damaged circuit in addition to emulating the wild-type circuit. A record of this paper's transparent peer review process is included in the Supplemental Information.

SUBMITTER: Rabinowitch I 

PROVIDER: S-EPMC7979504 | biostudies-literature | 2021 Mar

REPOSITORIES: biostudies-literature

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Circumventing neural damage in a C. elegans chemosensory circuit using genetically engineered synapses.

Rabinowitch Ithai I   Upadhyaya Bishal B   Pant Aaradhya A   Galski Dolev D   Kreines Lena L   Bai Jihong J  

Cell systems 20210119 3


Neuronal loss can considerably diminish neural circuit function, impairing normal behavior by disrupting information flow in the circuit. Here, we use genetically engineered electrical synapses to reroute the flow of information in a C. elegans damaged chemosensory circuit in order to restore organism behavior. We impaired chemotaxis by removing one pair of interneurons from the circuit then artificially coupled two other adjacent neuron pairs by ectopically expressing the gap junction protein,  ...[more]

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