Abstract
For most metazoans, oxygen deprivation leads to cell dysfunction and if severe, death. Sublethal stress prior to a hypoxic or anoxic insult (“preconditioning”) can protect cells from subsequent oxygen deprivation. The molecular mechanisms by which sublethal stress can buffer against a subsequent toxic insult and the role of the nervous system in the response are not well understood. We studied the role of neuronal activity preconditioning to oxygen deprivation in Caenorhabditis elegans. Animals expressing the histamine gated chloride channels (HisCl1) in select cell populations were used to temporally and spatially inactivate the nervous system or tissue prior to an anoxic insult. We find that inactivation of the nervous system for 3 h prior to the insult confers resistance to a 48-h anoxic insult in 4th-stage larval animals. Experiments show that this resistance can be attributed to loss of activity in cholinergic and GABAergic neurons as well as in body wall muscles. These observations indicate that the nervous system activity can mediate the organism's response to anoxia.
| Original language | English (US) |
|---|---|
| Article number | e12713 |
| Journal | Genes, Brain and Behavior |
| Volume | 20 |
| Issue number | 4 |
| DOIs | |
| State | Published - Apr 2021 |
Funding
Les Turner ALS Foundation; National Insitute of Health (NIH), Grant/Award Numbers: NS05225, NS087077; National Institute of General Medical Sciences of the National Institutes of Health, Grant/Award Number: K12GM081259; NIH Office of Research Infrastructure Programs, Grant/Award Number: P40 OD010440 Funding information We would like to thank Cornelia Bargmann and Paul Sternberg for generously sharing with us several strains to test in our experimental paradigm. We would like to thank Michael Crowder at the University of Washington Seattle and David M. Raizen at the University of Pennsylvania for providing intellectual support and guidance in our experimental design and results. We also thank the Worm Group laboratories at the University of Pennsylvania for their feedback and support. We thank the members of the Kalb, Fang‐Yen, Burkhardt, Argon, laboratories for support. We would like to thank Janis Burkhardt, Yair Argon and Steven Seeholzer for generously providing reagents, equipment, and space to conduct our experiments. We also thank Erika Perez at Xavier University of Louisiana and Gabriel Perron at Bard College for guidance on statistical analyses. Some strains were provided by the CGC, which is funded by NIH Office of Research Infrastructure Programs (P40 OD010440). The research reported in this publication was supported by the National Institutes of Health K12GM081259 (H. L. B), NS087077 and NS05225 (R. G. K.) and the Les Turner ALS Center at Northwestern University (R. G. K.). We would like to thank Cornelia Bargmann and Paul Sternberg for generously sharing with us several strains to test in our experimental paradigm. We would like to thank Michael Crowder at the University of Washington Seattle and David M. Raizen at the University of Pennsylvania for providing intellectual support and guidance in our experimental design and results. We also thank the Worm Group laboratories at the University of Pennsylvania for their feedback and support. We thank the members of the Kalb, Fang-Yen, Burkhardt, Argon, laboratories for support. We would like to thank Janis Burkhardt, Yair Argon and Steven Seeholzer for generously providing reagents, equipment, and space to conduct our experiments. We also thank Erika Perez at Xavier University of Louisiana and Gabriel Perron at Bard College for guidance on statistical analyses. Some strains were provided by the CGC, which is funded by NIH Office of Research Infrastructure Programs (P40 OD010440). The research reported in this publication was supported by the National Institutes of Health K12GM081259 (H. L. B), NS087077 and NS05225 (R. G. K.) and the Les Turner ALS Center at Northwestern University (R. G. K.).
Keywords
- C. elegans
- GABAergic neurons
- anoxia
- cholinergic neurons
- ischemia
- muscle activity
- neural circuits
- oxygen deprivation
- preconditioning
- stress
ASJC Scopus subject areas
- Neurology
- Genetics
- Behavioral Neuroscience