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Isoflurane Exposure in Juvenile Caenorhabditis elegans Causes Persistent Changes in Neuron Dynamics
Gregory S Wirak1, Christopher V Gabel, Christopher W Connor
1From the Department of Physiology and Biophysics, Boston University School of Medicine, Boston, Massachusetts (G.S.W., C.V.G., C.W.C.) the Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Boston, Massachusetts (C.W.C.).
Anesthesiology
|May 27, 2020
Summary
Developmental exposure to isoflurane anesthesia in C. elegans causes lasting changes in locomotion and neuronal activity. These effects are linked to stress-response pathways involving daf-16 and mTOR.
Area of Science:
- Neuroscience
- Developmental Biology
- Anesthesiology
Background:
- Anesthetic exposure during neurodevelopment can cause persistent behavioral deficits in animal models.
- The precise neuronal mechanisms underlying these postanesthetic effects remain unclear.
- The nematode Caenorhabditis elegans offers a powerful model for studying postanesthetic effects on neuronal activity due to its well-defined neurocircuitry and suitability for functional imaging.
Purpose of the Study:
- To investigate the long-term effects of developmental isoflurane exposure on neuronal activity and locomotion in C. elegans.
- To examine how isoflurane impacts the neurocircuitry controlling C. elegans movement.
Main Methods:
- C. elegans were exposed to 8% isoflurane during the L1 larval stage, a critical period for neurodevelopment.
- Locomotion was assessed in adulthood, and spontaneous neuronal activity in the command interneuron circuitry was measured using calcium imaging (GCaMP6s).
- Functional imaging employed confocal and light-sheet microscopy techniques.
Main Results:
- Isoflurane-exposed worms exhibited reduced spontaneous reversal behavior throughout adulthood.
- Anesthetic exposure altered the activity dynamics of the AVA command interneuron, increasing state transition rates.
- These age-dependent effects on neuronal activity and locomotion were modulated by daf-16 (FoxO transcription factor) and mechanistic Target of Rapamycin (mTOR) signaling.
Conclusions:
- Developmental isoflurane exposure induces persistent alterations in C. elegans locomotion and interneuron circuit function.
- The observed effects suggest a pathological activation of stress-response pathways, influenced by daf-16 and mTOR.
- This study highlights the long-lasting impact of early-life anesthetic exposure on neural circuit dynamics.
