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Optogenetic Activation of Afferent Pathways in Brain Slices and Modulation of Responses by Volatile Anesthetics
Published on: July 23, 2020
Anaesthetics differentially modulate the trigeminocardiac reflex excitatory synaptic pathway in the brainstem
Xin Wang1, Christopher Gorini, Douglas Sharp
1Department of Pharmacology and Physiology, and Department of Anesthesiology and Critical Care Medicine, The George Washington University, 2300 Eye Street, NW, Washington, DC 20037, USA.
The Journal of Physiology
|September 21, 2011
Summary
This study reveals how ketamine, isoflurane, and fentanyl affect the trigeminocardiac reflex (TCR) by modulating glutamatergic pathways. These anesthetics differentially impact synaptic responses, clarifying mechanisms behind TCR modulation.
Area of Science:
- Neuroscience
- Anesthesiology
- Physiology
Background:
- The trigeminocardiac reflex (TCR) involves bradycardia and hypotension upon trigeminal nerve excitation.
- Mechanisms by which anesthetics and analgesics modulate TCR are not fully understood.
Purpose of the Study:
- To investigate the synaptic mechanisms of ketamine, isoflurane, and fentanyl on the TCR.
- To examine their effects on trigeminal neurons in the Sp5I nucleus and cardiac vagal neurons (CVNs) in the Nucleus Ambiguus (NA).
Main Methods:
- Electrophysiological recordings of excitatory postsynaptic currents (EPSCs) in Sp5I and CVNs.
- Stimulation of trigeminal afferent fibers and assessment of synaptic responses.
- Application of glutamatergic receptor antagonists (AMPA/kainate and NMDA).
- Administration of ketamine, isoflurane, and fentanyl to evaluate their modulatory effects.
Main Results:
- TCR involves glutamatergic pathways mediated by AMPA/kainate and NMDA receptors.
- Ketamine inhibited EPSCs in both Sp5I and CVNs.
- Isoflurane significantly inhibited EPSCs in CVNs, while fentanyl significantly enhanced them.
- Fentanyl and isoflurane showed no effect on Sp5I neuronal responses.
Conclusions:
- Glutamatergic excitatory synaptic pathways are crucial for the TCR.
- Ketamine, isoflurane, and fentanyl differentially modulate TCR synaptic pathways through distinct receptor interactions.
- Understanding these mechanisms can inform anesthetic choices and management of TCR.
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