Tooth pulp- and facial hair mechanoreceptor-evoked responses of trigeminal sensory neurons are attenuated during ketamine anesthesia.
BACKGROUND
Evidence exists that ketamine, administered systemically using a dose required for inducing a state of anesthesia, may antagonize nociceptive but not innocuous input to lumbar dorsal horn neurons. However, it is unclear whether ketamine exerts this selective action on sensory inputs to trigeminal sensory neurons. The current study was undertaken to compare the responses evoked in trigeminal sensory neurons by electrical stimuli applied to the tooth pulp versus air-puff stimuli applied to facial hair mechanoreceptors (FHMs) during quiet wakefulness versus ketamine anesthesia.


METHODS
Accordingly, responses of rostral trigeminal sensory nuclear complex (TSNC) and trigeminothalamic tract neurons evoked by tooth pulp (a source of small-diameter fiber input) and FHMs (a source of larger-diameter fiber input) were recorded extracellularly from chronically instrumented cats before, during, and after recovery from the anesthetic state induced by a single (2.2 mg/kg) intravenous injection of ketamine.


RESULTS
Overall, tooth pulp-evoked responses of TSNC neurons were maximally suppressed by 50% within 5 min after the intravenous administration of ketamine. Ketamine also suppressed the FHM-evoked responses of TSNC and trigeminothalamic neurons by 45%. The time course of ketamine's suppressive action was equivalent for tooth pulp- and FHM-evoked responses. However, the recovery of tooth pulp-evoked TSNC neuronal responses at suprathreshold intensities was markedly prolonged compared with neuronal responses driven by threshold stimuli or FHM.


CONCLUSIONS
These electrophysiologic results in the chronically instrumented cat preparation indicate that a nonselective suppression of orofacial somatosensory information occurs during ketamine anesthesia. The prolonged recovery of suprathreshold responses of TSNC neurons mediated by small-diameter afferent fiber input may partly underlie the analgesic action of ketamine that is clinically relevant at subanesthetic doses.
Cairns
B E
BE
Department of Oral Physiology, Faculty of Dentistry, The University of Toronto, Ontario, Canada.
McErlane
S A
SA
Fragoso
M C
MC
Soja
P J
PJ
D000778:Anesthetics, Dissociative / Q000494:pharmacology*; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D002415:Cats; D003782:Dental Pulp / Q000187:drug effects* / Q000502:physiology; D004558:Electric Stimulation; D004594:Electrophysiology; D005145:Face; D006197:Hair / Q000187:drug effects* / Q000502:physiology; D007649:Ketamine / Q000494:pharmacology*; D008465:Mechanoreceptors / Q000187:drug effects* / Q000502:physiology; D009475:Neurons, Afferent / Q000187:drug effects* / Q000502:physiology; D014278:Trigeminal Nuclei / Q000187:drug effects* / Q000502:physiology
D000778:Anesthetics, Dissociative; D007649:Ketamine