title: Is the human masticatory system devoid of recurrent inhibition?
abstract: The aim of the present study was to investigate the existence or otherwise of a functional recurrent inhibitory system (Renshaw cell system) in the motoneurons that innervate human masticatory muscles. In a previous study, L: -acetylcarnitine (L: -Ac), a substance known to potentiate recurrent inhibition in humans was found to alter, in a specific way, the discharge variability, and the synchronous activity of motor units depending on the presence or absence of recurrent inhibition in the corresponding motoneuron pool. Using a similar paradigm, we have recorded the tonic discharge activity of motor unit pairs from the masseter muscle during voluntary isometric contraction while subjects were undergoing continuous intravenous saline (SAL, NaCl 0.9%) perfusion. Following a brief baseline-recording period, the subjects were given a test injection of either L: -Ac or isotonic saline (SAL) in a double blind manner. The variability, synchronization, and coherence between the motor unit discharges were analysed during three successive periods: pre-injection, during injection, and post-injection, each lasting 2-3 min. Neither L: -Ac nor SAL injection induced a significant change in the inter-spike interval (ISI) or the coefficient of variation of the ISIs in the motor units tested. There were also no significant changes in the pattern of synchronous activity or in the coherence, which reflects the common frequency content of the unit discharges. Reminiscent of what had been observed previously with motoneurons without recurrent inhibition in the Abductor Digitorum Minimi muscle, the lack of effects of L: -Ac injection on the firing behaviour of masseter motoneurons may suggest that classical Renshaw cell inhibition is lacking in this motoneuron pool.
authors.affiliation: Research Centre for Human Movement Control, Discipline of Physiology, School of Molecular and Biomedical Sciences, University of Adelaide, Adelaide, SA 5005, Australia. kemal.turker@adelaide.edu.au
authors.forename: K S
authors.initials: KS
authors.lastname: Türker
authors.forename: A
authors.initials: A
authors.lastname: Schmied
authors.forename: A
authors.initials: A
authors.lastname: Rossi
authors.forename: R
authors.initials: R
authors.lastname: Mazzocchio
authors.forename: P F
authors.initials: PF
authors.lastname: Sowman
authors.forename: J P
authors.initials: JP
authors.lastname: Vedel
mesh_terms: D000108:Acetylcarnitine / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000328:Adult; D001732:Bite Force; D004576:Electromyography; D005246:Feedback / Q000187:drug effects / Q000502:physiology; D005260:Female; D006801:Humans; D007537:Isometric Contraction / Q000187:drug effects / Q000502:physiology; D008297:Male; D008409:Mastication / Q000187:drug effects / Q000502:physiology; D008410:Masticatory Muscles / Q000294:innervation* / Q000502:physiology*; D008875:Middle Aged; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology*; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D018697:Nootropic Agents / Q000494:pharmacology; D012965:Sodium Chloride / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology; D014276:Trigeminal Nerve / Q000187:drug effects / Q000502:physiology*; D014278:Trigeminal Nuclei / Q000187:drug effects / Q000502:physiology*
chemical_list: D018697:Nootropic Agents; D012965:Sodium Chloride; D000108:Acetylcarnitine