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Biomedical subjects

E Godaux

Publications and source records attributed to E Godaux.

80 records · Page 5Linked to original sources
PubMed1975

Exteroceptive suppression and motor control of the masseter and temporalis muscles in normal man.

Single electrical stimuli to the gums and mucosa inside the mouth elicit two successive exteroceptive suppressions (ES1 and ES2) in the voluntary electromyogram of the masseter and temporalis muscles in normal man. The same afferent axons appear to be involved in the two effects, as indicated by the intensity function, the electrical excitability, the afferent conduction velocity and the lack of differential effect of Xylocaine infiltration of the inferior alveolar nerve. Two similar phases of inhibition involve the monosynaptic masseter reflex and the synchronized electromyographical spikes induced by jaw vibration. Exteroceptive suppression is thought to be mediated, in the brain stem, by both an oligosynaptic (ES1) and a multisynaptic (ES2) mechanism.

Action Potentials↗
PubMed1975

Human masseter muscle: H- and tendon reflexes. Their paradoxical potentiation by muscle vibration.

We developed a method for direct electrical stimulation of the masseter nerve in man. Both direct M-reponses and genuine H-reflexes were recorded from the ipsilateral masseter muscle. Muscle vibration that inhibits the Achilles tendon reflex and the soleus H-reflex was found to potentiate the masseter tendon reflex and also the masseter H-reflex. This unexpected contrast may be related to peculiar brain stem circuitry of the masseter reflex mechanism.

Achilles Tendon↗
PubMed1975

Vibration-induced discharge patterns of single motor units in the masseter muscle in man.

Single motor unit potentials were recorded with small bipolar wires from intact masseter muscles in the adult man and a detailed parametric analysis of the effects of muscle vibration on motor unit discharges was carried out. 2. When the vibration amplitude was kept constant, each unit started firing at a definite threshold of vibration frequency. With higher frequencies the rate of firing rapidly reached a maximum. Units recruited at higher frequencies presented a lower maximum rate of firing. 3. When the vibration frequency was kept constant, each masseter unit discharged at a definite threshold of vibration amplitude. With higher amplitudes the unit quickly reached a maximum rate of discharge. Units with a higher frequency threshold tended to also present a higher amplitude threshold. Motor unit "excitability" curves could be plotted using the combined threshold conditions for frequency and amplitude of applied vibrations. 4. With a given parametric set of vibration, the units only started firing at a given delay after the onset of vibration. The delay was quite different for different units and it increased considerably, sometimes by several seconds, when the vibration amplitude was made smaller. 5. In all the experimental conditions tested, and even when the unit discharge did not start until several seconds after vibration onset, the unit potential presented a close and highly consistent temporal relation to the vibration cycles. The slow recruitment process is thought to involve a polysynaptic excitatory mechanism which progressively depolarizes the masseter motoneurones close to their threshold, the actual firing being triggered by monosynaptic excitatory post-synaptic potentials from I(a) afferents, hence the small latency jitter recorded. This special pattern of tonic vibration reflex in jaw-closing muscles in man may result from the lack of reciprocal inhibition from the jaw-opening muscles.

Action Potentials↗
PubMed1975

Evidence for a monosynaptic mechanism in the tonic vibration reflex of the human masseter muscle.

Vibration of the masseter and temporalis muscles in normal human adult subjects elicits a tonic vibration reflex with unexpected features. The electromyographic response is not asynchronous as in the limb muscles, but involves well-defined spikes with a one-to-one temporal relation to the vibration cycles. The effect of various parameters such as muscle stretch, vibration frequency or amplitude, etc, has been investigated. The small latency fluctuation of the vibration-induced spikes is compatible with a monosynaptic reflex mechanism which is considered to be assisted by a polysynaptic facilitatory background of proprioceptive origin.

Adult↗
PubMedDate not supplied

Effects of ketamine on ocular movements of the cat.

We studied the effects of ketamine, an antagonist of the N-methyl-D-aspartate receptors, on (1) the spontaneous saccades, (2) the vestibulo-ocular reflex (VOR), and (3) the optokinetic nystagmus (OKN) in 8 cats. Ketamine was given intramuscularly at four dosages (1, 2, 8, and 16 mg/kg). Eye movements were measured using the magnetic field-search coil technique. Ketamine did not prevent the occurrence of saccades, but each of them was followed by a centripetal postsaccadic drift. The time-constant of the drift induced by ketamine was 1.0 s when the given dosage was 1 mg/kg and 0.35 s when the given dosage was 16 mg/kg. Post-saccadic drift caused by a low dosage of ketamine may reflect only a mismatch between the pulse and the step commands that create saccades. The highest used dosages of ketamine aggravated the post-saccadic drift probably by disturbing the oculomotor neural integrator. To elicit the horizontal VOR, the head was submitted either to sinusoidal rotations (+/- 20 degrees; 0.05 to 1 Hz) or to a rotation at a constant velocity (100 degrees/s during 40 s). In darkness, the VOR step gain was reduced by ketamine in a dosage-dependent manner. VOR phase lead at 0.10 Hz oscillation in darkness increased from 4.0 degrees +/- 2.4 degrees to 51.6 degrees +/- 7.5 degrees after administration of ketamine at 16 mg/kg. This suggests that ketamine, at least at higher dosages, induces a failure of the neural integrator. Chemical blockade of the vestibular commissure by ketamine may also be responsible for the reduction of the VOR gain. Horizontal OKN was tested using a step stimulus (30 degrees/s during 40 s). When ketamine was given at 1 mg/kg, the average steady-state gain of the OKN diminished from 0.6 +/- 0.2 to 0.3 +/- 0.1. After administration of ketamine at 2 mg/kg, the OKN was abolished. The sensitivity of OKN to ketamine is explained at least partly by the fact that ketamine acts against the visual pathways in the retina, in the geniculate nucleus, and in the visual cortex. The time course of the optokinetic afternstagmus (OKAN) and that of the decrease of the prerotatory and postrotatory VOR were not reduced by ketamine administered at 1 or 2 mg/kg. This shows that ketamine does not affect the velocity-storage mechanism at these dosages.

Animals↗