Biting intentions modulate digastric reflex responses to sudden unloading of the jaw.

Reflex responses in jaw-opening muscles can be evoked when a brittle object cracks between the teeth and suddenly unloads the jaw. We hypothesized that this reflex response is flexible and, as such, is modulated according to the instructed goal of biting through an object. Study participants performed two different biting tasks when holding a peanut half stacked on a chocolate piece between their incisors. In one task, they were asked to split the peanut half only (single-split task), and in the other task, they were asked to split both the peanut and the chocolate in one action (double-split task). In both tasks, the peanut split evoked a jaw-opening muscle response, quantified from electromyogram (EMG) recordings of the digastric muscle in a window 20-60 ms following peanut split. Consistent with our hypothesis, we found that the jaw-opening muscle response in the single-split trials was about twice the size of the jaw-opening muscle response in the double-split trials. A linear model that predicted the jaw-opening muscle response on a single-trial basis indicated that task settings played a significant role in this modulation but also that the presplit digastric muscle activity contributed to the modulation. These findings demonstrate that, like reflex responses to mechanical perturbations in limb muscles, reflex responses in jaw muscles not only show gain-scaling but also are modulated by subject intent.

Task-dependent control of the jaw during food splitting in humans.

Although splitting of food items between the incisors often requires high bite forces, rarely do the teeth harmfully collide when the jaw quickly closes after split. Previous studies indicate that the force-velocity relationship of the jaw closing muscles principally explains the prompt dissipation of jaw closing force. Here, we asked whether people could regulate the dissipation of jaw closing force during food splitting. We hypothesized that such regulation might be implemented via differential recruitment of masseter muscle portions situated along the anteroposterior axis because these portions will experience a different shortening velocity during jaw closure. Study participants performed two different tasks when holding a peanut-half stacked on a chocolate piece between their incisors. In one task, they were asked to split the peanut-half only (single-split trials) and, in the other, to split both the peanut and the chocolate in one action (double-split trials). In double-split trials following the peanut split, the intensity of the tooth impact on the chocolate piece was on average 2.5 times greater than in single-split trials, indicating a substantially greater loss of jaw closing force in the single-split trials. We conclude that control of jaw closing force dissipation following food splitting depends on task demands. Consistent with our hypothesis, converging neurophysiological and morphometric data indicated that this control involved a differential activation of the jaw closing masseter muscle along the anteroposterior axis. These latter findings suggest that the regulation of jaw closing force after sudden unloading of the jaw exploits masseter muscle compartmentalization.

The trigeminal circuits responsible for chewing.

Mastication is a vital function that ensures that ingested food is broken down into pieces and prepared for digestion. This review outlines the masticatory behavior in terms of the muscle activation patterns and jaw movements and gives an overview of the organization and function of the trigeminal neuronal circuits that are known to take part in the generation and control of oro-facial motor functions. The basic pattern of rhythmic jaw movements produced during mastication is generated by a Central Pattern Generator (CPG) located in the pons and medulla. Neurons within the CPG have intrinsic properties that produce a rhythmic activity, but the output of these neurons is modified by inputs that descend from the higher centers of the brain, and by feedback from sensory receptors, in order to constantly adapt the movement to the food properties.

Assessment of the potential role of muscle spindle mechanoreceptor afferents in chronic muscle pain in the rat masseter muscle.

BACKGROUND: The phenotype of large diameter sensory afferent neurons changes in several models of neuropathic pain. We asked if similar changes also occur in "functional" pain syndromes. METHODOLOGY/PRINCIPAL FINDINGS: Acidic saline (AS, pH 4.0) injections into the masseter muscle were used to induce persistent myalgia. Controls received saline at pH 7.2. Nocifensive responses of Experimental rats to applications of Von Frey Filaments to the masseters were above control levels 1-38 days post-injection. This effect was bilateral. Expression of c-Fos in the Trigeminal Mesencephalic Nucleus (NVmes), which contains the somata of masseter muscle spindle afferents (MSA), was above baseline levels 1 and 4 days after AS. The resting membrane potentials of neurons exposed to AS (n = 167) were hyperpolarized when compared to their control counterparts (n = 141), as were their thresholds for firing, high frequency membrane oscillations (HFMO), bursting, inward and outward rectification. The amplitude of HFMO was increased and spontaneous ectopic firing occurred in 10% of acid-exposed neurons, but never in Controls. These changes appeared within the same time frame as the observed nocifensive behaviour. Ectopic action potentials can travel centrally, but also antidromically to the peripheral terminals of MSA where they could cause neurotransmitter release and activation of adjacent fibre terminals. Using immunohistochemistry, we confirmed that annulospiral endings of masseter MSA express the glutamate vesicular transporter VGLUT1, indicating that they can release glutamate. Many capsules also contained fine fibers that were labelled by markers associated with nociceptors (calcitonin gene-related peptide, Substance P, P2X3 receptors and TRPV1 receptors) and that expressed the metabotropic glutamate receptor, mGluR5. Antagonists of glutamatergic receptors given together with the 2(nd) injection of AS prevented the hypersensitivity observed bilaterally but were ineffective if given contralaterally. CONCLUSIONS/SIGNIFICANCE: Low pH leads to changes in several electrical properties of MSA, including initiation of ectopic action potentials which could propagate centrally but could also invade the peripheral endings causing glutamate release and activation of nearby nociceptors within the spindle capsule. This peripheral drive could contribute both to the transition to, and maintenance of, persistent muscle pain as seen in some "functional" pain syndromes.

From movement to pain: a tribute to professor James P. Lund.

This tribute article to Professor James P. Lund stems from 6 of the presentations delivered at the July 1, 2008, symposium that honored 3 "giants" in orofacial neuroscience: B. J. Sessle, A. G. Hannam, and J. P. Lund. It was noted that soon after his training as a dentist in Australia, Jim Lund became interested in research. At the time he decided to do a PhD, there was a lot of discussion about how rhythmic movements were programmed. The early belief, based on Sherrington's studies of motor systems, was that these movements were simply an alternating series of reflexes. In the late 1960s and early 1970s, some still shared this belief, whereas others favored Graham Brown's hypothesis that repetitive movements were centrally programmed and did not depend on reflexes triggered by sensory inputs. There was no strong evidence then for either scenario except for the rhythmic movements of respiration. Lund's pioneering work during his PhD proved the existence of a central pattern generator (CPG) for mastication in the brainstem. Since then he has been interested in understanding how CPGs function and how sensory feedback works to adjust the motor patterns that they produce. Sections in this tribute article to Lund are written by some of his close collaborators and reflect the evolution of his work throughout the years. The first 4 presentations in this article (by K.-G. Westberg, D. McFarland, A. Kolta, and C. Stohler) highlight various aspects of these interests, and the final 2 presentations (by J. Feine and A. Woda) focus especially on clinical aspects of Lund's interests. The last section of this article is a final commentary from Professor Lund.