Jaw movement kinematics and jaw muscle (EMG) activity during drinking in the pigeon (Columba livia)

1992 ◽  
Vol 170 (3) ◽  
Author(s):  
R. Bermejo ◽  
M. Remy ◽  
H.P. Zeigler
Keyword(s):  
Columba Livia ◽  
Emg Activity ◽  
Movement Kinematics ◽  
Jaw Movement ◽  
Jaw Muscle

Characteristics of Glutamate-Evoked Temporomandibular Joint Afferent Activity in the Rat

2001 ◽  
Vol 85 (6) ◽  
pp. 2446-2454 ◽  
Author(s):  
Brian E. Cairns ◽  
Barry J. Sessle ◽  
James W. Hu
Keyword(s):  
Temporomandibular Joint ◽  
Receptive Fields ◽  
Male Rats ◽  
Emg Activity ◽  
Digastric Muscle ◽  
Afferent Activity ◽  
Jaw Muscles ◽  
M 10 ◽  
Jaw Muscle ◽  
Evoked Activity

Injection of glutamate into the rat temporomandibular joint (TMJ) capsule can reflexly induce a prolonged increase in the electromyographic (EMG) activity of the jaw muscles, however, the characteristics of TMJ afferents activated by glutamate have not been investigated. In the present study, we examined the effect of glutamate injection into the TMJ capsule on jaw muscle EMG activity and the extracellularly recorded activity of single trigeminal afferents that had receptive fields in the TMJ tissue and antidromically identified projections to the brain stem subnucleus caudalis (Vc) in rats of both sexes. Glutamate (0.05–1.0 M, 10 μl) injection into the TMJ capsule evoked EMG activity in a dose-related manner; however, at concentrations of 0.5 and 1.0 M, glutamate-evoked digastric muscle responses were greater in female than in male rats. In experiments where jaw muscle EMG and afferent activity were recorded simultaneously, glutamate (0.5 M, 10 μl) injection into the TMJ capsule evoked activity in the jaw muscles as well as in 27 (26 Aδ and 1 C-fiber afferent) of 34 trigeminal afferents that could be activated by blunt mechanical stimulation of the TMJ tissue. In these experiments, glutamate-evoked jaw muscle activity was significantly increased for 6 min after the glutamate injection, whereas afferent activity was significantly increased only during the first minute after the glutamate injection. The glutamate-evoked afferent activity was inversely related to conduction velocity and, in afferents with conduction velocities <10 m/s, was significantly greater in female ( n = 6) than in male ( n = 10) rats. These results suggest that glutamate excites putative nociceptive afferents within the TMJ to a greater degree in female than in male rats. This sex-related difference in afferent discharge may, in part, underlie sex-related differences in glutamate-evoked jaw muscle EMG activity.

Activation of Peripheral GABAA Receptors Inhibits Temporomandibular Joint–Evoked Jaw Muscle Activity

1999 ◽  
Vol 81 (4) ◽  
pp. 1966-1969 ◽  
Author(s):  
Brian E. Cairns ◽  
Barry J. Sessle ◽  
James W. Hu
Keyword(s):  
Receptor Antagonist ◽  
Temporomandibular Joint ◽  
Gabaa Receptors ◽  
Muscle Activity ◽  
Mustard Oil ◽  
Emg Activity ◽  
Dose Response Relationship ◽  
Jaw Muscle ◽  
Nociceptive Information ◽  
Masseter Muscles

Activation of peripheral GABAA receptors inhibits temporomandibular joint–evoked jaw muscle activity. We have previously shown that injection of mustard oil or glutamate into rat temporomandibular joint (TMJ) tissues, an experimental model of acute TMJ injury, can reflexly induce a prolonged increase in the activity of both digastric (jaw-opener) and masseter (jaw-closer) muscles. In this study, GABA was applied to the TMJ region by itself or in combination with glutamate, and the magnitude of evoked jaw muscle electromyographic (EMG) activity was measured. Application of GABA alone to the TMJ region did not evoke significant jaw muscle EMG activity when compared with normal saline controls. In contrast, co-application of GABA and glutamate into the TMJ region decreased the magnitude of glutamate-evoked EMG activity. This GABA-mediated inhibition of glutamate-evoked EMG activity followed an inverse dose-response relationship with an estimated median inhibitory dose (ID50) of 0.17 ± 0.05 (SE) μmol and 0.031 ± 0.006 μmol for the digastric and masseter muscles, respectively. Co-administration of the GABAA receptor antagonist bicuculline (0.05 μmol) but not the GABABreceptor antagonist phaclofen (0.05 or 0.15 μmol) reversed the suppressive actions of GABA, indicating that this action of GABA may be mediated by peripheral GABAA receptors located within the TMJ region. Our results suggest that activation of peripheral GABAA receptors located within the TMJ region could act to decrease the transmission of nociceptive information.

Modulation of Jaw Muscle Spindle Discharge During Mastication in the Rabbit

1997 ◽  
Vol 77 (4) ◽  
pp. 2227-2231 ◽  
Author(s):  
Y. Masuda ◽  
T. Morimoto ◽  
O. Hidaka ◽  
T. Kato ◽  
R. Matsuo ◽  
...  
Keyword(s):  
Muscle Spindle ◽  
High Frequency ◽  
Low Frequency ◽  
Phase Relationship ◽  
Muscle Spindles ◽  
Jaw Movement ◽  
Firing Rates ◽  
Jaw Opening ◽  
Jaw Muscle ◽  
Opening Phase

Masuda, Y., T. Morimoto, O. Hidaka, T. Kato, R. Matsuo, T. Inoue, M. Kobayashi, and A. Taylor. Modulation of jaw muscle spindle discharge during mastication in the rabbit. J. Neurophysiol. 77: 2227–2231, 1997. Discharges of jaw muscle spindles were recorded during chewing carrot from mesencephalic trigeminal nucleus (Mes V) in the awake rabbit to evaluate contribution of the muscle spindles to the development of complete sequences of masticatory movements. The Mes V spindle units were divided into two types according to the maximum firing rates during mastication, with a dividing line at 200 Hz; high-frequency units and low-frequency units. Although both types of units fired maximally during the jaw-opening phase of chewing cycles, their firing rates and pattern varied according to three sequential stages of mastication (stages I, IIa, and IIb). The high-frequency units often increased firing before the start of mastication and built up firing in the first few chewing cycles. Their maximal firing rate was sometimes lower during stage IIa (chewing stage) than during stage I (ingestion stage) and stage IIb (preswallowing stage), although the jaw movements were greater in stage IIa than in other stages. The phase relationship of the firing to a jaw movement cycle in stage IIa was consistent in individual units. The low-frequency units did not build up activity before the onset of movements. They fired mostly during the jaw-opening phase, but the peak of firing did not necessarily coincide with the time of maximal opening. It was concluded that the difference in the firing pattern among masticatory stages may be ascribed to a stage-dependent modulation of both fusimotor activity and jaw movement pattern.

Administration of opiate antagonist naloxone induces recurrence of increased jaw muscle activities related to inflammatory irritant application to rat temporomandibular joint region

1994 ◽  
Vol 72 (3) ◽  
pp. 1430-1433 ◽  
Author(s):  
X. M. Yu ◽  
B. J. Sessle ◽  
H. Vernon ◽  
J. W. Hu
Keyword(s):  
Temporomandibular Joint ◽  
Mineral Oil ◽  
Mustard Oil ◽  
Emg Activity ◽  
Opiate Antagonist ◽  
Joint Region ◽  
Naloxone Administration ◽  
Opioid Mechanisms ◽  
Jaw Muscle ◽  
Oil Injection

1. Our recent studies in rats have demonstrated that the small-fiber excitant and inflammatory irritant mustard oil injected into the temporomandibular joint (TMJ) region can evoke a sustained and reversible increase of electromyographic (EMG) activity in jaw muscles and an acute inflammatory response. The aim of the present study was to test if opioid mechanisms are involved in modulating the EMG increase evoked by mustard oil. 2. Mustard oil injected into the rat TMJ region evoked significant increases of jaw muscle EMG activity; the vehicle mineral oil had no such effect. The increased EMG activity lasted up to 20 min, and by 30 min after the mustard oil injection had returned to control (preinjection) levels, at which time administration of the opiate antagonist naloxone (1.3 mg/kg i.v.) induced a significant recurrence of the increase in EMG activity. This "rekindling" of EMG activity appeared at 5 to 10 min after the naloxone administration and lasted for 10 to 20 min. In contrast, naloxone administration in the animals receiving mineral oil injection into the TMJ region did not "rekindle" the EMG activity, nor did the administration of the peripherally acting opiate antagonist methylnaloxone or the vehicle of naloxone. 3. These findings reveal that the application of the opiate antagonist naloxone produces a recurrence of increased jaw muscle activity reflexively evoked by mustard oil injection into the rat TMJ region. They suggest that central opioid depressive mechanisms activated by the mustard oil-induced afferent barrage limit the duration of the evoked EMG changes.

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