Angiotensin II-induced rhythmic jaw movements in the ketamine-anesthetized guinea pig
Department of Oral Biology, School of Dentistry, University of California, Los Angeles 90024. Brain Research
(Impact Factor: 2.84).
02/1989; 478(2):233-40. DOI: 10.1016/0006-8993(89)91503-5
The EMG activity of the left anterior digastric muscle as well as associated jaw movements were studied in ketamine-anesthetized guinea pigs that had received i.v. infusions of angiotensin II (ANG-II). Rhythmic jaw movements with two distinct movement profiles were associated with ANG-II infusion. One movement profile was typified by vertical jaw opening and closing movements with little or no associated horizontal movement. The second rhythmical jaw movement profile was unlike the first in that jaw closing was accompanied by a significant horizontal deflection of the jaw. Both jaw movement profiles were similar in that little or no horizontal movement occurred during jaw opening. Tongue protrusions were also observed during jaw opening in both cases. The results show that ANG-II induces rhythmic jaw movements in anesthetized guinea pigs. ANG-II-induced jaw movement profiles and digastric muscle EMG activity are similar to those seen after an i.v. injection of apomorphine in the anesthetized guinea pig, and to those associated with lapping in the awake animal.
Available from: Takafumi Kato
- ") to activate glutamate and glycine/inhibitory • Reduces oral tardive dyskynesia neurons that induce REM muscle atonia (OTD*) induced by DA (Siegel, 2000) Adenosine Role in hypothalamic oral aggressive/ Promotes deep sleep (SWA)/caffeine is defensive behavior (Nagy et al., 1986; opposite (Gallopin et al., 2000) Amir et al., 1997; Gottesmann, 1997) Adrenaline (Adr) or Facilitates RJM induced by glutamate: NA triggers above ACh-induced atonia; noradrenaline (NA) Ó in SB? (Nakamura and Katakura, 1995; promotes alertness/arousal (Gallopin et al., Sjöholm et al., 1996; Amir et al., 1997; 2000; Siegel, 2000) Gottesmann, 1997) Angiotensin Facilitates DA-induced RJM ? (Gerstner et al., 1989) Calcium (Ca) channels Synaptic activation Synaptic key event that contributes to (Soto-Trevino et al., 2001) GABA inhibition of arousal center/essential to sleep (Kandel et al., 2000; Siegel, 2000) Cholecystokinin (CCK) Promotes rhythmic jaw movement (RJM) Controversial effect (Pietrowsky et al., 1990; (Nishikawa et al., 1985; Kojima et al., 1992; Kapás et al., 1991; Jones, 2000) Stoessl and Polanski, 1993) Dopamine (DA) Promotes RJM and OTD Promotes alertness/arousal (e.g., ventrotegmental DA 1 receptor = ++ agonist area of hypothalamus) and is a major factor DA 2 receptors = + antagonist, -agonist in the pathophysiology of PLMS DA 3 receptor = no effect (Gunne et al., 1982; (Jones, 2000; Montplaisir et al., 2000) Lambert et al., 1986; Johansson et al., 1987; Koshikawa et al., 1989; Spooren et al., 1991; Lublin et al., 1992; Lublin, 1995; Nakamura and Katakura, 1995) GABA • Facilitation of RJM (minor role) or inhibition • Promote sleep onset and non-REM thalamoof RMJ induced by DA cortical EEG pattern • Twitches secondary to lack of inhibition • In REM, it contributes to NA and 5-HT neuron (Gunne et al., 1982; Lambert et al., 1986; inhibition that normally facilitates ACh action Johansson et al., 1987; Cools et al., 1989; (Nitz and Siegel, 1997a,b; Gallopin et al., Koshikawa et al., 1989; Spooren et al., 1991; 2000; Kandel et al., 2000; Siegel, 2000) Lublin et al., 1992; de Beltrán et al., 1993; Lublin, 1995; Nakamura and Katakura, 1995) Glutamate/NMDA • Facilitates RJM/dorsal nPC. Involved in reticular activating/arousal • Blocks phasic RJM/ventral nPO. "
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ABSTRACT: Sleep bruxism (SB) is reported by 8% of the adult population and is mainly associated with rhythmic masticatory muscle activity (RMMA) characterized by repetitive jaw muscle contractions (3 bursts or more at a frequency of 1 Hz). The consequences of SB may include tooth destruction, jaw pain, headaches, or the limitation of mandibular movement, as well as tooth-grinding sounds that disrupt the sleep of bed partners. SB is probably an extreme manifestation of a masticatory muscle activity occurring during the sleep of most normal subjects, since RMMA is observed in 60% of normal sleepers in the absence of grinding sounds. The pathophysiology of SB is becoming clearer, and there is an abundance of evidence outlining the neurophysiology and neurochemistry of rhythmic jaw movements (RJM) in relation to chewing, swallowing, and breathing. The sleep literature provides much evidence describing the mechanisms involved in the reduction of muscle tone, from sleep onset to the atonia that characterizes rapid eye movement (REM) sleep. Several brainstem structures (e.g., reticular pontis oralis, pontis caudalis, parvocellularis) and neurochemicals (e.g., serotonin, dopamine, gamma aminobutyric acid [GABA], noradrenaline) are involved in both the genesis of RJM and the modulation of muscle tone during sleep. It remains unknown why a high percentage of normal subjects present RMMA during sleep and why this activity is three times more frequent and higher in amplitude in SB patients. It is also unclear why RMMA during sleep is characterized by co-activation of both jaw-opening and jaw-closing muscles instead of the alternating jaw-opening and jaw-closing muscle activity pattern typical of chewing. The final section of this review proposes that RMMA during sleep has a role in lubricating the upper alimentary tract and increasing airway patency. The review concludes with an outline of questions for future research.
Critical reviews in oral biology and medicine: an official publication of the American Association of Oral Biologists 02/2003; 14(1):30-46. DOI:10.1177/154411130301400104
Available from: icta.ufl.edu
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ABSTRACT: The electromyograph (EMG) activity of the left anterior digastric and the genioglossus muscles was studied in ketamine-anesthetized guinea pigs under 3 separate jaw movement paradigms. The first paradigm has been previously named spontaneous rhythmic jaw movements. These jaw movements occur 1-2 h after the onset of ketamine anesthesia. After spontaneous rhythmic jaw movements began, a single dose of apomorphine caused a new, second jaw movement paradigm to occur, apomorphine-induced rhythmic jaw movements. The final paradigm, cortically-evoked rhythmic jaw movements, was elicited by electrical stimulation of the masticatory area of the cerebral cortex. Genioglossus EMG activity was complex and highly variable in spontaneous rhythmic jaw movements; however, apomorphine-induced jaw movements were characterized by simultaneously occurring rhythmic EMG bursts of approximately 230 ms duration in both the digastric and genioglossus muscles. In 4 of 5 animals, genioglossus muscle activity onset preceded digastric muscle activity onset by approximately 20 ms. These results support the hypothesis that apomorphine-induced rhythmic jaw movements are an analog of lapping in the awake animal. In cortically-evoked rhythmic jaw movements, both digastric and genioglossus EMG activity were time-locked to the cortical electrical stimulation, with an onset latency of approximately 11 ms for the digastric EMG activity and of 16 ms for the genioglossus EMG activity. These results support the hypothesis that both trigeminal and hypoglossal motoneuron pools are closely coupled in certain coordinative movement patterns.
Brain Research 11/1991; 562(1):79-84. DOI:10.1016/0006-8993(91)91189-8 · 2.84 Impact Factor
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