Involvement of NMDA receptor mechanisms in jaw electromyographic activity and plasma extravasation induced by inflammatory irritant application to temporomandibular joint region of rats

Abstract

The aim of this study was to examine the possible role of N-methyl-D-aspartate (NMDA) receptor mechanisms in responses induced by the small-fibre excitant and inflammatory irritant mustard oil injected into the temporomandibular joint (TMJ) region of rats. The effects of the non-competitive NMDA antagonist MK-801 were tested on the mustard oil-evoked increases in electromyographic (EMG) activity of the masseter and digastric muscles and Evans Blue plasma extravasation. Five minutes before the mustard oil injection, MK-801 or its vehicle was administered systemically (i.v.), into the third ventricle (i.c.v.), or locally into the TMJ region. Compared with control animals receiving vehicle, the rats receiving MK-801 at an i.v. dose of 0.5 mg/kg (n = 5) showed a significant reduction in the incidence and magnitude of EMG responses as well as in the plasma extravasation evoked by mustard oil; MK-801 at an i.v. dose of 0.1 mg/kg (n = 5) had no significant effect on plasma extravasation or on the incidence and magnitude of EMG responses but did significantly increase the latency of EMG responses. An i.c.v. dose of 0.1 mg/kg (n = 5) or 0.01 mg/kg (n = 5) had no significant effect on plasma extravasation or incidence of EMG responses but did significantly reduce the magnitudes of the masseter EMG response; the 0.01 mg/kg dose also significantly increased the latency of the digastric EMG response. The magnitudes of both the masseter and digastric EMG responses were also significantly reduced by MK-801 administered into the TMJ region at a dose of 0.1 mg/kg (n = 5) but not by 0.01 mg/kg (n = 5); neither dose significantly affected the incidence of EMG responses or the plasma extravasation. These data suggest that both central and peripheral NMDA receptor mechanisms may play an important role in EMG responses evoked by the small-fibre excitant and inflammatory irritant mustard oil, but that different neurochemical mechanisms may be involved in the plasma extravasation induced by mustard oil.

Craniofacial Pain and Motor Function: Pathogenesis, Clinical Correlates, and Implications

“…These increases occur during the first 7 to 8 mins and between approximately 15 and 30 mins following the injection of the small fiber excitant. This motor response is abolished by the pre-administration of local anesthetic into the site in which the noxious stimulation is subsequently applied (Yu et al, 1995), or is attenuated by the intravenous administration of the non-competitive N-methyl-D-aspartate (NMDA) antagonist MK-801 (Yu et al, 1996).…”

Src, a molecular switch governing gain control of synaptic transmission mediated by N- methyl- d -aspartate receptors

“…On the other hand, inappropriate alteration of synaptic transmission is a fundamental underpinning of various pathological conditions, including epilepsy and chronic pain. In the case of chronic pain, enhanced transmission in nociceptive pathways, i.e., pathways conveying pain-related information, is known from animal experiments to occur at various levels of the neuraxis including the dorsal horn of the spinal cord (1-3) and the trigeminal nucleus caudalis, the homologous region in the brainstem (4,5). Synaptic transmission at fast excitatory synapses in the dorsal horn, as in most regions of the CNS, is mediated by glutamate receptors, and there is a growing body of evidence indicating that these receptors are crucial in conditions of enhanced nociceptive transmission (6)(7)(8).…”

Influence of ethanol and morphine on pain perception evoked by deep tissue injury

“…Since most of the molecules mediating ethanol effects are the same associated with the modulation of pain arising from deep tissues, for example, GABA A -R (Kenji et al, 2001), GIRK (Ikeda et al, 2001), NMDA receptors (Yu et al, 1996), 5HT-receptors (Garraway, Hochman, 2001) and ATP-R (Hu et al, 2002), its possible that ethanol can influence nociceptive mechanisms related to deep tissue injuries, which have characteristics different from those related to cutaneous injuries (Sessle, Hu, 1991).…”