The underlying nociceptive mechanisms in temporomandibular joint (TMJ) and masticatory muscles in many pain conditions are still unclear, largely due to the limited study of peripheral and central neural mechanisms affecting craniofacial musculoskeletal tissues. This study provided evidence in support of Hypothesis 1: Peripheral glutamatergic and capsaicin-sensitive mechanisms modulate the properties of primary afferents and brainstem neurons processing deep craniofacial nociceptive information. Effects of glutamate and capsaicin injected into the receptive field of deep craniofacial nociceptive afferents or TMJ of TMJ-responsive nociceptive neurons in trigeminal subnucleus caudalis/upper cervical cord (Vc/UCC) were studied in halothane-anesthetized rats. When injected alone, glutamate and capsaicin activated and induced peripheral sensitization in many afferents. Following glutamate injection, capsaicin-evoked activity was greater than that evoked by capsaicin alone, whereas following capsaicin injection, glutamate-evoked responses were similar to those of glutamate alone. When injected alone, glutamate and capsaicin also activated and induced central sensitization in most Vc/UCC neurons. Following glutamate injection, capsaicin evoked greater activity and less sensitization compared with capsaicin alone, whereas following capsaicin, glutamate was less effective in activating and sensitizing most Vc/UCC neurons. This apparent desensitizing effect of capsaicin on glutamate-evoked excitability of Vc/UCC neurons contrasts with the lack of capsaicin-induced modulation of glutamate-evoked afferent excitability, suggesting that peripheral and central sensitization may be differentially involved in the nociceptive effects of glutamate and capsaicin applied to deep craniofacial tissues. Further evidence of glutamate-capsaicin interactions was documented in the attenuation by TMJ pre-injection of glutamate receptor antagonists of jaw muscle activity reflexly evoked by TMJ injection of capsaicin. Moreover, additional findings support Hypothesis 2: Surgical cutaneous incision modulates the properties of brainstem neurons processing deep craniofacial nociceptive information. TMJ-responsive nociceptive Vc/UCC neurons could be activated by surgical incision of the skin overlying the TMJ and this incision-induced afferent barrage caused nociceptive neurons to be temporarily refractory to further capsaicin-induced central sensitization.
These novel findings suggest that peripheral glutamate and capsaicin receptor mechanisms as well as surgical cutaneous incision may be involved in the nociceptive processing of deep craniofacial afferent inputs and may interact to modulate both activation as well as sensitization evoked from these tissues.
| Identifer | oai:union.ndltd.org:TORONTO/oai:tspace.library.utoronto.ca:1807/16742 |
| Date | 19 January 2009 |
| Creators | Lam, David King |
| Contributors | Hu, James W., Sessle, Barry John |
| Source Sets | University of Toronto |
| Language | en_ca |
| Detected Language | English |
| Type | Thesis |
| Format | 2535197 bytes, application/pdf |
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