The long term objectives of this project are to determine the role of craniofacial sensory feedback in the control of jaw movement and to determine how these sensori-motor processes may be altered in oro-facial dysfunctions including bruxism, masticatory muscle and temporomandibular disorders. Three hypotheses are proposed: 1) Sensory feedback from trigeminal ganglion masticatory muscle afferents reaches trigeminal motoneurons via disynaptic and trisynaptic neuronal circuits involving the spinal trigeminal nucleus and adjacent reticular formation. This hypothesis will be tested by investigating relationships between intracellularly labeled trigeminal ganglion jaw-muscle afferent neurons and retrogradely-labeled trigeminal premotor neurons. 2) Brainstem interneurons which respond to jaw movement include one type which manifests responses similar to low-threshold muscle proprioceptive afferents and responds to small amplitude jaw displacement and a second type which is activated by large amplitude jaw displacement and provides sensory feedback related to the extremes of mandibular movement and masticatory muscle stress. Both groups include interneurons which project to the trigeminal motor nucleus and others which project to higher centers. This hypothesis will be tested by examining the physiology and morphology of trigeminal and reticular formation neurons which respond to jaw movement via intracellular recording and staining. 3) Sensory integration occurs in the mesencephalic trigeminal nucleus (Vme) via interactions between jaw-muscle spindle primary afferent neurons and between muscle spindle and periodontal mechanoreceptor primary afferent neurons. This hypothesis will be tested by: a) Examining the morphological relationships between Vme muscle spindle and Vme periodontal afferent neurons using intracellular staining and retrograde neuronal labeling and b) investigating cellular interactions between Vme neurons using intracellular stimulus, and spike-triggered averaging techniques. These studies will provide data fundamental to understanding on the role of sensory feedback in normal oral motor function and insight into the pathophysiological mechanisms involved in craniofacial dysfunctions and the effects of craniofacial clinical manipulations.

Agency
National Institute of Health (NIH)
Institute
National Institute of Dental & Craniofacial Research (NIDCR)
Type
Research Project (R01)
Project #
5R01DE010132-09
Application #
2897028
Study Section
Oral Biology and Medicine Subcommittee 1 (OBM)
Project Start
1991-07-01
Project End
2002-09-29
Budget Start
1999-09-30
Budget End
2000-09-29
Support Year
9
Fiscal Year
1999
Total Cost
Indirect Cost
Name
University of Maryland Baltimore
Department
Dentistry
Type
Schools of Dentistry
DUNS #
003255213
City
Baltimore
State
MD
Country
United States
Zip Code
21201
Dessem, Dean (2011) Physiological, morphological and neurochemical characterization of neurons modulated by movement. J Vis Exp :
Dessem, Dean; Ambalavanar, Ranjinidevi; Evancho, Melena et al. (2010) Eccentric muscle contraction and stretching evoke mechanical hyperalgesia and modulate CGRP and P2X(3) expression in a functionally relevant manner. Pain 149:284-95
Ambalavanar, R; Dessem, D (2009) Emerging peripheral receptor targets for deep-tissue craniofacial pain therapies. J Dent Res 88:201-11
Ambalavanar, R; Yallampalli, C; Yallampalli, U et al. (2007) Injection of adjuvant but not acidic saline into craniofacial muscle evokes nociceptive behaviors and neuropeptide expression. Neuroscience 149:650-9
Dessem, Dean; Moritani, Masayuki; Ambalavanar, Ranjinidevi (2007) Nociceptive craniofacial muscle primary afferent neurons synapse in both the rostral and caudal brain stem. J Neurophysiol 98:214-23
Ambalavanar, Ranjinidevi; Moutanni, Aicha; Dessem, Dean (2006) Inflammation of craniofacial muscle induces widespread mechanical allodynia. Neurosci Lett 399:249-54
Masri, Radi; Ro, Jin Y; Dessem, Dean et al. (2006) Classification of muscle spindle afferents innervating the masseter muscle in rats. Arch Oral Biol 51:740-7
Ambalavanar, Ranjinidevi; Moritani, Masayuki; Moutanni, Aicha et al. (2006) Deep tissue inflammation upregulates neuropeptides and evokes nociceptive behaviors which are modulated by a neuropeptide antagonist. Pain 120:53-68
Ambalavanar, R; Dessem, D; Moutanni, A et al. (2006) Muscle inflammation induces a rapid increase in calcitonin gene-related peptide (CGRP) mRNA that temporally relates to CGRP immunoreactivity and nociceptive behavior. Neuroscience 143:875-84
Ambalavanar, Ranjinidevi; Moritani, Masayuki; Dessem, Dean (2005) Trigeminal P2X3 receptor expression differs from dorsal root ganglion and is modulated by deep tissue inflammation. Pain 117:280-91

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