The objective of this project is to define neuronal mechanisms for mandibular kinesthesia. Orofacial position and movement information originates from receptors in jaw muscles, the temporomandibular joint (TMJ), and skin. This information is conveyed to trigeminal brainstem nuclei via neurons in the trigeminal ganglion and the mesencephalic nucleus. Our previous studies suggest the hypothesis that deep tissue inputs are somatotopically distributed in the trigeminal nuclei and in the thalamus so that perception old precise jaw movements results from spatially and temporally related activation of both deep (muscle and joint) and cutaneous receptors. Kinesthesia from postcranial structures requires thalamic relay of information to the somatosensory cortex. Although studies of cortical neurons support the existence of these pathways for jaw kinesthesia, little is known about the specific brainstem sources or the thalamic representation of this neural input. The first specific aim is to define the distribution, receptive field properties, and movement-related-responses of thalamic neurons by studying evoked potentials from nerve supplying the masseter muscle, the TMJ, and perioral region. Although kinesthetic information is signalled by larger diameter afferents, it is known that many smaller diameter afferents also respond to non-noxious mechanic;il stimuli including muscle stretch and joint movement in spinal systems. Similar properties for smaller diameter fibers supplying cranial tissues have not been documented. We hypothesize that some smaller diameter differents modulate central trigeminal neurons that process kinesthetic information. The second specific aim will examine the capacity of trigeminothalamic neurons to signal rate and positional changes during passive jaw movement. Algesic substances reliably activate small diameter muscle and joint afferents. The effects of intramuscular injections with an algesic substances on movement related-responses will be studied. The receptive fields of these neurons will be defined by graded mechanical and electrical stimulation, thalamic projections will be identified by antidromic stimulation. The third specific aim is to define the central distribution of physiologically-defined masseter muscle and TMJ afferents in Vi by intraaxonal staining. In the same experiment, thalamic projection neurons will be labeled by retrograde axonal transport methods. Ultrastructure of the synaptic input from identified afferents onto trigeminothalamic neurons will be studied. These experiments will lead to a fundamental understanding of oral sensory mechanisms important for adapting to acute changes in craniomandibular relationships and long term alterations related to aging or adaptation to dental prostheses.
|Capra, Norman F; Hisley, Calvin K; Masri, Radi M (2007) The influence of pain on masseter spindle afferent discharge. Arch Oral Biol 52:387-90|
|Capra, N F; Bernanke, J M; Porter, J D (1991) Ultrastructural changes in the masseter muscle of Macaca fascicularis resulting from intramuscular injections of botulinum toxin type A. Arch Oral Biol 36:827-36|
|Capra, N F; Wax, T D (1989) Distribution and central projections of primary afferent neurons that innervate the masseter muscle and mandibular periodontium: a double-label study. J Comp Neurol 279:341-52|
|Capra, N F (1987) Localization and central projections of primary afferent neurons that innervate the temporomandibular joint in cats. Somatosens Res 4:201-13|