Direct evidence of trigeminal innervation of the cochlear blood vessels

Oregon Health and Science University, Portland, Oregon, United States
Neuroscience (Impact Factor: 3.36). 05/1998; 84(2):559-67. DOI: 10.1016/S0306-4522(97)00503-4
Source: PubMed

ABSTRACT This paper provides the first detailed description of the trigeminal innervation of the inner ear vasculature. This system provides a newly discovered neural substrate for rapid vasodilatatory responses of the inner ear to high levels of activity and sensory input. Moreover, this discovery may provide an alternative mechanism for a set of clinical disturbances (imbalance, hearing loss, tinnitus and headache) for which a central neural basis has been speculated. Iontophoretic injections of biocytin were made via a glass microelectrode into the trigeminal ganglion in guinea-pigs. Tissue for histological sections was obtained 24 h later. Labeled fibers from the injection site were observed as bundles around the ipsilateral spiral modiolar blood vessels, as individual labeled fibers in the interscala septae, and in the ipsilateral stria vascularis. The dark cell region of the cristae ampullaris in the vestibular labyrinth was also intensively labeled. No labeled fibers were observed in the neuroepithelium of the cristae ampullaris or the semicircular canals. These results confirm and localize an earlier indirect observation of the trigeminal ganglion projection to the cochlea. This innervation may play a role in normal vascular tone and in some inner ear disturbances, e.g., sudden hearing loss may reflect an abnormal activity of trigeminal ganglion projections to the cochlear blood vessels.

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    • "The circled minus signs in Fig. 1 indicate sites where a triptan (e.g., rizatriptan) can act on ganglion cells and brainstem trigeminal, solitary nucleus and vestibular nuclear neuronal 5-HT 1B and 5-HT 1D receptors to reduce nociceptive [17,29,35], vestibular activity, and vascular activity. It is suggested that these triptan actions have a net impact on migraine and motion sickness sensitivity by modulating activity of the the trigeminal nerve innervation of the inner ear vascular supply [67] [68]. Finally, it is worth noting that the spiral ganglion and cochlea show similar patterns of TRPV1, P2X 3 , 5-HT 1B , 5-HT 1D and 5-HT 1F receptor expression [2] [4] [8]. "
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    ABSTRACT: This review develops the hypothesis that co-morbid balance disorders and migraine can be understood as additive effects of processing afferent vestibular and pain information in pre-parabrachial and pre-thalamic pathways, that have consequences on cortical mechanisms influencing perception, interoception and affect. There are remarkable parallel neurochemical phenotypes for inner ear and trigeminal ganglion cells and these afferent channels appear to converge in shared central pathways for vestibular and nociceptive information processing. These pathways share expression of receptors targeted by anti-migraine drugs. New evidence is also presented regarding the distribution of serotonin receptors in the planum semilunatum of the primate cristae ampullaris, which may indicate involvement of inner ear ionic homeostatic mechanisms in audiovestibular symptoms that can accompany migraine.
    Journal of Vestibular Research 01/2011; 21(6):315-21. DOI:10.3233/VES-2011-0428 · 1.19 Impact Factor
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    • "Indirect evidence suggests a functional connection between the vestibular and trigeminal systems. For example, painful trigeminal stimulation can trigger or modulate auditory and vestibular symptoms, such as spontaneous nystagmus, in patients with migraine headaches.48,49 Buisseret et al. (1990) used peroxidase injection into the oculomotor muscles as a marker to observe diffusion into several areas of the nervous system: the Gasser node, the interpolaris and the caudalis portion of the spinal trigeminal nucleus, the paratrigeminal nucleus, and the dorsal horn of the cervical spinal cord (C1 - C2).45 "
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    ABSTRACT: In recent years, many researchers have investigated the various factors that can influence body posture: mood states, anxiety, head and neck positions, oral functions (respiration, swallowing), oculomotor and visual systems, and the inner ear. Recent studies indicate a role for trigeminal afferents on body posture, but this has not yet been demonstrated conclusively. The present study aims to review the papers that have shown a relationship between the stomatognathic system and body posture. These studies suggest that tension in the stomatognathic system can contribute to impaired neural control of posture. Numerous anatomical connections between the stomatognathic system's proprioceptive inputs and nervous structures are implicated in posture (cerebellum, vestibular and oculomotor nuclei, superior colliculus). If the proprioceptive information of the stomatognathic system is inaccurate, then head control and body position may be affected. In addition, the present review discusses the role the myofascial system plays in posture. If confirmed by further research, these considerations can improve our understanding and treatment of muscular-skeletal disorders that are associated with temporomandibular joint disorders, occlusal changes, and tooth loss.
    Clinics (São Paulo, Brazil) 03/2009; 64(1):61-6. DOI:10.1590/S1807-59322009000100011 · 1.19 Impact Factor
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    • "A few projection neurons are located in the maxillary division (Shore et al., 2000). The locations of these projection neurons overlap with the regions that innervate both the cochlea and the middle ear: The ophthalmic division innervates the cochlea, and the mandibular region innervates the middle ear (Vass et al., 1997,1998). The TG neurons that project to the CN are generally smaller, with a smaller nucleus (compared to those labeled by skin injections) and have uneven surfaces (Shore et al., 2000). "
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    ABSTRACT: This review outlines the anatomical and functional bases of somatosensory influences on auditory processing in the normal brainstem and midbrain. It then explores how interactions between the auditory and somatosensory system are modified through deafness, and their impact on tinnitus is discussed. Literature review, tract tracing, immunohistochemistry, and in vivo electrophysiological recordings were used. Somatosensory input originates in the dorsal root ganglia and trigeminal ganglia, and is transmitted directly and indirectly through 2nd-order nuclei to the ventral cochlear nucleus, dorsal cochlear nucleus (DCN), and inferior colliculus. The glutamatergic somatosensory afferents can be segregated from auditory nerve inputs by the type of vesicular glutamate transporters present in their terminals. Electrical stimulation of the somatosensory input results in a complex combination of excitation and inhibition, and alters the rate and timing of responses to acoustic stimulation. Deafness increases the spontaneous rates of those neurons that receive excitatory somatosensory input and results in a greater sensitivity of DCN neurons to trigeminal stimulation. Auditory-somatosensory bimodal integration is already present in 1st-order auditory nuclei. The balance of excitation and inhibition elicited by somatosensory input is altered following deafness. The increase in somatosensory influence on auditory neurons when their auditory input is diminished could be due to cross-modal reinnervation or increased synaptic strength, and may contribute to mechanisms underlying somatic tinnitus.
    American Journal of Audiology 01/2009; 17(2):S193-209. DOI:10.1044/1059-0889(2008/07-0045) · 1.28 Impact Factor
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