Direct evidence of trigeminal innervation of the cochlear blood vessels.
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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ABSTRACT: Betahistine has been used to treat several vestibular disorders of both central and peripheral origin. The objective of this work has been to study the betahistine action mechanism at the peripheral level. Experiments were carried out in wild larval axolotl (Ambystoma tigrinum). Multiunit extracellular recordings were obtained from the semicircular canal nerve using a suction electrode. Betahistine (10 µM to 10 mM, n = 32) inhibited the basal spike discharge of the vestibular afferent neurons with an IC50 of 600 µM. To study if betahistine action on the afferent nerve discharge was somehow related to nitric oxide (NO) generation, betahistine 1 mM (n = 5) was co-administered with NG-nitro-L-arginine 3 µM. The action of betahistine remained as in control experiments. To determine the influence of betahistine on the efferent innervation of hair cells its interactions with carbachol (200 µM, n = 5), and with cholinergic antagonists: atropine (10 µM, n = 3) and d-tubocurarine (10 µM, n = 3) were also studied. Betahistine 1 mM reduced the excitatory action of carbachol in a 30 ±3.4%. Cholinergic antagonists did not modify betahistine actions. Postsynaptic actions of betahistine were analized on the basis of its capability to interact01/2000;
Article: Surdités brusques et fluctuantes[Show abstract] [Hide abstract]
ABSTRACT: Idiopathic sudden hearing loss may be isolated or associated with vertiginous symptoms. The pathophysiologic mechanism is unclear. Probably it represents the common end point of numerous and various pathologic processes: viral infection, microcirculatory disorders, autoimmune disorders, intralabyrinthine membrane ruptures. Acoustic neuromas and vertebrobasilar dissection are rare cause of sudden hearing loss but should be considered in the differential diagnosis. The treatment is nihilistic (no therapy) or based on the use of blood flow promoting drugs with steroids. A number of other treatments have been advocated including antiviral drugs and carbogen. The principal factor that makes the analysis of treatment efficacy difficult is the high rate of early spontaneous resolution. Principal prognosis factors are: the severity of the loss, flat or downsloping audiograms, and the presence of vertigo that all must be taken into account when trying to ascertain the benefit of any treatment. Fluctuating sensorineural hearing loss is a poorly defined clinical entity with the potential for progressive serious hearing impairment. While the aetiology includes syphilis, cochlear malformations, autoimmune and perilymphatic fistulas, the most common origin is Meniere disease. In the early stage, episodic vertigo may be absent but appears within 6 months. Very often, the origin remains unknown. Any specific treatment may be advised.EMC - Oto-rhino-laryngologie 01/2004; 1(3):133-156.
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ABSTRACT: Soto E, Chavez H, Valli P, Benvenuti C, Vega R. Betahistine produces post-synaptic inhibition of the excitability of the primary afferent neurons in the estibular endorgans. Acta Otolaryngol 2001; Suppl 545: 19-24. Betahistine has been used to treat several vestibular disorders of both central and peripheral origin. The objective of this work was to study the action of betahistine in the vestibular endorgans. Experiments were done in wild larval axolotl (Ambystoma tigrinum). Multiunit extracellular recordings were obtained from the semicircular canal nerve using a suction electrode. Betahistine (10 Mt o 10 mM;n= 32) inhibited the basal spike discharge of the vestibular afferent neurons with an IC50 of 600 M. To define the site of action of betahistine, its interactions with the nitric oxide synthase inhibitor NG-nitro-L-arginine (3 M) and with the cholinergic antagonists atropine (10 M; n =3) and d-tubocurarine (10 M; n= 3) were studied. The action of betahistine when co-administered with these drugs was the same as that in control experiments, indicating that its effects did not include nitric oxide production or the activation of cholinergic receptors. In contrast, 0.01-1 mM betahistine reduced the excitatory action of kainic acid (10 M; n =6) and quiscualic acid (1 M; n= 13). These results indicate that the action of betahistine on the spike discharge of afferent neurons seems to be due to a post-synaptic inhibitory action on the primary afferent neuron response to the hair cell neurotransmitter. Key words: afferent transmission, Ambystoma tigrinum, excitatory amino acids, histamine, Meniere's disease, nitric oxide, quiscualic acid, synapse, ertigo.Acta Oto-laryngologica - ACTA OTO-LARYNGOL. 01/2001; 121(6):19-24.