Endolymphatic hydrops reduces retrograde labeling of trigeminal innervation to the cochlea.

Abstract:

:This paper reports that endolymphatic hydrops causes a significant reduction of retrogradely labeled cell bodies of the ipsilateral trigeminal ganglion following application of horseradish peroxidase in the cochlea. We previously showed that the trigeminal ganglion is a source of primary sensory innervation to the cochlear blood vessels. The innervation of the cochlea from the trigeminal ganglion may provide the basis of an alternative mechanism for Ménière's syndrome (imbalance, hearing loss, tinnitus, and a sensation of fullness in the ear) for which a central neural basis has been speculated. Innervation patterns of sensory nerves from the trigeminal ganglion to the cochlear blood vessels were studied using retrograde transport of wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP). Healthy and hydropic guinea pigs were unilaterally implanted with an osmotic pump and a cannula for cochlear delivery of 2% WGA-HRP or vehicle alone. In other guinea pigs the cochlea was pretreated with 100 micromol capsaicin before administering 2% WGA-HRP. Histological sections of the ipsi- and contralateral trigeminal ganglia were obtained 48 h after WGA-HRP infusion. In the hydropic guinea pig, the number of labeled nerve cell bodies observed in the anteriomedial portion of the trigeminal ganglion at the origin of the ophthalmic nerve was reduced by 70% relative to normal animals. Capsaicin pretreatment nearly eliminated the labeled sensory fibers as expected. These data indicate that the trigeminal innervation to the cochlea could be involved in inner ear homeostatic disturbances, including the hydrops that is symptomatic of Ménière's disease.

journal_name

Exp Neurol

journal_title

Experimental neurology

authors

Vass Z,Shore SE,Nuttall AL,Miller JM

doi

10.1006/exnr.1998.6813

subject

Has Abstract

pub_date

1998-06-01 00:00:00

pages

241-8

issue

2

eissn

0014-4886

issn

1090-2430

pii

S0014-4886(98)96813-3

journal_volume

151

pub_type

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