Use of calcium-binding proteins to map inputs in vestibular nuclei of the gerbil

Abstract

We wished to determine whether calbindin and/or calretinin are appropriate markers for vestibular afferents, a population of neurons in the vestibular nuclear complex, or cerebellar Purkinje inputs. To accomplish this goal, immunocytochemical staining was observed in gerbils after lesions of the vestibular nerve central to the ganglion, the cerebellum, or both. Eleven to fourteen days after recovery, the brain was processed for immunocytochemical identification of calretinin and calbindin. After lesion of the vestibular nerve, no calretinin staining was seen in any of the vestibular nuclei except for a population of intrinsic neurons, which showed no obvious change in number or staining pattern. Calbindin staining was reduced in all nuclei except the dorsal part of the lateral vestibular nuclei. The density of staining of each marker, measured in the magnocellular medial vestibular nucleus, was significantly reduced. After the cerebellar lesion, no differences in calretinin staining were noted. However, calbindin staining was greatly reduced in all nuclei. The density of staining, measured in the caudal medial vestibular nucleus, was significantly lower. After a combined lesion of the cerebellum and vestibular nerve, the distribution and density of calretinin staining resembled that after vestibular nerve section alone, whereas calbindin staining was no longer seen. This study demonstrates that calretinin and calbindin are effective markers for the identification of vestibular afferents.

Immunoreactivity for calcium-binding proteins defines subregions of the vestibular nuclear complex of the cat

“…For calbindin and parvalbumin, but not calretinin, a second major source is Purkinje cells of the cerebellum (Celio 1990). Work in the rodent suggests that the cerebellum and the eighth nerve are in fact the only sources of calbindin-immunoreactive fibers in the VNC (Kevetter and Leonard 1997;Bäurle et al 1998). The possible sources of parvalbuminimmunoreactive fibers are more numerous, as several brainstem structures with parvalbuminimmunoreactive cells, including the interstitial nucleus of Cajal (Kokkoroyannis et al 1996;Horn et al 1999), the rostral interstitial nucleus of the MLF (Horn and Büttner-Ennever 1998) and inhibitory and excitatory burst neurons of the reticular formation (Horn et al 1995) may contribute the parvalbumin-immunoreactive fibers that are seen in the MLF and VNC.…”

“…Kevetter and Leonard (1997) showed that the two populations of calbindin-labeled fibers were differentially distributed, with cerebellar and not vestibular afferents going to the parvocellular and central subdivisions of the VMN, regions which on geographic grounds would include the dense zones of calbindin fiber immunoreactivity seen in cat. Further evidence for the cerebellum as the source of the calbindin dense fiber patches comes from a study of a mouse mutant that lacks Purkinje cells (Bäurle et al 1998).…”

“…Studies using immunoreactivity to calcium-binding proteins noted a small region of calretininimmunoreactive cells in the medial vestibular nucleus, and further found that immunoreactivity to parvalbumin and calbindin defined different fiber populations (Arai et al 1991;Résibois and Rogers 1992;Kevetter and Leonard 1997;Paxinos et al 1999). We have extended this approach to the cat, an animal widely used in studies of vestibular anatomy, physiology and behavior (references in Wilson and Melvill Jones 1979;Gerrits 1990;Barmack 2003).…”

Temporal Changes of the Calcium-binding Proteins in the Medial Vestibular Nucleus following Unilateral Labyrinthectomy in Rats

“…There have been many studies on the calcium-binding protein levels in the auditory brainstem and central visual nervous system (Lane et al, 1996;Caicedo et al, 1997). However, there are only a few reports on the central vestibular system, and they mainly been focused on the role of calcium-binding proteins as a marker of afferent input, by using calretinin only or calretinin and calbindin after the recovery of static vestibular symptoms (Sans et al, 1995;Kevetter & Neonard, 1997). Sans et al (1995) reported that unilateral sensory deprivation induces permanent asymmetry in the expression of calretinin between the ipsilateral and contralateral MVN, and suggested that the calretinin expression in the MVN depends upon the integrity and activity of the sensorineural peripheral vestibular influences.…”

“…Sans et al (1995) reported that unilateral sensory deprivation induces permanent asymmetry in the expression of calretinin between the ipsilateral and contralateral MVN, and suggested that the calretinin expression in the MVN depends upon the integrity and activity of the sensorineural peripheral vestibular influences. Kevetter and Neonard (1997) reported that the level of calretinin and calbindin expression decreases after a vestibular neurectomy, and suggested that calretinin and calbindin are effective markers for identifying the vestibular afferents.…”