Course and targets of the calbindin D-28k subpopulation of primary vestibular afferents.
The subpopulation of primary vestibular afferents (PVA) displaying immunoreactivity for the calcium binding protein Calbindin D-28k (Calb) is constituted of particularly large bipolar neurons in the vestibular ganglion (VG) that innervate the central regions of the vestibular end organs exclusively via calyx endings on type I vestibular hair cells. These large-diameter PVA are characterized by irregular spontaneous discharge patterns and predominantly phasic firing properties with respect to natural vestibular stimulation. The present study describes the complete course and terminations of Calb+ PVA in the cerebellar cortex, the cerebellar (CN) and vestibular nuclei (VN) of the mouse. To eliminate the two sources of Calb+ fibers in the cerebellum, i.e., the Calb+ primary vestibular input and the axons of cerebellar Purkinje cells (PC), in their totality, a unilateral eighth nerve transection was performed in the PC-deficient mutant mice, Purkinje cell degeneration (pcd/pcd) and Lurcher (Lc/+). Neurectomy in these mutants results in a complete ipsilateral loss of Calb+ fibers in the cerebellar cortex, the CN and VN. The Calb+ primary vestibular input on the contralateral side terminates solely in the rostral half of the ventral uvula and in the nodulus of the cerebellar cortex. Calb+ fibers traverse all three subdivisions of the CN, but terminations were found only in the lateral and medial cerebellar nuclei. In the VN, Calb+ PVA terminations were restricted to the superior, the ventral part of the lateral, the lateral portion of the medial, and the inferior vestibular nuclei. Calb + terminals were also present in the small cell group Y and Cajal's interstitial nucleus of the vestibular nerve as well as in defined areas of the reticular formation. All Calb + PVA are strictly unilateral. The results show that the Calb+ subpopulation of VG neurons is the sole source of Calb+ fibers and terminals in the PC-deficient cerebellum and the VN. The central input of this distinct subgroup of PVA is distributed in narrow posterior vermal areas and parts of the CN and VN. The cerebellar mutants, Purkinje cell degeneration and Lurcher, provide excellent tools to selectively investigate the subgroup of Calb+ PVA in the mouse in its entirety.
Bäurle
J
J
Freie Universität Berlin, Fachbereich Humanmedizin, Universitätsklinikum Benjamin Franklin, Department of Physiology, Germany. baeurle@zedat.fu-berlin.de
Vogten
H
H
Grüsser-Cornehls
U
U
D000818:Animals; D001306:Auditory Pathways / Q000737:chemistry / Q000166:cytology; D001369:Axons / Q000737:chemistry / Q000502:physiology; D064026:Calbindins; D002470:Cell Survival / Q000502:physiology; D003714:Denervation; D005260:Female; D008297:Male; D051379:Mice; D008818:Mice, Neurologic Mutants; D009154:Mutation; D009410:Nerve Degeneration / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D009419:Nerve Tissue Proteins / Q000032:analysis; D009475:Neurons, Afferent / Q000737:chemistry* / Q000473:pathology / Q000648:ultrastructure; D010320:Parvalbumins / Q000032:analysis; D011689:Purkinje Cells / Q000737:chemistry* / Q000473:pathology / Q000648:ultrastructure; D064030:S100 Calcium Binding Protein G / Q000032:analysis*; D014725:Vestibular Nerve / Q000737:chemistry / Q000473:pathology* / Q000601:surgery
D064026:Calbindins; D009419:Nerve Tissue Proteins; D010320:Parvalbumins; D064030:S100 Calcium Binding Protein G