K Accumulation and Clearance in the Calyx Synaptic Cleft of Type I Mouse Vestibular Hair Cells.

Vestibular organs of Amniotes contain two types of sensory cells, named Type I and Type II hair cells. While Type II hair cells are contacted by several small bouton nerve terminals, Type I hair cells receive a giant terminal, called a calyx, which encloses their basolateral membrane almost completely. Both hair cell types release glutamate, which depolarizes the afferent terminal by binding to AMPA post-synaptic receptors.

An allosteric gating model recapitulates the biophysical properties of I expressed in mouse vestibular type I hair cells.

Key Points: Vestibular type I and type II hair cells and their afferent fibres send information to the brain regarding the position and movement of the head. The characteristic feature of type I hair cells is the expression of a low-voltage-activated outward rectifying K current, I , whose biophysical properties and molecular identity are still largely unknown. In vitro, the afferent nerve calyx surrounding type I hair cells causes unstable intercellular K concentrations, altering the biophysical properties of I .

Distinct roles of Eps8 in the maturation of cochlear and vestibular hair cells.

Several genetic mutations affecting the development and function of mammalian hair cells have been shown to cause deafness but not vestibular defects, most likely because vestibular deficits are sometimes centrally compensated. The study of hair cell physiology is thus a powerful direct approach to ascertain the functional status of the vestibular end organs. Deletion of Epidermal growth factor receptor pathway substrate 8 (Eps8), a gene involved in actin remodeling, has been shown to cause deafness in mice.

Corrigendum: Glutamic acid decarboxylase 67 expression by a distinct population of mouse vestibular supporting cells.

[This corrects the article on p. 428 in vol. 8, PMID: 25565962.

Glutamic acid decarboxylase 67 expression by a distinct population of mouse vestibular supporting cells.

The function of the enzyme glutamate decarboxylase (GAD) is to convert glutamate in γ-aminobutyric acid (GABA). Glutamate decarboxylase exists as two major isoforms, termed GAD65 and GAD67, that are usually expressed in GABA-containing neurons in the central nervous system. GAD65 has been proposed to be associated with GABA exocytosis whereas GAD67 with GABA metabolism.