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Darwin, E. (1794). Zoonomia; or, the laws of organic life (Vol. I).
London, UK.
Darwin, E. (1796). Zoonomia; or, the laws of organic life (Vol. II).
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Flourens, P. (1824). Recherches expérimentales sur les propriétés
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Flourens, P. (1842). Recherches expérimentales sur les propriétés
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Ontogeny of the Vestibular
System and Balance
Timothy A. Jones and Sherri M. Jones
introduCtion and baCkground
In the human, embryonic development begins at fertilization of the ovum and lasts until the end of the
eighth week after fertilization. The fetal period then
extends from the ninth week until birth (36 to 40 weeks
after fertilization). There are a number of major events
occurring during weeks 3 and 4 of embryonic development that are critical for normal formation of the head
and neck, including the ear. This period includes the
appearance of the cranial placodes and development
of the pharyngeal apparatus. Disturbances in these
and other important early processes, as may be produced by genetic variation or exposure to physiological stressors, teratogens, or other factors, can lead to
serious head and neck developmental abnormalities,
including deafness and vestibular dysgenesis. Our
purpose here is to present the normal ontogeny of vestibular sensors. Detailed consideration of the ontogeny
of the auditory system as well as the consequences of
genetic variation on vestibular and auditory development is available elsewhere (Jones & Jones, 2011). Considered here are developmental events common to both
modalities during the early formation of the inner ear
and important differences in developmental programs
where appropriate. We begin during embryonic development and in particular emphasize the appearance of
the first outward structural sign of the emerging inner
ear, the otic placode. The chapter concludes with vestibular functional maturation and subsequent acquisition of postural control and balance.
Detailed knowledge regarding the development
of vestibular and auditory function comes largely from
the study of animals. Much of the information presented below is based on studies using chick or mouse
models, and the corresponding developmental ages in
the human are given in weeks post fertilization based
on the work of a number of investigators, including
Bredberg (1968), Anniko (1983a), Dechesne (1992),
Pujol, Lavigne-Rebillard, and Lenoir (1998), Jeffery
and Spoor (2004), Sans and Dechesne (1985), and Sulik
and Cotanche (2004). Much, if not all, of the postnatal
developmental changes observed in mammalian models occur prior to birth in the human. We will indicate
human ages estimated or found to correspond to those
of animal models, when possible.
During the first week of human development following fertilization, the zygote undergoes cleavage to
form a blastocyst which then attaches to the uterine
wall (i.e., endometrium). By the end of the second week
the blastocyst is fully implanted within the endometrium and has formed the bilaminar embryonic disk
(Figures 2–1A and D). The laminae are termed epiblast
and hypoblast. The cells of the epiblast will give rise
to all the cells of the adult. Cells of the hypoblast will
form extra-embryonic structures. The basic anatomical
axes and planes illustrated are already established by
this stage prior to morphogenesis, which is initiated
during gastrulation (week 3). The orientation of axes
and planes shown are standard conventions and will
be referenced throughout the chapter.
Morphogenesis begins with gastrulation, which is
a process of epiblast cellular proliferation and migration
15
16 BALANCE FUNCTION ASSESSMENT AND MANAGEMENT
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A.
Epiblast
Hypoblast
Superior/Cranial
C.
A/V P/D
Inferior/Caudal
A
Anterior
Cranial
R
Embryonic
disc
B.
Connecting
stalk
L
V
Cranial
Rostral
V
Caudal
Dorsal
Ventral
P
D.
D
Two dimensional
dorsal view
Posterior
Caudal
Intersecting planes
L
transverse
median
horizontal
A
R
P
figure 2–1. Anatomical axes and planes in the developing embryo. A. Isolated 3-dimen-
sional bilaminar embryonic disk with connecting stalk. B.
median (also called sagittal plane) and horizontal.
the left-right (
terior (AP) and dorsal-ventral axes.
left-right axes. C. Anatomical directions in the adult human, embryo, and one amphibian
species. D. Schematic representation of an isolated bilaminar embryonic disk as seen
from the dorsal view. Anterior-posterior and left-right axes are shown as dashed lines. From
Genetics, Embryology, and Development of Auditory and Vestibular Systems (2011) (p. 98)
by Sherri M. Jones and Timothy A. Jones.
LR) and dorsal-ventral (DV) axes. The medial plane contains the anterior-pos-
The horizontal plane contains the anterior-posterior and
to produce three distinct germ layers: the ectoderm,
mesoderm, and endoderm. All tissues develop from
these three germ layers. With the induction of the neural plate, progression of neurulation, and formation of
the neural tube, a systematic regional segmentation
emerges, which distinguishes the forebrain (prosencephalon), midbrain (mesencephalon), and hindbrain
(rhomencephalon) of the incipient brain. The hindbrain is further segmented into seven neuromeres
(rhombomeres), where the cells of each neuromere
Intersecting planes: transverse,
The transverse or lateral plane contains
acquire specific identities such that the cells of each
neuromere have unique characteristics and collectively respond to external signals in a manner that differs from neighboring segments. During this period
(week 3), cranial placodes develop from ectodermal
regions very near their respective neuromeres. Olfactory, visual, and auditory sensory organs as well as
cranial sensory ganglia develop from their respective
placodes. The inner ear develops from the otic placode
(Figure 2–2).
2. ONTOGENY OF THE VESTIBULAR SYSTEM AND BALANCE 17
Otic Vesicle
CD
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r6
r5
cross section
24d
OC
OP
D
hindbrain
SE
OP
21–23d
EN
delaminating
neuroblasts
NP
Mesoderm
Notochord
ED
OC
OP
SE
CC
NT
Lens
26–28d
OV
SAG
L
V
Figure 2–2. Formation of the otic vesicle (OV) from the otic placode (OP) over a period
from approximately 3 to 4 weeks in the human embryo (follow arrows: 21–23 to 28–35
days post fertilization. [E8.5 to just beyond E10.5 in mouse]). d = days post fertilization.
D = endolymphatic duct; EN = endoderm; CC = central canal; CD = cochlear duct; D =
E
dorsal; L = lateral; Mesoderm = mesenchyme presumptive mesoderm; NP = neural plate;
NT = neural tube; OC = otic cup; OP = otic placode; OV = otic vesicle; r5-r6 = rhombomeres
5 and 6; SAG = statoacoustic ganglion; SE = surface ectoderm (epidermis); V = ventral.
From Genetics, Embryology, and Development of Auditory and Vestibular Systems (2011)
(p. 158) by Sherri M. Jones and Timothy A. Jones.
OV
FORMATION OF THE OTIC
PLA
CODE AND OTIC VESICLE
The inner ear is formed from primordial ectodermal
cells near neuromeres (rhombomeres) 5 and 6 in the
embryonic hindbrain. These cells form a flat, thickened
patch of ectoderm called the otic placode during week 3
SAG
28–35d
(see Figure 2–2). The otic placode appears morphologically as the first step in the formation of the inner ear.
A variety of genetic signals define a region of tissue
committed to form the otic placode, and subsequent
molecular signaling leads to the separation of the otic
placode from epidermal tissue (reviewed by Ohyama,
Groves, & Martin [2007]). According to Groves (2005),
the cells ultimately forming the placode are not simply
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gathered from adjacent cells, but rather it appears likely
that the cells migrate from a wide area and somehow
collect to form the placode.
Cells of the otic placode give rise to the otic vesicle
(also called the otocyst) at about week 4 (day 26), from
which sensory, nonsensory, and most neural cells of the
inner ear will be derived (see Figure 2–2). The otic vesicle, however, does not give rise to olivocochlear and
vestibular efferent fibers or to autonomic innervation
of blood vessels. Shortly after forming, the otic placode
begins to bend and fold inward, producing a shallow
dimple. This invagination of ectoderm continues until
a deep pit is formed, which is called the otic pit or otic
cup (see Figure 2–2). The dorsal edge of the otic tissue remains in close approximation to the hindbrain/
neural plate during this process. This association favors
molecular signaling and formation of asymmetric
molecular signal fields. Ultimately, the otic cup closes
to form the otic vesicle. Closure of the otic cup and the
proximal neural groove (thus forming the neural tube
locally) occurs at about the same time during week 4.
During and after its formation, the otic vesicle is
influenced by signals from the hindbrain as well as the
mesenchyme surrounding the otic vesicle (known as
the periotic mesenchyme or mesoderm) that becomes
the bony labyrinth of the inner ear. Several important
signaling molecules play a dominant role in establishing the dorsal-ventral morphological axis within the
otocyst. The dorsal-ventral boundary of the otic vesicle (a line midway between the bottom and top of the
otic vesicle) distinguishes the dorsal vestibular sensors
from the ventral cochlear sensors. Molecular signals are
thought to form gradients of influence along the dorsal-ventral extent of otic tissue (Schneider-Maunoury
& Pujades, 2007). Tissue elements at any given position experience a unique combination of signal levels
and each combination of signals has the potential to
favor one program of development or another. Molecular signals within the otocyst and in the surrounding
regions are also responsible for the order and layout of
structures along the anteroposterior and mediolateral
dimensions of the otic vesicle.
DELAMINATION AND FORMATION OF
THE STATOACOUSTIC GANGLION
the statoacoustic ganglion (Figures 2–2 and 2–3). This
process is called delamination; it begins in epithelial
regions of the presumptive utricle and cristae as early
as week 4 (22 to 28 days) and represents the beginning
of neurogenesis. The epithelial neuroblasts divide and
ultimately differentiate into auditory and vestibular
neurons. Delamination expands to include prosensory
regions (i.e., regions containing cells that will become
sensory hair cells) within or adjacent to the sacculus
and eventually the cochlea. Delamination continues
through periods as late as week 9. We will consider the
formation of the statoacoustic ganglion in more detail
later in the chapter.
FORMATION OF PROSENSORY PATCHES
For warm-blooded vertebrates, there are six or seven
sensory patches in the mature inner ear (utricle, saccule, cochlea, three cristae, and the macula lagena in
birds). This list does not include the very small sensory
patch called the crista neglecta, about which little is
known (Montandon, Gacek, & Kimura, 1970). The sensory epithelia form in close association with the nonsensory components (i.e., cristae with canals, maculae
with vestibule, and cochlea with cochlear duct). There
is evidence that molecular signals from the sensory
patches guide the surrounding nonsensory structures in
morphogenesis (reviewed in Bok, Chang, & Wu, 2007).
Before such cooperative signaling can occur, the
proneural and prosensory cells must be specified and
distinguished from the surrounding epithelium. These
precursor “neurosensory” cells (cells that in the future
may take on a neural or sensory cell fate) are specified
early in the development of the otocyst. A neurosensory domain (i.e., region of cells that will become hair
cells or neurons) can be identified at late week 4 with
the expression of genes that may be viewed as markers
for cells destined to become neurons or sensory cells
(Bok et al., 2007; Morsli, Choo, Ryan, Johnson, & Wu,
1998). Inactivation of these genes or of corresponding
pathways interferes with the formation of the statoacoustic ganglion and sensory organs. Those cells destined to become neural cells will soon delaminate (as
described above) while the remaining cells will become
the sensory epithelia.
Under the influence of specific proteins, proneural
cells (neuroblasts, i.e., cells that will become afferent
neurons) detach from and leave the epithelium of the
otic cup and vesicle and then migrate medially and
ventrally into the mesenchyme, ultimately to form
Sensory Patches
At late week 4, certain regions of the otic vesicle
(regions A, B, and C of Figure 2–3) express specific
D
E
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P
A
4–5w
V
A
ED
B
C
delaminating
neuroblasts
A
pc
B
5w
hc
ac
um
A
pc
cd
ED
hc
sm
C
cd
5–6w
B
ac
um
C
figure 2–3. Lateral views of locations for important
markers of prosensory and sensory domains during
development. Regions forming the most dorsal sensory
epithelia (cristae of semicircular canals) are distinguished early by the expression of particular genes
(labels A and B), whereas the more ventral regions
are marked with a different combination of signals
(labeled C).
the sensory epithelia of the utricular macula (um),
saccular macula (sm) and cochlear duct (cd) in
that order. ac = anterior crista. hc = horizontal (lateral)
crista. pc = posterior crista. Schematics are based on
data from the mouse. Corresponding ages in human
are given (weeks post fertilization). Adapted from Bok,
Chang, and Wu, 2007 with permission from Interna-
tional Journal of Developmental Biology, 51, 526.
The ventral prosensory domains elaborate
A
pc
organ of Corti
ED
hc
sm
9–10w
B
ac
um
C
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genes that outline the neurosensory domain, including
presumptive cristae, maculae, and cochlear prosensory
fields as well as the proneural fields where neuroblasts
delaminate. The dorsal fields (A and B of Figure 2–3)
are distinguished from ventral prosensory regions (C
of Figure 2–3) by being marked with different combinations of gene signals. The patterns mark and distinguish which domains become cristae and which
become macular and cochlear sensors. The pattern of
expression for one gene (Otx1) highlights the region of
the presumptive lateral (horizontal) canal, and in its
absence (Otx1
-/-
) the lateral canal fails to form (Morsli
et al., 1999).
Anteroventral regions of the otocyst form in
sequence: first the utricle, then the saccule, and finally
the cochlea. As noted above, neuroblasts delaminate
from this region and migrate anteriorly to form the
statoacoustic ganglion over the period from week 4 to
week 9. Initially, there is no distinction between presumptive macular and cochlear regions (see Figure 2–3,
week 4); however, development proceeds from dorsal
to ventral revealing first the more dorsal utricular maculae (see Figure 2–3, weeks 5 to 6) and then, later, the
saccular macula and cochlea (see Figure 2–3, weeks 9
to 10). By week 5, the utricle is clearly segregated and
(by late week 5) the saccule is easily recognized, but a
clear segregation from cochlear fields is evident only
after week 6 (Morsli et al., 1998). Segregation of these
macular and cochlear sensory patches requires signals
from nonsensory regions of the otic vesicle after week 4
(Nichols et al., 2008). In the absence of such signaling,
the utricle, saccule, and cochlea form a combined malformed single mosaic sensory epithelium. The progressive segregation of sensory epithelia also appears to be
linked to the simultaneous delamination process as cells
migrate from the prosensory regions to become neurons
of the statoacoustic ganglion (Fritzsch et al., 2002).
formation of the CoChlea and
Zone of non-Proliferation
The emerging cochlear duct can be seen initially as a
lengthening of the ventral pole of the otocyst beginning at about week 5 in humans (see Figure 2–3). The
duct continues to extend first ventromedially, then it
turns abruptly, anteriorly forming a curved hook by
late week 5 (Morsli et al., 1998). This represents initiation of the cochlear coil, and by the sixth week a full
half turn is achieved (see Figure 2–3). The cochlea will
continue to elongate and increase the number of coils
(~2.5 turns in the human adult).
At the early stages of cochlea formation (e.g.,
weeks 5 to 6), the cochlear duct (Figures 2–3 and 2–4B)
houses a thick (four to five cells thick) undifferentiated
epithelium that forms a ridge or sheet extending from
the base to apex. This ridge of cells contains prosensory
cells that have segregated ventrally from the sacculus.
The ridge contains the presumptive organ of Corti. All
cochlear hair cells and supporting cells will arise from
this epithelial ridge.
Elongation and coiling of the cochlea continues
with the leading edge of extension represented at the
apical tip. Beginning at about late week 5, a central
strip of the apical epithelial ridge begins to exit the cell
cycle and terminate mitosis (Figure 2–4) (Chen, Johnson, Zoghbi, & Segil, 2002; Chen & Segil, 1999; Lee,
Liu, & Segil, 2006). Over a period of about a week in
humans (late week 5 to week 6), a wave of terminal
mitosis sweeps along a central strip of the epithelial
ridge from the cochlear apex to base. This is followed
shortly afterward by a wave of cells exiting the cell
cycle, which also moves along the central strip from
the cochlear apex to base forming a cellular zone of
nonproliferation (ZNP) along the epithelial ridge (see
Figure 2–4) (Chen et al., 2002; Chen & Segil, 1999; Lee
et al., 2006). These postmitotic cells form the undifferentiated prosensory domain of the organ of Corti, and
its formation is presumably completed before weeks 7
to 8 in humans (Chen et al., 2002; Chen & Segil, 1999;
Lee et al., 2006; Ruben, 1967).
By approximately week 8, the cochlear coil has
reached 1.5 turns and the ZNP is in place (Chen &
Segil, 1999). The region of the initial ventromedial
cochlear extension in the otocyst continues to elongate
during the coiling process, thus (importantly) increasing the distance between the saccular macula and the
first turn of the cochlea (Morsli et al., 1998). Elongation
of the cochlear epithelium after weeks 7 to 8 must be
accomplished without ZNP cell division, since prosensory cells in the ZNP have exited the cell cycle. Completion of the adult number of coils (~2.5 turns) is not
accomplished until weeks 9 to 10 (Chen & Segil, 1999;
Morsli et al., 1998; Sher, 1971; Suli & Cotanche, 2004).
The cochlea continues to elongate in the human from
20 mm to 35 mm between 10 and 16 weeks (Bredberg,
1968; Sulik & Cotanche, 2004).
Coiling and elongation of the ZNP is thought to
be accomplished largely through the process of convergent extension. For this reason, the cochlea is subject
to abnormal morphogenesis (short, thickened organ of
Corti) when alterations in planar cell polarity (PCP) signaling are present (Jones & Chen, 2007; Kelley & Chen,
2007; McKenzie, Krupin, & Kelley, 2004; Montcouquiol
et al., 2003; Wang et al., 2005; Wang, Guo, & Nathans,
2. ONTOGENY OF THE VESTIBULAR SYSTEM AND BALANCE 21
A.
Radial neurites
F
l
a
c
e
O
ZNP
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Cochlear Duct
ZNP
B.
Apical surface
L
5w
Cochlear duct
ROHC
Lumen
RIHC
ZNP
~8w
5.5w
KO
Roof
Floor
oor
7w
8w
M
GER
LER
figure 2–4. A. Formation of the zone of non-proliferation (ZNP, marked gray) in the cochlear
duct at four periods of development, based on studies in the mouse model (e.g., Chen et
al., 2002, Lee et al., 2006). Corresponding estimated ages for the human are shown. The ZNP
appears first in the apex and then sweeps towards the base over the next week (48 hours in
mouse).
al., 2002,
9 to 10 (P0, mouse). During this latter period of elongation, the sensory epithelium thins and
narrows. B. Schematic of the cochlear duct circa week 6 (E14 mouse). According to Lim and
Rueda (1992), the greater epithelial ridge (GER) incorporates the region of inner hair cells,
whereas the lesser epithelial ridge (LER) incorporates the region where outer hair cells will
form.
The zone of non-proliferation identifies the epithelial region of prospective inner and outer
hair cells. Kolliker’s organ (KO) has been defined a number of ways. Here, Kolliker’s organ
includes only that portion of the GER that does not include prospective sensory hair cells.
RIHC = region of inner hair cells. ROHC = region of outer hair cells. From Genetics, Embryol-
ogy, and Development of Auditory and Vestibular Systems (2011) (pp. 164, 166) by Sherri M.
Jones and Timothy A. Jones.
The formation of ZNP is completed by approximately week 6 (E14 mouse, Chen et
Lee et al., 2006), however, the cochlea continues to elongate and coil until weeks
Together they form the floor of the early cochlear duct, also called the epithelial ridge.
2006). Mutations in, or knock outs of, core PCP genes
(or related signaling pathways) prevent elongation
and result in a shortened cochlea. The extent to which
vestibular sensors depend on the convergent extension process is not clear. However, like the cochlea, the
vestibular epithelia start out as a layered partition of
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four to five epithelial cells and at maturity are reduced
to an apical layer of sensory cells supported by one or
two non-sensory cells (Dechesne, 1992). Whether the
thinning process involves convergent extension has not
been clarified (to our knowledge).
hair Cell differentiation
Before differentiation can begin, vestibular and auditory prosensory epithelial cells must complete the last
(or terminal) cell division. This is often referred to as
terminal mitosis and is an event noted above in the
formation of the cochlear ZNP. The postmitotic prosensory epithelial cells appear structurally like any
other cells in the epithelium. There are no superficial
structural distinctions and no obvious evidence of axial
polarization. Prosensory cells must initiate differentiation before such outward distinctions will appear.
Vestibular afferent and efferent neurons are present in sensory regions at about week 6. Prosensory
cells demonstrate ongoing mitosis at this time. Within
vestibular epithelia there are temporal and spatial gradients over the course of mitosis. In general, central
regions (apex of cristae and striolar regions of maculae) initiate and reach peak levels of mitosis well before
peripheral regions (base cristae, edges of maculae).
Terminal mitosis occurs in a similar order (Mbiene &
Sans, 1986; Sans & Chat, 1982). Although these general
trends may hold, for any given vestibular region there
is a more or less continual eruption of new immature
stereociliary bundles until late fetal periods, thus suggesting that some cells do not complete terminal cell
division until very late.
Differentiation of prosensory cells of the cristae,
maculae, and cochlea all require the induction of the
gene atonal homolog 1 (Atoh1) (also known as mouse
atonal homolog 1, Math1; Bermingham et al., 1999).
Prosensory cells exit the cell cycle and ultimately must
express Atoh1 before differentiating into hair cells.
Atoh1 expression and differentiation of hair cells begin
in the cristae and maculae well before similar levels
are expressed in the cochlea (Bermingham et al., 1999;
Chen et al., 2002; Lanford, Shailam, Norton, Gridley,
& Kelley, 2000; Woods, Montcouquiol, & Kelley, 2004).
Atoh1 expression is presumably present throughout
the sensory epithelium by weeks 8 to 10 and then is
downregulated during later fetal periods (Driver et al.,
2013; Lanford et al., 2000; Shailam et al., 1999).
During differentiation of the sensory epithelium,
a remarkable pattern of hair cells and supporting cells
emerges. Our understanding of the molecular signals
orchestrating these events is more detailed for the
cochlea than vestibular sensors, but in either case, there
are many more questions to answer. One feature of
both auditory and vestibular epithelia suggests a common organizing mechanism. The presence of orderly
patterned mosaics of hair cells and supporting cells in
all inner ear sensory epithelia implies a role for Notchmediated lateral inhibition (Lanford et al., 1999, 2000).
In particular, all epithelia are arranged such that every
hair cell is isolated from other hair cells by a ring of
supporting cells or their processes. Lateral inhibition is
one strategy that produces a “center on, surround off”
pattern, where “on” refers to a hair cell and “off” to a
non-sensory supporting cell.
In due course across the entire postmitotic sensory
epithelium, a molecular scheme can be postulated to
produce a mosaic of patches, where each patch is composed of a hair cell surrounded by supporting cells.
This scheme is simplistic and incomplete, but it provides a basis for us to begin to understand how such
mosaics can be shaped by molecular signaling and how
the remarkable structures of the vestibular system and
cochlea may be formed.
Prior to differentiation, prosensory cells appear
as homogeneous epithelial cells interconnected to each
other by gap junctions (Dechesne, 1992; Ginzberg &
Gilula, 1979). Gap junctions are subsequently lost only
in cells committed to a hair cell fate. This occurs during
the earliest period of hair cell differentiation (Bryant,
Forge, & Richardson, 2005; Forge, Souter, & DenmanJohnson, 1997). Thus, one of the earliest events of hair
cell differentiation includes the isolation of hair cells
from surrounding supporting cells by eliminating
direct electrochemical coupling between them.
Vestibular stereoCiliary bundles
The traditional definitive structural sign of hair cell
differentiation is the elaboration of microvilli and
formation of stereociliary bundles. Using scanning
electron microscopy, vestibular hair cells can be definitively identified by about week 8 in the cristae with
the appearance of stereociliary bundles (Bryant et al.,
2005; Dechesne, 1992; Denman-Johnson & Forge, 1999;
Mbiene & Sans, 1986). In contrast, the first morphological evidence of cochlear stereocilia begins to emerge
between weeks 10 and 12 (Anniko, 1983b; Lim &
Anniko, 1985; Pujol et al., 1998; Sulik & Cotanche, 2004).
The earliest hair cells appear with microvilli or stereocilia encircling a single kinocilium in the center of
the cell (Figure 2–5). The first sign of intrinsic hair cell
Developing Vestibular Sensory Epithelium
Week 7 (cristae)
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-Undifferentiated epithelial patch
-Microvilli
-Single central cilium
Week 8
-Differentiating hair cells
-Stereocilia surroundcentral
kinocilium
-Early polarization
-Tip links may be present
Weeks 8–12
-Lateral and tip stereociliary links present
-Cuticular plate is forming
-Sharp Line of Polarization Reversal
-KC & S height continue to grow
S
HC
BB
Weeks 12–15
KC
S
HC
KC
BB
LPR
E16.5
-Cuticular plate is formed
-Bundle length increases
-KC & S height comparable
-Transduction channels appear
S
HC
S
KC
BB
KC
figure 2–5. Development of vestibular stereociliary bundles. Estimated human ages in weeks post fertilization are shown. The earliest stages of development are similar for both auditory and vestibular hair cells
although vestibular hair bundles begin appearing much earlier than cochlear bundles. Later developmental stages for auditory hair bundles are very different than those for vestibular bundles. Stereociliary bundles
for vestibular epithelia are mature by weeks 20 to 23 (Dechesne, 1992). KC = kinocilium; S = stereocilia; HC =
hair cell; BB = basal body; LPR = line of polarity reversal; CP = cuticular plate. From Genetics, Embryology, and
Development of Auditory and Vestibular Systems (2011) (p. 174) by Sherri M. Jones and Timothy A. Jones.
CP
BB
HC
Maturation and
refinement continues
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