296
The otic placode, one of several dorsolateral placodes, is an epithelial thickening
of the ectoderm near the middle of the developing hindbrain (Nelsen 1953 ; Kelly
and Corwin 1992 ). The hindbrain develops from the neural tube and has a complex
series of rhombomeres or bulges that have differential gene expression, particularly
Hox gene expression, allowing for rhombomere specifi c differentiation, which in
turn forms the basis of nerve patterning in the hindbrain (Keynes and Krumlauf
1994 ; Gilland and Baker 1993 ). The otic placode and later developing otocyst is
located in close proximity to this rhombencephalon and the infl uence of the rhombencephalon is necessary and suffi cient to induce the ectoderm to develop the otic
placode (Model et al. 1981 ; Van De Water 1983 ; see Fig. 3 ). It is likely that molecular cues from the developing hindbrain are responsible for inducing the development of fi sh inner ear (Ekker et al. 1992 ). In addition to rhombencephalilization, the
notochordal mesoderm, paraxial mesoderm and neural crest play a role in otic placode induction (Yntema 1955 ; Van De Water 1983 ; Jacobson and Sater 1988 ).
As the brain develops, the telencephalon and diencephalon begin to differentiate.
Just after cephalic fl exure increases, the otic pit forms as the otic placode invaginates. It has been demonstrated in amphibians that the axis polarity is fi xed during
early otic pit formation (Harrison 1945 ). This is likely true for all vertebrates including fi sh. Fixation of the anteroposterior axis occurs fi rst, followed by the dorsoventral axis during otic pit formation (Yntema 1955 ). Once polarized, the locations for
inner ear structures become fi xed within the otic pit and disruptions in the orientation of the otic pit or later the otocyst will cause deformities in the inner ear (Harrison
1945 ; Detwiler and van Dyke 1950 ; Mansour et al. 1993 ).
The otic pit next separates from the ectoderm and closes to form the otocyst. As
the otocyst forms, cells in the anteroventral portion of the otocyst give rise to the
otic ganglia, which migrates away and breaks contact from the otocyst (Von Kupffer
1895 ; Webb and Noden 1993 ; Haddon and Lewis 1996 ). Populations of embryonic
stem cells that make up part of the neural crest give rise to the support and glial cells
found in the otic ganglion (Ayer-Le Liver and Le Douarin 1982 ; D’Amico-Martel
and Noden 1983 ). Shortly after the otocyst separates from the ectoderm, there is a
proliferation of undifferentiated epithelial cells along the ventro-medial surface of
the otocyst. This proliferation of undifferentiated epithelial cells precedes segregation and differentiation of the otocyst into the various vestibular and auditory sensory epithelia. These undifferentiated epithelial cells later develop into hair and
support cells within the otic endorgans. In amphibians transplantation and grafting
experiments have demonstrated that the otocyst must be in close proximity to both
the hindbrain and cephalic mesenchyme, at least during a critical period in an early
stage otocyst, in order for differentiation to occur (Kaan 1930 ; Detwiler and van
Dyke 1950 ). Although the length of this critical period varies among other vertebrate groups, it is likely that fi sh undergo a similar critical period where proximity
to the hindbrain and cephalic mesenchyme is necessary for segregation and differentiation of the sensory epithelia.
As the otocyst develops and differentiates, the otic ganglia must grow distal processes to innervate the sensory epithelia of the auditory end organs. Studies in other
vertebrate groups have demonstrated that the otocyst releases trophic factors to
R.O. Vasconcelos et al.
The otic placode, one of several dorsolateral placodes, is an epithelial thickening
of the ectoderm near the middle of the developing hindbrain (Nelsen 1953 ; Kelly
and Corwin 1992 ). The hindbrain develops from the neural tube and has a complex
series of rhombomeres or bulges that have differential gene expression, particularly
Hox gene expression, allowing for rhombomere specifi c differentiation, which in
turn forms the basis of nerve patterning in the hindbrain (Keynes and Krumlauf
1994 ; Gilland and Baker 1993 ). The otic placode and later developing otocyst is
located in close proximity to this rhombencephalon and the infl uence of the rhombencephalon is necessary and suffi cient to induce the ectoderm to develop the otic
placode (Model et al. 1981 ; Van De Water 1983 ; see Fig. 3 ). It is likely that molecular cues from the developing hindbrain are responsible for inducing the development of fi sh inner ear (Ekker et al. 1992 ). In addition to rhombencephalilization, the
notochordal mesoderm, paraxial mesoderm and neural crest play a role in otic placode induction (Yntema 1955 ; Van De Water 1983 ; Jacobson and Sater 1988 ).
As the brain develops, the telencephalon and diencephalon begin to differentiate.
Just after cephalic fl exure increases, the otic pit forms as the otic placode invaginates. It has been demonstrated in amphibians that the axis polarity is fi xed during
early otic pit formation (Harrison 1945 ). This is likely true for all vertebrates including fi sh. Fixation of the anteroposterior axis occurs fi rst, followed by the dorsoventral axis during otic pit formation (Yntema 1955 ). Once polarized, the locations for
inner ear structures become fi xed within the otic pit and disruptions in the orientation of the otic pit or later the otocyst will cause deformities in the inner ear (Harrison
1945 ; Detwiler and van Dyke 1950 ; Mansour et al. 1993 ).
The otic pit next separates from the ectoderm and closes to form the otocyst. As
the otocyst forms, cells in the anteroventral portion of the otocyst give rise to the
otic ganglia, which migrates away and breaks contact from the otocyst (Von Kupffer
1895 ; Webb and Noden 1993 ; Haddon and Lewis 1996 ). Populations of embryonic
stem cells that make up part of the neural crest give rise to the support and glial cells
found in the otic ganglion (Ayer-Le Liver and Le Douarin 1982 ; D’Amico-Martel
and Noden 1983 ). Shortly after the otocyst separates from the ectoderm, there is a
proliferation of undifferentiated epithelial cells along the ventro-medial surface of
the otocyst. This proliferation of undifferentiated epithelial cells precedes segregation and differentiation of the otocyst into the various vestibular and auditory sensory epithelia. These undifferentiated epithelial cells later develop into hair and
support cells within the otic endorgans. In amphibians transplantation and grafting
experiments have demonstrated that the otocyst must be in close proximity to both
the hindbrain and cephalic mesenchyme, at least during a critical period in an early
stage otocyst, in order for differentiation to occur (Kaan 1930 ; Detwiler and van
Dyke 1950 ). Although the length of this critical period varies among other vertebrate groups, it is likely that fi sh undergo a similar critical period where proximity
to the hindbrain and cephalic mesenchyme is necessary for segregation and differentiation of the sensory epithelia.
As the otocyst develops and differentiates, the otic ganglia must grow distal processes to innervate the sensory epithelia of the auditory end organs. Studies in other
vertebrate groups have demonstrated that the otocyst releases trophic factors to
R.O. Vasconcelos et al.