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Hirano, 1985; Alderdice, 1988). Hiroi et al. (1998) studied the changes in
chloride cell distribution during early development of the Japanese fl ounder
by whole-mount immunocytochemistry using antiserum against Na+, K+-
ATPase, which is supposedly located specifi cally on the chloride cells. In
larvae immediately after hatching, the immunoreactive cells are distributed
only on the yolk-sac membrane and body skin. Thereafter, premetamorphic
larvae become to possess both cutaneous and newly appeared branchial
chloride cells. Cutaneous chloride cells often form multicellular complexes.
The complex is considered advantageous to Na+secretion (Shiraishi et al.,
1997), since Na+ is transported through the paracellular pathway in the
complex down its electrical gradient (McCormick, 1995). Thus, cutaneous
chloride cells seem to play the major role in Na+secretion during this period.
Cutaneous chloride cells decrease in size and density at the beginning
of metamorphosis and disappear completely at metamorphic climax. In
contrast, the number of branchial chloride cells located on gill fi laments
increases during metamorphosis. From these results, Hiroi et al. (1998)
concluded that the site for ion secretion probably shift from cutaneous to
branchial chloride cells during the metamorphosis of the Japanese fl ounder.
Schreiber and Specker (1999a) also reported the development of chloride
cells in the gills of the summer fl ounder during metamorphosis. At the start
of metamorphosis, the gills possess one type of larval MRCs, which are
characterized by large electron-lucent mitochondria, absence of well-defi ned
apical pit, and relatively weak immunoreactivity of Na+, K+-ATPase.
Towards the end of metamorphosis, Na+, K+-ATPase immunoreactivity
of MRCs increases, and by the end of metamorphosis, larval type MRCs
disappear, and instead, two juvenile type MRCs, which are characterized
by smaller electron-dense mitochondoria, develop. One type is weakly
osmiophilic with well developed apical pit, and the other is strongly
osmiophillic and positioned adjacent to the former MRC. From the location
of the cell and its morphology, the authors designate the latter as accessory
cells of the former MRCs. At present, it is uncertain whether juvenile type
MRCs develop from larval type MRCs or from a different origin. Schreiber
and Specker (2000) reported that administration of T4 to premetamorphic
larvae of summer fl ounder stimulated the development of juvenile type
MRCs precociously. They also showed that, while the treatment with
thiourea (TU) arrested the development, T4 administration to TU-treated
fi sh compensated the effect of TU and stimulated the development of
juvenile type MRCs. These results not only indicate that thyroid hormone
stimulates the development of juvenile type gill MRCs but also strongly
suggest that thyroid hormone regulates the shift of functional site of ion
secretion from cutaneous chloride cells to gill chloride cells during fl atfi sh
metamorphosis.
