dramatically in function and gene expression. The sound-producing elements in males but not females are surrounded by elastic cartilage.The male
larynx is made up entirely of fast-twitch muscle fibers, whereas the female
larynx is mostly composed of slow-twitch fibers; all male muscle fibers
express a distinct myosin heavy-chain isoform, LM, found in only a subset
of fibers in females (reviewed in Kelley 1996).
How do these sexually differentiated cellular features of the vocal system
come about? In X. laevis, removal of the testis at any point during the first
six months after metamorphosis blocks addition of new muscle fibers. Castration also blocks expression of the LM gene, the transcription of which
appears to require androgen secretion. Transplantation of a testis into a
female at any point during her development results in a masculinized
program of laryngeal development and the ability to produce male songs
(Watson and Kelley 1992). Administering androgen antagonists to tadpoles
blocks the rescue of laryngeal motor neurons that underlies sex differences
in cell number while exogenous androgens rescue dying cells in females
(Kay et al. 1999). Although testicular androgens appear necessary for masculinization of the song system, they are not sufficient. Exogenous androgens do not masculinize cell numbers in juvenile females, nor can those
females sing when adult (even when given activational androgens), whereas
testis implants fully masculinize the muscle cell numbers in females.
Are these cellular differences that parallel vocal differences between
males and females caused by the organizational effect of hormones? The
control of cell number appears to result from organizational effects of
androgen because castration of juvenile males does not reverse muscle fiber
addition. The ability of gonadal androgen to increase muscle fiber number
depends on another hormone, thyroxine. Thyroxine, a thyroid hormone, is
responsible for metamorphosis in amphibians; without thyroxine, androgen
cannot induce laryngeal cell proliferation (Robertson and Kelley 1996).
Premature exposure to thyroxine induces premature androgen sensitivity
of the larynx (Cohen and Kelley 1996). The ability of hormones to masculinize muscle fiber extends past early juvenile stages. Even adult females
can achieve male-like numbers of fibers after testis transplants. Thus, the
critical period for androgen regulation of muscle fiber number is opened
by exposure to thyroxine. Females maintain androgen sensitivity and can
respond to testis transplants even when adult. In males, the critical period
ends when the full complement of muscle fibers is achieved, perhaps due
to depletion of the stem cell population (myoblasts) that generates new
fibers.
In addition to the number of muscle fibers, contractile properties of
muscle fibers are also controlled by a developmental program. After all
muscle fibers have been generated in males, slow-twitch fibers gradually
start to convert to fast-twitch fibers. If animals are castrated at any point
during this process, fiber type switching is halted but can be resumed if
androgen is provided (Tobias et al. 1991). Female muscle fibers can be
6. Hormonal Control of Communication
303
larynx is made up entirely of fast-twitch muscle fibers, whereas the female
larynx is mostly composed of slow-twitch fibers; all male muscle fibers
express a distinct myosin heavy-chain isoform, LM, found in only a subset
of fibers in females (reviewed in Kelley 1996).
How do these sexually differentiated cellular features of the vocal system
come about? In X. laevis, removal of the testis at any point during the first
six months after metamorphosis blocks addition of new muscle fibers. Castration also blocks expression of the LM gene, the transcription of which
appears to require androgen secretion. Transplantation of a testis into a
female at any point during her development results in a masculinized
program of laryngeal development and the ability to produce male songs
(Watson and Kelley 1992). Administering androgen antagonists to tadpoles
blocks the rescue of laryngeal motor neurons that underlies sex differences
in cell number while exogenous androgens rescue dying cells in females
(Kay et al. 1999). Although testicular androgens appear necessary for masculinization of the song system, they are not sufficient. Exogenous androgens do not masculinize cell numbers in juvenile females, nor can those
females sing when adult (even when given activational androgens), whereas
testis implants fully masculinize the muscle cell numbers in females.
Are these cellular differences that parallel vocal differences between
males and females caused by the organizational effect of hormones? The
control of cell number appears to result from organizational effects of
androgen because castration of juvenile males does not reverse muscle fiber
addition. The ability of gonadal androgen to increase muscle fiber number
depends on another hormone, thyroxine. Thyroxine, a thyroid hormone, is
responsible for metamorphosis in amphibians; without thyroxine, androgen
cannot induce laryngeal cell proliferation (Robertson and Kelley 1996).
Premature exposure to thyroxine induces premature androgen sensitivity
of the larynx (Cohen and Kelley 1996). The ability of hormones to masculinize muscle fiber extends past early juvenile stages. Even adult females
can achieve male-like numbers of fibers after testis transplants. Thus, the
critical period for androgen regulation of muscle fiber number is opened
by exposure to thyroxine. Females maintain androgen sensitivity and can
respond to testis transplants even when adult. In males, the critical period
ends when the full complement of muscle fibers is achieved, perhaps due
to depletion of the stem cell population (myoblasts) that generates new
fibers.
In addition to the number of muscle fibers, contractile properties of
muscle fibers are also controlled by a developmental program. After all
muscle fibers have been generated in males, slow-twitch fibers gradually
start to convert to fast-twitch fibers. If animals are castrated at any point
during this process, fiber type switching is halted but can be resumed if
androgen is provided (Tobias et al. 1991). Female muscle fibers can be
6. Hormonal Control of Communication
303