maintain hypertrophied sonic muscle well beyond the breeding season
(Connaughton and Taylor 1995b). Thus, T and/or its metabolites are
involved in modifying the periphery in adulthood in male weakfish. It is not
clear whether androgen-induced modification of sonic muscles is required
for vocal production. Hypertrophied muscle is, however, necessary to masculinize some acoustic properties of calls. Hypertrophied sonic muscles of
males produce vocalizations with increased amplitude by generating a
greater burst of force (Connaughton et al. 1997). Thus, the amplitude of
male calls encodes the circulating levels of androgen in this species.
Although circulating androgens have a dramatic effect on sonic muscles
in the male weakfish, the smaller sonic muscles of females are not due to
low levels of androgens in adulthood. Exogenous androgen can induce
muscle growth in adult males, but the same treatment does not masculinize
the muscle in female adults. Thus, sonic muscle is probably differentiated
during development in males and females such that females lose responsiveness to androgen in adulthood (Connaughton and Taylor 1995b).
At the level of the CNS, the activational role of androgen has not been
explored. However, recent reports show that AVT and vasoactive intestinal
polypeptide (VIP) play inhibitory roles in humming vocalization in plainfin midshipman fish. Many of the brain nuclei that are involved in vocal production are shown to contain AVT and VIP immunoreactive neurons
(Foran and Bass 1998; Powers and Ingleton 1998; Goodson and Bass 2000a).
Infusion of AVT into preoptic area–anterior hypothalamus and VIP into
the paralemniscal midbrain inhibited electrically induced fictive vocalizations in type I (humming) midshipman fish (Goodson and Bass 2000b,
2000c), suggesting that endogenous AVT and VIP may exert opposing
actions on vocalization to 11-ketoT.
In summary, androgens that activate the courtship vocalizations modify
the structure of the vocal organ in weakfish. These structural changes
modify the acoustic quality of calls; it is not clear whether they are required
for vocal production per se. Although activational effects of androgens in
the CNS are not clear, AVT and VIP act directly on vocal nuclei to inhibit
vocal production.
3.2. Unreceptive Vocalizations
Unreceptive vocalizations are given by many species of frogs. When nongravid female frogs are clasped by a sexually active male, they give release
calls that result in termination of the clasp attempt (Schmidt 1965; Kelley
and Tobias 1999). Sexually unreceptive female X. laevis tick; ticking functions as a release call but also suppresses male vocalizations (Tobias et al.
1998). Gonadectomy increases ticking rates, but application of estrogen
combined with progesterone had no effect on calling (Weintraub et al.
1985). Testosterone, synthesized by the ovary as a precursor to E 2 and circulating during ovulation, decreases ticking rates (Kelley 1982; Hannigan
298
A. Yamaguchi and D.B. Kelley
(Connaughton and Taylor 1995b). Thus, T and/or its metabolites are
involved in modifying the periphery in adulthood in male weakfish. It is not
clear whether androgen-induced modification of sonic muscles is required
for vocal production. Hypertrophied muscle is, however, necessary to masculinize some acoustic properties of calls. Hypertrophied sonic muscles of
males produce vocalizations with increased amplitude by generating a
greater burst of force (Connaughton et al. 1997). Thus, the amplitude of
male calls encodes the circulating levels of androgen in this species.
Although circulating androgens have a dramatic effect on sonic muscles
in the male weakfish, the smaller sonic muscles of females are not due to
low levels of androgens in adulthood. Exogenous androgen can induce
muscle growth in adult males, but the same treatment does not masculinize
the muscle in female adults. Thus, sonic muscle is probably differentiated
during development in males and females such that females lose responsiveness to androgen in adulthood (Connaughton and Taylor 1995b).
At the level of the CNS, the activational role of androgen has not been
explored. However, recent reports show that AVT and vasoactive intestinal
polypeptide (VIP) play inhibitory roles in humming vocalization in plainfin midshipman fish. Many of the brain nuclei that are involved in vocal production are shown to contain AVT and VIP immunoreactive neurons
(Foran and Bass 1998; Powers and Ingleton 1998; Goodson and Bass 2000a).
Infusion of AVT into preoptic area–anterior hypothalamus and VIP into
the paralemniscal midbrain inhibited electrically induced fictive vocalizations in type I (humming) midshipman fish (Goodson and Bass 2000b,
2000c), suggesting that endogenous AVT and VIP may exert opposing
actions on vocalization to 11-ketoT.
In summary, androgens that activate the courtship vocalizations modify
the structure of the vocal organ in weakfish. These structural changes
modify the acoustic quality of calls; it is not clear whether they are required
for vocal production per se. Although activational effects of androgens in
the CNS are not clear, AVT and VIP act directly on vocal nuclei to inhibit
vocal production.
3.2. Unreceptive Vocalizations
Unreceptive vocalizations are given by many species of frogs. When nongravid female frogs are clasped by a sexually active male, they give release
calls that result in termination of the clasp attempt (Schmidt 1965; Kelley
and Tobias 1999). Sexually unreceptive female X. laevis tick; ticking functions as a release call but also suppresses male vocalizations (Tobias et al.
1998). Gonadectomy increases ticking rates, but application of estrogen
combined with progesterone had no effect on calling (Weintraub et al.
1985). Testosterone, synthesized by the ovary as a precursor to E 2 and circulating during ovulation, decreases ticking rates (Kelley 1982; Hannigan
298
A. Yamaguchi and D.B. Kelley