trating males gradually decreases vocal production, whereas T replacement
restores calling behavior. Estrous females of some rodent species also
produce ultrasonic vocalizations to attract males. Female ultrasonic vocalizations are regulated by synergistic activity of two gonadal steroids, estradiol (E 2 ) and progesterone (P). A peak of E 2 followed by P is typical of the
ovulatory menstrual cycles of female mammals. Gonadectomizing adult
females decreases calling rates, and injection of E 2 followed by P reinstates
calling behavior in rats (Matochik et al. 1992) and hamsters (Floody 1979;
Floody and Comerci 1987). Thus, in both sexes, gonadal steroids play a
potent activational role in the production of courtship vocalizations.
The activational effects of T may be mediated by its metabolites, as we
have seen in other vertebrates. For example, E 2 implants in castrated males
can restore ultrasonic vocalizations in mice and gerbils (Holman et al. 1991;
Nyby et al. 1992). In hamsters, the aromatase inhibitor, l,4,6-androstatriene3,17-dione, blocks effects of T in reinstating vocal activity in castrated males
(Floody and Petropoulos 1987). These results suggest that aromatization of
endogenous T to E 2 is involved in the activation of vocalizations in males.
In rats, there is evidence that both T and E 2 receptors are required for the
activation of vocalizations. Using recently developed androgen and estrogen receptor blockers, hydroxyflutamide and RU58668, Vagell and
McGinnis (1998) demonstrated that both types of intracellular receptors
need to be bound to activate vocalizations in castrated males with T
implants; blocking of either type of receptor prevented reinstatement of the
vocal behavior. Taken together, these studies in rats suggest that ultrasonic
vocalizations of males are activated when some of the circulating T binds
to androgen receptors and the remaining T is aromatized to E 2 and binds
to estrogen receptors. Hormonal modifications of the larynx in rodents have
not received much attention.
In addition to steroid hormones, recent reports reveal a role for peptide
hormones in activation of vocalizations. In hamsters, injection of oxytocin
(OXT) into the hypothalamus of naturally estrous females increases the
rate of ultrasonic vocalizations within 30 minutes (Floody et al. 1998). As
discussed in the section on AVT-induced vocal production in frogs, OXT
may interact with gonadal steroids to activate vocalizations. It will be of
interest to examine whether elevated levels of estrogen and progesterone
are required for OXT to activate vocal production. Involvement of OXT in
vocal production is particularly interesting in light of recent revelations that
AVP and OXT play important roles in controlling the social behavior of
rodents (e.g., Young et al. 1998). In summary, courtship vocalizations of
male and female rodents are largely activated by gonadal steroids, although
the exact combination of metabolites required differs across species. In
addition, neuropeptides, such as OXT, in combination with steroid hormones may play potent roles in activating vocalizations.
Although the neural substrates for vocal production encompass a
number of brain regions, most research has been focused on the medial
6. Hormonal Control of Communication
295
restores calling behavior. Estrous females of some rodent species also
produce ultrasonic vocalizations to attract males. Female ultrasonic vocalizations are regulated by synergistic activity of two gonadal steroids, estradiol (E 2 ) and progesterone (P). A peak of E 2 followed by P is typical of the
ovulatory menstrual cycles of female mammals. Gonadectomizing adult
females decreases calling rates, and injection of E 2 followed by P reinstates
calling behavior in rats (Matochik et al. 1992) and hamsters (Floody 1979;
Floody and Comerci 1987). Thus, in both sexes, gonadal steroids play a
potent activational role in the production of courtship vocalizations.
The activational effects of T may be mediated by its metabolites, as we
have seen in other vertebrates. For example, E 2 implants in castrated males
can restore ultrasonic vocalizations in mice and gerbils (Holman et al. 1991;
Nyby et al. 1992). In hamsters, the aromatase inhibitor, l,4,6-androstatriene3,17-dione, blocks effects of T in reinstating vocal activity in castrated males
(Floody and Petropoulos 1987). These results suggest that aromatization of
endogenous T to E 2 is involved in the activation of vocalizations in males.
In rats, there is evidence that both T and E 2 receptors are required for the
activation of vocalizations. Using recently developed androgen and estrogen receptor blockers, hydroxyflutamide and RU58668, Vagell and
McGinnis (1998) demonstrated that both types of intracellular receptors
need to be bound to activate vocalizations in castrated males with T
implants; blocking of either type of receptor prevented reinstatement of the
vocal behavior. Taken together, these studies in rats suggest that ultrasonic
vocalizations of males are activated when some of the circulating T binds
to androgen receptors and the remaining T is aromatized to E 2 and binds
to estrogen receptors. Hormonal modifications of the larynx in rodents have
not received much attention.
In addition to steroid hormones, recent reports reveal a role for peptide
hormones in activation of vocalizations. In hamsters, injection of oxytocin
(OXT) into the hypothalamus of naturally estrous females increases the
rate of ultrasonic vocalizations within 30 minutes (Floody et al. 1998). As
discussed in the section on AVT-induced vocal production in frogs, OXT
may interact with gonadal steroids to activate vocalizations. It will be of
interest to examine whether elevated levels of estrogen and progesterone
are required for OXT to activate vocal production. Involvement of OXT in
vocal production is particularly interesting in light of recent revelations that
AVP and OXT play important roles in controlling the social behavior of
rodents (e.g., Young et al. 1998). In summary, courtship vocalizations of
male and female rodents are largely activated by gonadal steroids, although
the exact combination of metabolites required differs across species. In
addition, neuropeptides, such as OXT, in combination with steroid hormones may play potent roles in activating vocalizations.
Although the neural substrates for vocal production encompass a
number of brain regions, most research has been focused on the medial
6. Hormonal Control of Communication
295