168 
Crews 
intromission is achieved. In addition, copula- 
tion in this species is prolonged, often lasting 
more than 20 minutes. 
During the breeding season, females 
undergo regularly recurring periods of sex- 
ual receptivity which are correlated with 
their cyclic pattern of ovarian activity (see 
above; Fig. 12). The inhibition, by mating, 
of further sexual receptivity during each 
follicular cycle, but not during subsequent 
cycles, could serve to minimize possible 
predation and maximize the probability of 
a female realizing her reproductive potential 
during a breeding season. Similarly, the 
specialized sperm-storage ducts that have 
been described in this species (Fox, 1963) 
probably function to insure that, following 
a single successful mating, a female could 
continue to lay fertile eggs even if the terri- 
torial male were no longer present. 
CONTROL OF THE REFRACTORY 
PERIOD IN THE LIZARD, 
Anolis carolinensis 
The annual ovarian cycle of the lizard A. 
carolinensis may be divided into three dis- 
tinct periods: previtellogenesis, vitellogene- 
sis, and regression (see Fig. 2). Previtello- 
genesis lasts from November to February 
and is characterized by inactive ovaries con- 
taining only small, translucent, unyolked 
follicles and atrophic oviducts. During this 
phase, the follicles are initially relatively 
uniform, ranging from 1.2-1. 8 mm in di- 
ameter, but gradually increase to 1. 8-2.0 mm 
by late February (Crews, 1973a). Yolk 
deposition (vitellogenesis) begins in March; 
at this time a single follicle begins to ac- 
cumulate yolk and enlarges rapidly until it 
is ovulated at about 8.0 mm. During the en- 
suing breeding season, a single ovarian fol- 
licle matures and is ovulated alternately be- 
tween ovaries every 10-14 days (see above). 
Vitellogenesis ceases in late August and the 
yolking follicles already present in the ovary 
begin to degenerate rapidly. Follicles under- 
going atresia differ from normal follicles 
and from corpora lutea in that they are 
highly vascularized, discolored (orange- 
yellow instead of the bright yellow of a 
normal follicle), flaccid, and mottled in ap- 
pearance (Crews and Licht, 1974). These 
corpora atretica (CA) are gradually ab- 
sorbed and disappear completely from the 
ovary during October. 
Experimental studies indicate that female 
A. carolinensis are sexually refactory dur- 
ing the early portion of the regressive phase 
of the annual cycle (see Fig. 2). For example, 
environmental (both social and climatic) 
stimuli that promote rapid ovarian growth 
in winter and spring are generally ineffec- 
tive in stimulating females in September and 
October (Crews, 1973a; Licht, 1973). Fe- 
males constantly maintained under stimula- 
tory environmental conditions undergo three 
to four complete ovarian cycles per year 
(Crews, unpublished data), suggesting that 
seasonal ovarian growth and regression are 
under endogenous control. Furthermore, fe- 
males appear to respond less rapidly to 
exogenous gonadotropic hormones in the fall 
than in winter and spring (Licht, 1970; 
unpublished data). Females exposed to a 
stimulatory environmental regime in late 
August, the beginning of the refractory 
period, continue to undergo follicular atresia, 
responding to the unseasonal environmental 
conditions only after the CA have been 
resorbed (Crews and Licht, 1974). These 
lines of evidence suggest, therefore, that 
refractoriness may be due partly to changes 
in ovarian hormonal sensitivity as a conse- 
quence of the presence of the atretic follicle. 
To test this hypothesis, Paul Licht and I 
conducted an experiment in which refractory 
females were given daily injection of mam- 
malian (bovine) FSH following the removal 
of either the CA or a normal follicle. The 
results were quite clearcut. Females lacking 
the CA were at least five times more sensi- 
tive to the exogenous gonadotropin, as in- 
dicated by ovarian and oviducal growth, than 
females which had had a normal follicle 
removed (Fig. 13) ; this suggested that the 
CA produces a substance (s) which inhibits 
ovarian sensitivity to gonadotropin stimula- 
tion. These results also indicate that the 
