Ka. Young et al., Testicular apoptosis is down-regulated during spontaneous recrudescence inwhite-footed mice (Peromyscus leucopus), J BIOL RHYT, 16(5), 2001, pp. 479-488
Among individuals of many nontropical species, seasonal breeding is timed b
y tracking changes in the daily photoperiod. Transfer of rodents to short (
< 12 h of light/day) day lengths for 6 to 14 weeks can induce regression of
the testes mediated by apoptosis. After 16 to 20 weeks of short day exposu
re, reproductive function is "spontaneously" initiated, and testicular recr
udescence is observed. The gonadal mechanisms that underlie testicular recr
udescence are not fully understood. If the onset of testicular regrowth tha
t occurs during spontaneous recrudescence reflects a down-regulation of apo
ptotic signals, then a decline in apoptosis should be noted concurrent with
increased testis mass. This experiment sought to assess the role of apopto
sis in the restoration of reproductive capacity to photoperiod-inhibited wh
ite-footed mice. Males were assigned to long (16:8 LD) or short (8:16 LD) p
hotoperiods for 0,14,18,22,26, or 30 weeks. At each of these time points, t
estis mass and testosterone concentrations were assessed. In addition, apop
totic activity was measured using both in situ terminal deoxynucleotidyl tr
ansferase dNTP end labeling (TUNEL) and DNA laddering. Short photoperiod ex
posure induced maximal decreases in testicular parameters after 14 weeks (p
< 0.05). After 26 weeks of short days, testis mass was no longer different
between males housed in long days and those housed in short days. In contr
ast, the high incidence of apoptotic TUNEL labeling and DNA laddering obser
ved at 14 weeks was reduced to long day values after 22 weeks of short day
exposure. Together, our results establish that a decrease in testicular apo
ptosis coincides with testicular recrudescence in white-footed mice. The cu
rrent study demonstrates a decline in the incidence of testicular cell deat
h concomitant with changes in testis mass or length, elucidating a timeline
of changes at the cellular level related to the onset of recrudescence.