title: Testicular apoptosis is down-regulated during spontaneous recrudescence in white-footed mice (Peromyscus leucopus).
abstract: Among individuals of many nontropical species, seasonal breeding is timed by 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 exposure, reproductive function is "spontaneously" initiated, and testicular recrudescence is observed. The gonadal mechanisms that underlie testicular recrudescence are not fully understood. If the onset of testicular regrowth that occurs during spontaneous recrudescence reflects a down-regulation of apoptotic signals, then a decline in apoptosis should be noted concurrent with increased testis mass. This experiment sought to assess the role of apoptosis in the restoration of reproductive capacity to photoperiod-inhibited white-footed mice. Males were assigned to long (16:8 LD) or short (8:16 LD) photoperiods for 0, 14, 18, 22, 26, or 30 weeks. At each of these time points, testis mass and testosterone concentrations were assessed. In addition, apoptotic activity was measured using both in situ terminal deoxynucleotidyl transferase dNTP end labeling (TUNEL) and DNA laddering. Short photoperiod exposure 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 contrast, the high incidence of apoptotic TUNEL labeling and DNA laddering observed 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 apoptosis coincides with testicular recrudescence in white-footed mice. The current study demonstrates a decline in the incidence of testicular cell death concomitant with changes in testis mass or length, elucidating a timeline of changes at the cellular level related to the onset of recrudescence.
authors.affiliation: Division of Reproductive Sciences, Oregon Regional Primate Research Center, Oregon Health Sciences University, Beaverton 97006, USA.
authors.forename: K A
authors.initials: KA
authors.lastname: Young
authors.forename: B R
authors.initials: BR
authors.lastname: Zirkin
authors.forename: R J
authors.initials: RJ
authors.lastname: Nelson
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001835:Body Weight / Q000502:physiology; D004247:DNA / Q000235:genetics / Q000302:isolation & purification; D053938:DNA Fragmentation / Q000502:physiology; D015536:Down-Regulation / Q000502:physiology*; D012739:Gonadal Steroid Hormones / Q000378:metabolism; D017403:In Situ Hybridization; D008297:Male; D009929:Organ Size / Q000502:physiology; D010542:Peromyscus / Q000502:physiology*; D017440:Photoperiod; D011863:Radioimmunoassay; D012098:Reproduction / Q000502:physiology; D012621:Seasons; D013091:Spermatogenesis / Q000502:physiology; D013737:Testis / Q000254:growth & development / Q000502:physiology*; D013739:Testosterone / Q000378:metabolism
chemical_list: D012739:Gonadal Steroid Hormones; D013739:Testosterone; D004247:DNA