| Popis: |
This study investigated whether central glutamatergic pathways are involved in sexual maturation in the Siberian hamster, a species in which puberty is regulated by photoperiod. The aim of the initial experiments was to determine whether exogenous activation of N-methyl-D-aspartate (NMDA) receptor-mediated glutamatergic pathways could induce premature testicular development in photoinhibited hamsters. Male hamsters raised in an inhibitory short-day photoperiod (8L:16D) received systemic injections of the glutamate agonist NMDA. Twice-daily treatment with 20 or 40 mg/kg BW caused significant increases in testicular weight within 4 wk, but this was not accompanied by a significant increase in circulating testosterone. Subsequent experiments revealed that the degree of testicular development induced by NMDA was comparable to that induced by daily treatment with GnRH (1 microg). This study demonstrates the potential for increased glutamatergic activity to induce testicular development. The aim of the second series of experiments was to determine whether blockade of endogenous NMDA receptor-mediated glutamatergic pathways could prevent testicular development in photostimulated hamsters. Males were transferred from short (SD) to long days (LD; 16L:8D) at 80-100 days of age to induce rapid testicular growth and were concurrently treated with MK801, a noncompetitive NMDA receptor antagonist (2 mg/kg BW per day), or CGP40116, a competitive NMDA receptor antagonist (5 or 10 mg/kg BW per day) for 4 wk. LD photoperiod caused a rapid increase in testicular weight in vehicle-treated hamsters within 4 wk. Both antagonists significantly reduced the LD-stimulated testicular growth. MK801 treatment induced a degree of sedation and a loss of body weight, suggesting that the reduced testicular development in this group may have been secondary to decreased growth rates; but no behavioral changes or loss of body weight was observed in the hamsters treated with CGP40116. These observations in a photoperiodic species provide support for the hypothesis that activation of NMDA receptor-mediated glutamatergic pathways contributes to sexual maturation. |
