The suprachiasmatic nucleus in organotypic slice cultures of the common vole (Microtus arvalis): comparison of development with rat and hamster and the effect of age.

The intrinsic properties of the suprachiasmatic nucleus (SCN), the site of the main circadian pacemaker in mammals, have recently been studied in vitro by means of organotypic slice culturing. So far, only neonatal rats and mice have been used for such developmental and functional analyses of the isolated pacemaker. Here, the authors present a comparative developmental study of the SCN of voles, rats, and hamsters in organotypic slice cultures. In contrast to strictly circadian organization of behavior in rats and hamsters, common voles (Microtus arvalis) are characterized by large variability in the strength of circadian organization of behavior. It is not known to what extent this variability is reflected in the intrinsic features of the SCN. Cultures were prepared from rat, hamster, and vole pups (6 to 9 days old) for the purpose of species comparison. In addition, the authors studied the relation between age and development in cultures from pup (7 to 10 days old), juvenile (15 to 16 days old), and young adult (1 to 2 months old) voles. In contrast to the situation in rat and hamster, the most striking feature in neonatal voles is the variability in shape of the final, fully developed culture and its poor resemblance with the in vivo SCN. The SCN of adult voles, however, could be cultured successfully while retaining its morphological organization seen in situ. Phase-contrast microscopy and immunocytochemical staining for vasopressin and glial fibrillary acidic protein revealed that cultures of pup and juvenile voles still have potential for neurogenesis and morphological reorganization. Young voles, therefore, can serve as a model to study the developmental establishment of a functional circadian pacemaker, while adult voles allow the study of intrinsic pacemaker properties in relation to previously recorded behavior of the donor and aging-related pacemaker dysfunction.