Destruction of the hypothalamic suprachiasmatic nucleus (SCN) disrupts
circadian behavior. Transplanting SCN tissue from fetal donors into S
CN-lesioned recipients can restore circadian behavior to the arhythmic
hosts. In the transplantation model employing fetal hamster donors an
d SCN-lesioned hamsters as hosts, the period of the restored circadian
behavior is hamster-typical. However, when fetal rat anterior hypotha
lamic tissue containing the SCN is implanted into SCN-lesioned rats, t
he period of the restored circadian rhythm is only rarely typical of t
hat of the intact rat. The use of an anterior hypothalamic heterograft
model provides new approaches to donor specificity of restored circad
ian behavior and with the aid of species-specific markers, provides a
means for assessing connectivity between the graft and the host. Using
an antibody that stains rat and mouse neuronal tissue but not hamster
neurons, it has been demonstrated that rat and mouse anterior hypotha
lamic heterografts containing the SCN send numerous processes into the
host (hamster) neuropil surrounding the graft, consistent with graft
efferents reported in other hypothalamic transplantation models in whi
ch graft and host tissue can be differentiated (i.e., Brattleboro rat
and hypogonadal mouse). Moreover, SCN neurons within anterior hypothal
amic grafts send an appropriately restricted set of efferent projectio
ns to the host brain which may participate in the functional recovery
of circadian locomotor activity.