THE suprachiasmatic nuclei (SCN) contain a circadian clock whose activ
ity can be recorded in vitro for several days. This clock can be reset
by the application of neuropeptide Y. In this study, we focused on de
termination of the receptor responsible for neuropeptide Y phase shift
s of the hamster circadian clock in vitro. Coronal hypothalamic slices
containing the SCN were prepared from Syrian hamsters housed under a
14 h:10 h light:dark cycle. Tissue was bathed in artificial cerebrospi
nal fluid (ACSF), and the firing rates of individual cells were sample
d throughout a 12 h period. Control slices received either no applicat
ion or application of 200 nl ACSF to the SCN at zeitgeber time 6 (ZT6;
ZT12 was defined as the time of lights off). Application of 200 ng/20
0 nl of neuropeptide Y at ZT6 resulted in a phase advance of 3.4 h. Ap
plication of the Y2 receptor agonist, neuropeptide Y (3-36), induced a
similar phase advance in the rhythm, while the Y1 receptor agonist, [
Leu(31), Pro(34)]-neuropeptide Y had no effect. Pancreatic polypeptide
(rat or avian) also had no measurable phase-shifting effect. Neuropep
tide Y applied at ZT20 or 22 had no detectable phase-shifting effect.
These results suggest that the phase-shifting effects of neuropeptide
Y are mediated through a Y2 receptor, similar to results found in vivo
.