A single gene defect of the circadian clock (tau mutation) has recentl
y been described that results in a shortening of the circadian activit
y cycle of the Syrian hamster. In the homozygous animal, free running
activity is shortened by 4 h, resulting in a circadian period of appro
ximately 20 h. Here, we examine the effect of the tau mutation on nonc
ircadian oscillators by comparing the frequency of episodic secretion
of LH and cortisol in normal period wild-type (similar to 24-h circada
n rhythm) and tau mutant (similar to 20-h circadian rhythm) castrate f
emales. Animals were ovariectomized at 14 weeks of age and maintained
thereafter under conditions of constant illumination. Wheel-running re
cords were obtained, and only those animals exhibiting clear single bo
uts of circadian activity were used in the experiment. Two days after
intraatrial cannulation, blood samples were collected for a 5-h period
every 5 min during the subjective day at the same relative phase of t
he circadian cycle. Deconvolution analysis revealed that LH pulse freq
uency was significantly reduced in the tau mutant females (33.3 +/- 2.
25- and 28.7 +/- 2.0-min interpulse intervals for tau and normal perio
d females, respectively). Cortisol pulse frequency also exhibited sign
ificant differences, with a reduced pulse frequency (32.8 +/- 3.6- and
27.8 +/- 1.4-min interpulse intervals for tau and wild-type females,
respectively). There were no significant differences with respect to s
ecretory pulse amplitude, hormone half-life or estimated burst amplitu
de, or mass of hormone secreted per burst for either hormone. We concl
ude that a genetic defect that affects the circadian clock located in
the suprachiasmatic nucleus may have a more general effect on neural o
scillators, including those controlling episodic hormone secretion.