The acute and residual entraining effects of a 15 min pulse of light o
n rat pineal function in individual animals were investigated using th
e excretion rate of the melatonin metabolite, 6-sulphatoxymelatonin, a
s an index of melatonin production. In animals maintained in a 12-hr L
:12-hr D photoperiod (lights off 1800), 15 min light exposure at 2000
had no significant effect on the metabolite rhythm. Light pulses at 22
00 (i.e., after the onset of excretion) decreased the melatonin metabo
lite excretion rate for 3 hr, after which the excretion rate increased
to normal. In contrast, pulses at 2400 and 0200 suppressed 6-sulphato
xymelatonin for the rest of the night such that total excretion was 58
+/- 8% and 66 +/- 6% of the amount excreted on the night before the p
ulse. A light pulse at 0400 had no significant effect on the 6-sulphat
oxymelatonin excretion when compared with the first night collection.
When the 6-sulphatoxymelatonin rhythm was assessed on the night follow
ing light guises at 2000 and 0400, the onset of metabolite excretion w
as unaffected (0.2 +/- 0.75-hr advance and 0.75 +/- 0.15-hr delay, res
pectively). In contrast, pulses at 2200, 2400, and 0200 resulted in si
gnificant delays in the onset of 2.4 +/- 0.2-hr, 1.5 +/- 0.1-hr, and 2
.1 +/- 0.3-hr, respectively (P < 0.05). The offset of metabolite excre
tion was not significantly affected by a prior light pulse, except in
animals receiving light treatment at 0400 when the offset was advanced
by 1.5 +/- 0.3 hr. In an associated experiment, the effect of constan
t darkness during the day after a 2200 light pulse was compared with o
ur standard condition of light exposure from 0900 to 1800. The phase d
elay provoked by the light pulse was similar in both conditions (2.9 /- 0.4 hr and 2.2 +/- 0.2 hr delays, respectively; P > 0.05). These re
sults confirm the differential responsiveness of the pineal gland to l
ight pulses during the night, both in terms of the acute suppression o
f melatonin production and the subsequent entraining effect of the mel
atonin rhythm, which had previously been assessed indirectly by seroto
nin-N-acetyltransferase (NAT) determinations.