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Department of Biology, Imperial College of Science Technology and Medicine, London, United Kingdom SW7 2AZ
Address all correspondence and requests for reprints to: Dr. Robert Lucas, Department of Biology, Sir Alexander Fleming Building, Imperial College Road, Imperial College of Science Technology and Medicine, London, United Kingdom SW7 2AZ. E-mail: r.j.lucas{at}ic.ac.uk
Pineal melatonin production is rapidly suppressed by light. In mammals,
the photoreceptors mediating this response are ocular; however,
definitive information regarding their nature and precise location is
absent. In an attempt to define these photoreceptors, we examined the
sensitivity of pineal melatonin production to inhibition by controlled
irradiance monochromatic green light (
max 509 nm) in C3H mice
bearing either of two mutations affecting the retina: retinal
degeneration (rd), a disruption of rod
phototransduction, and retinal degeneration slow (rds),
an ablation of photoreceptor outer segments. Diurnal profiles of pineal
melatonin content were similar in both mutant genotypes and in
wild-type mice; melatonin peaked between 35 h before lights on. All
three genotypes exhibited irradiance dependent inhibition of pineal
melatonin content; 2.6 x 10-2
microwatts/cm2 509 nm light induced complete suppression in
all three genotypes, whereas lower irradiances were ineffective in all
cases. Bilateral enucleation abolished responses even to 6
microwatts/cm2 509 nm light. These results demonstrate that
the process of irradiance detection for pineal melatonin inhibition is
buffered against considerable loss of photoreceptive capacity and that
neither rod photoreceptors nor rod or cone outer segments are required
for mediating this response in mice.
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