8. VISION AND BIOLUMINESCENCE
249
the delay period between the photoflash and the luminescent response
and the inhibitory period induced by a further photoflash and concludes
that a t least part of the excitatory delay period is controlled by factors
different from those controlling the inhibitory period. He suggests that
hormones may initiate the luminescent response but a more rapidly
acting nervous mechanism may instigate the extinguishing of the
luminescence. Hardy (1964) has demonstrated the presence of nerve
fibres entering the photophores and certainly if the ventral nerve cord
is cut then photophores posterior to the cut will not luminesce. Consequently, it is reasonable to assume that the photophores, to some
extent a t least, are under nervous control. Kay also found that light
of the same intensity and colour as the animals own luminescence
depresses, but does not completely inhibit, the previously optically
stimulated luminescence.
The stimulatory effect of 5-hydroxytryptamine on the luminescent
response of M . norvegica is interesting (Kay, 1962, 1965). Concentrations of 10-30 pg 5-HT per ml sea water cause half the animals, after
1-2 hr immersion, to luminesce for prolonged periods while concentrations greater than 50 pg per ml cause all the animals in the medium
to luminesce after 5-15 min immersion. As mentioned above, very low
concentrations of 5-HT, although not initiating luminescence, sensitize
the animals to luminesce in response to light. Adrenalin (4-100 pg/ml),
acetylcholine chloride (50-500 pg/ml), L-glutamic acid, sodium salt
(20-500 pg/ml) did not excite luminescence and y amino butyric acid
(10-100 pg/ml) was possibly inhibitory. Lysergic acid diethylamide
caused continuing luminescence in M . norvegica and low concentrations
of this drug (> 4 x
pg/ml) potentiated the luminescent response
to optical stimulation. Since 5-HT occurs naturally in the bodies of
crustaceans it seems probable that it may be involved in the control
system of bioluminescence used by the animal, and Doyle (1966) and
Doyle and Kay (1 967) found that 2'-( 3-dimethylaminopropy1thio)cinnamanilide, Squibb 10 643, an anti-serotonin which has been
shown, in low doses, to specifically inhibit 5-HT stimulation, also has
an inhibitory action on the bioluminescence of M . norvegica and
Thysanoessa raschii.
Kay (1965)) in the light of his experiments, discusses the probable
mechanisms controlling luminescence The delay between the application of the optical stimulus and the production by the animal, of a
luminescent response is relatively constant, being about 90 sec.
Lowering of the temperature from 10" to 0°C increases the delay time
to about 5 min but does not affect the immediate switching off of the
photophores which takes place when a fla'sh of light is applied to an
249
the delay period between the photoflash and the luminescent response
and the inhibitory period induced by a further photoflash and concludes
that a t least part of the excitatory delay period is controlled by factors
different from those controlling the inhibitory period. He suggests that
hormones may initiate the luminescent response but a more rapidly
acting nervous mechanism may instigate the extinguishing of the
luminescence. Hardy (1964) has demonstrated the presence of nerve
fibres entering the photophores and certainly if the ventral nerve cord
is cut then photophores posterior to the cut will not luminesce. Consequently, it is reasonable to assume that the photophores, to some
extent a t least, are under nervous control. Kay also found that light
of the same intensity and colour as the animals own luminescence
depresses, but does not completely inhibit, the previously optically
stimulated luminescence.
The stimulatory effect of 5-hydroxytryptamine on the luminescent
response of M . norvegica is interesting (Kay, 1962, 1965). Concentrations of 10-30 pg 5-HT per ml sea water cause half the animals, after
1-2 hr immersion, to luminesce for prolonged periods while concentrations greater than 50 pg per ml cause all the animals in the medium
to luminesce after 5-15 min immersion. As mentioned above, very low
concentrations of 5-HT, although not initiating luminescence, sensitize
the animals to luminesce in response to light. Adrenalin (4-100 pg/ml),
acetylcholine chloride (50-500 pg/ml), L-glutamic acid, sodium salt
(20-500 pg/ml) did not excite luminescence and y amino butyric acid
(10-100 pg/ml) was possibly inhibitory. Lysergic acid diethylamide
caused continuing luminescence in M . norvegica and low concentrations
of this drug (> 4 x
pg/ml) potentiated the luminescent response
to optical stimulation. Since 5-HT occurs naturally in the bodies of
crustaceans it seems probable that it may be involved in the control
system of bioluminescence used by the animal, and Doyle (1966) and
Doyle and Kay (1 967) found that 2'-( 3-dimethylaminopropy1thio)cinnamanilide, Squibb 10 643, an anti-serotonin which has been
shown, in low doses, to specifically inhibit 5-HT stimulation, also has
an inhibitory action on the bioluminescence of M . norvegica and
Thysanoessa raschii.
Kay (1965)) in the light of his experiments, discusses the probable
mechanisms controlling luminescence The delay between the application of the optical stimulus and the production by the animal, of a
luminescent response is relatively constant, being about 90 sec.
Lowering of the temperature from 10" to 0°C increases the delay time
to about 5 min but does not affect the immediate switching off of the
photophores which takes place when a fla'sh of light is applied to an