Synergic effects of tryptamine and octopamine on ophiuroid luminescence (Echinodermata)
Laboratoire de Biologie Marine, Université Catholique de Louvain, Bâtiment Kellner, Place Croix du Sud, 3, B-1348 Louvain-la-Neuve, Belgium
* Author for correspondence (e-mail: vanderlinden{at}bani.ucl.ac.be)
Accepted 26 July 2004
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Summary |
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Key words: Amphiura filiformis, Echinoderm, Ophiosila aranea, Ophiopsila californica, Ophiuroid, octopamine, pharmacology, tryptamine, luminescence
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Introduction |
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The aim of the present work was to further investigate the nervous control
mechanisms of bioluminescence in ophiuroids by a comparative study on three
species: Amphiura filiformis, Ophiopsila aranea and Ophiopsila
californica. We studied the putative involvement of two biogenic amines,
tryptamine and octopamine, present in trace levels in mammalian nervous
systems. These trace amines do not seem to play a main neurotransmitter role
in mammals (Borowsky et al.,
2001; Premont et al.,
2001
), but in invertebrates, octopamine serves as a major
neurotransmitter/neuromodulator (Roeder,
1999
; Premont et al.,
2001
). Boulton
(1976
,
1979
) had already suggested
that amines such as tryptamine and octopamine, with low endogenous
concentrations but a rapid turnover, may continuously be released from
synaptic terminals and act as modulators of neurotransmission mediated by the
metabolically related `classical' amine transmitters. Tryptamine is a
serotonin-related indolamine (Ramos et
al., 1999
), whose importance has been underestimated due to the
general assumption that it occurs as a byproduct of 5HT synthesis.
Nevertheless, tryptamine is not simply present as an accident of metabolism;
indeed, neuropharmacological and electrophysiological data strongly suggest
the existence of post-synaptic receptors for tryptamine independent of those
for 5HT (Jones, 1982
).
Recently, a new family of G protein-coupled receptors called trace amine
(TA) receptors has been described in humans
(Borowsky et al., 2001;
Yu et al., 2003
). Experiments
indicated that tryptamine plays some role in mammal neurotransmission
(McCormack et al., 1986
;
Juorio and Paterson, 1990
;
Mousseau, 1993
), but it has
never been shown to be a neuromediator involved in any invertebrate
physiological process. As a consequence, the present study brings an
innovative concept to ophiuroid luminescence control: a neurotransmitter role
for tryptamine. Octopamine, on the other hand, is well known to act as a
neurohormone, a neuromodulator and a neurotransmitter in various invertebrate
species (Roeder, 1999
) such as
annelids, molluscs and arthropods
(Dhainaut-Courtois, 1982
).
Since its discovery in the salivery glands of the cephalopod Octopus
(Erspamer and Boretti, 1951
),
it has been found in most invertebrate tissues studied so far. Several studies
indicate that octopamine is a neurotransmitter involved in many invertebrate
nervous control mechanisms (for a review, see
Roeder, 1999
). Octopamine is a
multipotent biogenic amine that also acts as a neurohormone, especially in
insects where it modulates the physiological state of the insect in a complex
way to enable it to cope with energy-demanding situations such as long-term
flying (Orchard et al., 1993
).
Moreover, octopamine is known to control glowing of the firefly lantern
(Nathanson, 1986
). Testing the
effect of octopamine on ophiuroid luminescence is thus entirely justified.
Trace amines have not yet been highlighted in echinoderms but might
potentially play some role in luminescence, such as in the firefly mechanism.
We therefore compared the effects of both tryptamine and octopamine in three
ophiuroid species: (i) O. aranea and O. californica, where
the neurotransmitters responsible for photogenesis are unknown, and (ii)
A. filiformis, where light emission seems to be under cholinergic
control (Dewael and Mallefet,
2002a). Our results from isolated photocytes and arm segments
suggest an involvement of octopamine and tryptamine in A. filiformis
luminescence control and of tryptamine in O. californica.
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Materials and methods |
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Experiments on dissociated photocytes
The method used to isolated the luminous cells (photocytes) is based on
that described by De Bremaeker et al.
(2000). First, the ophiuroids
were anaesthetized by immersion in 3.5% MgCl2 in artificial
seawater (ASW: 400.4 mmol l1 NaCl, 9.9 mmol
l1 CaCl2, 9.6 mmol l1 KCl, 52.3
mmol l1 MgCl2, 27.7 mmol l1
Na2SO4, 20 mmol l1 Tris, pH 8.3).
Since the arms are the only luminescent body parts of the ophiuroid species
studied, they were isolated from the disc and chopped into tiny pieces before
enzymatic digestion and differential centrifugation. The enriched
luminous-cell fraction was then divided into 100 µl samples.
Experiments on arm segments
After anaesthesia of the animals by immersion in 3.5% MgCl2,
arms were isolated from the disc and divided into 20 segments for A.
filiformis, 8 for O. aranea and 5 for O. californica,
and rinsed in ASW. These different preparations have roughly the same size.
Segments of each of the five arms cut at the same distance from the disc
produce light of similar intensity
(Mallefet et al., 1992;
Dewael and Mallefet, 2002b
).
Given this information, one segment was used for the control stimulation with
KCl while the four others were treated with the tested drugs.
Stimulations
A stock solution of 400 mmol l1 KCl was prepared in ASW
without NaCl to keep the osmolarity the same as normal ASW. Maximal light
emission was triggered by application of 200 mmol l1 KCl
(Mallefet et al., 1992). For
each experimental protocol, one aliquot part was stimulated in normal ASW, as
a control, while the other preparations were first immersed in ASW containing
the tested drug for 10 min before stimulation with KCl. For each experiment,
recordings were performed during the entire 10 min of the drug treatment for a
few aliquot parts. The remaining aliquot parts were only measured for the
first 2 min of drug treatments since none of the light emissions observed
exceeded those first two recorded minutes. For some experiments, calcium was
removed from the ASW (Ca2+-free ASW) by addition of 1 mmol
l1 EGTA.
Light emission was measured using a FB12 Berthold luminometer (Pforzheim, Germany) linked to a personal computer. Injections of corresponding volumes of ASW served as controls before the assays. These controls indicated that luminescence due to mechanical excitability was absent or negligible. Each light response was characterized by its maximal intensity (Lmax, in Mq s1) and expressed as a percentage of the control.
Drugs
In this study, we tested 3-[2-aminoethyl]indole (tryptamine; Sigma, Bornem,
Belgium) and 1-[p-hydroxyphenyl]-2-aminoethanol hydrochloride
(octopamine; Sigma) on arm segments and on isolated photocytes of the three
studied ophiuroid species. Solutions of tryptamine were dissolved in methanol
before dilution in ASW (or Ca2+-free ASW, depending on the
experiment), with a maximum of 1% methanol at final concentration. Octopamine
was dissolved and diluted in ASW or Ca2+-free ASW. We tested a wide
concentration range of tryptamine and octopamine
(1011104 mol l1)
on both isolated photocytes and on arm segments of the three species studied.
We also tested mixtures of tryptamine with each of the following drugs:
acetylcholine chloride (ACh, 103 mol l1;
Sigma), 2-aminoethylsulfonic acid (taurine, 103 mol
l1; Sigma) and 5-hydroxytyramine hydrochloride (dopamine,
104 mol l1; Sigma) on arm segments of
O. californica, and mixtures of octopamine (109 mol
l1) + taurine (103 mol
l1), tryptamine (105 mol
l1) + taurine (103 mol
l1), tryptamine (105 mol
l1) + octopamine (109 mol
l1), tryptamine (105 mol
l1) + ACh (103 mol l1),
octopamine (109 mol l1) + ACh
(103 mol l1) and tryptamine
(105 mol l1) + octopamine
(109 mol l1) + ACh (103
mol l1) on arm segments of A. filiformis. Fresh
solutions were prepared daily.
Statistics
Statistical analyses [analysis of variance (ANOVA), Dunnet and Tukey tests]
were performed using SAS/STAT® software
(SAS Institute Inc.,
1990).
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Results |
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Tryptamine
Tryptamine triggers light emissions (2% of KCl controls) of arm
segments in A. filiformis at concentrations between
104 and 107 mol l1
(Fig. 1). At lower
concentrations (1081011 mol
l1), a very weak luminescence (still distinguishable from
mechanical stimulation) remains but only reaches approximately 0.5% of KCl
controls. On photocytes isolated from A. filiformis, tryptamine does
not induce photogenesis except at a concentration of 1011
mol l1, which triggers a light emission representing 2% of
the controls.
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In O. aranea, tryptamine does not induce any light emission on either arm segments or isolated photocytes, at all the tested concentrations.
In O. californica, by contrast, tryptamine induced light responses
(2.5% of control) on arm segments at concentrations between
107 and 1010 mol l1;
higher and lower concentrations did not trigger any luminescence
(Fig. 2). On photocytes
isolated from this species, very weak light productions were observed at
104106 mol l1 and
1011 mol l1 tryptamine concentrations.
|
Tryptamine does not modify the KCl-induced luminescence of either preparation types (arm segments and photocytes) in all three species and at all tested concentrations.
Octopamine
Octopamine triggers light emission (1.7% of controls) of arm segments
in A. filiformis at concentrations of
1081011 mol l1
(Fig. 3). This was not observed
in isolated photocytes.
|
In O. aranea, no light production was observed after injection of octopamine on either arm segments or photocytes at all the tested concentrations.
Finally, a weak luminescence was observed in O. californica for octopamine treatments at 1081011 mol l1 on arm segments and at 1071010 mol l1 on isolated photocytes. Nevertheless, even if this luminescence was slightly different from a mechanical stimulation (injection of ASW), it is difficult to consider it as a proper light response since it only reached 0.2% of KCl controls.
Octopamine does not influence KCl-induced luminescence in any of the studied species.
Tryptamine and octopamine stimulations in Ca2+-free ASW
Tryptamine and octopamine were tested at the concentrations that induced
luminescence of A. filiformis and O. californica arm
segments in Ca2+-free ASW to see whether light production still
remained after Ca2+ removal.
Fig. 4 shows that in A.
filiformis, only 4.14% and 16.17% of tryptamine-induced luminescence
remained after Ca2+ removal at tryptamine concentrations of
104 mol l1 and 105 mol
l1, respectively. In O. californica,
107 mol l1 and 108 mol
l1 tryptamine only triggered 10.71% and 0.47% of control
(tryptamine 107 mol l1 and
108 mol l1 in normal ASW) in absence of
external Ca2+ (Fig.
5). Octopamine only triggered 13.84% and 1.38% of octopamine
controls (109 mol l1 and
1010 mol l1 in normal ASW, respectively)
in Ca2+-free ASW (Fig.
6). In both species, KCl still induces some light responses in
absence of Ca2+, reaching about 5% of the control stimulation in
normal ASW (results not shown).
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Synergic effects of tryptamine, octopamine and other drugs
We tested the effects of other drugs (ACh, dopamine, taurine) on
107 mol l1 tryptamine-induced luminescence
of O. californica arm segments. The results show that mixtures of
tryptamine + 103 mol l1 ACh as well as
tryptamine + 103 mol l1 taurine increase
the light response in comparison with tryptamine on its own
(Fig. 7). By contrast, no
increase of light emission is observed with the mixture of tryptamine +
104 mol l1 dopamine.
|
In A. filiformis, both tryptamine and octopamine alone triggered light emissions, so we tested the synergic effect of both drugs mixed together at concentrations of 105 mol l1 and 109 mol l1, respectively. The results showed no effect of this mixture on light production compared with both drugs administered on their own (Table 2). Synergic effects of 103 mol l1 taurine + 109 mol l1 octopamine were clearly seen (Fig. 8), however, since this drug mixture induced about 52% of KCl controls as against only 1% with octopamine on its own. By contrast, the combination of 105 mol l1 tryptamine + 103 mol l1 taurine did not potentiate the light response compared with the one triggered by tryptamine alone (Table 2). Finally, the following combinations were tested: 105 mol l1 tryptamine + ACh, 109 mol l1 octopamine + ACh and 105 mol l1 tryptamine + 109 mol l1 octopamine + ACh. Only the last combination increased luminescence compared with ACh treatment on its own (Fig. 9, Table 2).
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Discussion |
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The role of the trace amine tryptamine is not yet well understood in
vertebrates and is not documented in invertebrates. However, low levels of a
substance do not mitigate against an active function. Tryptamine is now
thought to function as a neuromodulator or a neurotransmitter in the mammalian
central nervous system (Yu et al.,
2003). The neuromodulator role of tryptamine is mainly illustrated
by its positive and negative modulation of 5HT transmission, but its action on
other systems such as ACh and glutamate cannot be ignored (for a review, see
Jones, 1982
). Previous studies
on the three ophiuroid species studied here have shown that 5HT does not play
a neurotransmitter role in photogenesis of those three species
(Dewael and Mallefet, 2002a
),
implying therefore that tryptamine does not modulate 5HT action. Our results
are in favour of a neurotransmitter function for tryptamine in A.
filiformis and O. californica, since tryptamine on its own
triggers light production in those species. As a neurotransmitter in
vertebrates, tryptamine interacts with the G protein-coupled TA2
receptor (Premont et al.,
2001
; Yu et al.,
2003
). This trace amine receptor is likely to be coupled to
conventional signalling pathways as demonstrated for TA1 (receptor
for octopamine; Borowsky et al.,
2001
), which will be discussed later, and their signalling is
probably regulated via mechanisms similar to those for other G
protein-coupled receptors. Moreover, we have tested the synergic effects of
tryptamine with other substances such as ACh, dopamine and taurine that had
been shown to trigger weak luminescence in O. californica
(Dewael and Mallefet, 2002a
).
Our results highlight that combinations of tryptamine+ACh and
tryptamine+taurine both increase light emission in comparison with
luminescence induced by tryptamine on its own, suggesting either a synergic
effect of several neurotransmitters or a modulatory effect of some substances
in luminescence control of this species. Nevertheless, according to classical
definitions, one can argue that the light-triggering effect of tryptamine is
more in favour of a neurotransmitter role than a neuromodulatory one alone.
Other examples of two neurotransmitters coexisting (e.g. 5HT and ACh) are
known in invertebrate neurones
(Dhainaut-Courtois, 1982
).
Octopamine, on the other hand, is a well-known neurotransmitter and
neuromodulator in invertebrates, but is only present as a trace amine in
vertebrates. Octopamine modulates almost every physiological process in
invertebrates studied so far. Indeed, most peripheral organs, sense organs,
and numerous targets within the central nervous system are modulated by
octopamine. Its presence has been demonstrated in several marine invertebrates
such as Aplysia californica
(Saavedra et al., 1974),
Octopus vulgaris (Saavedra,
1974
), Tapes watlini
(Dougan et al., 1981
), etc.
Moreover, octopamine is responsible for glowing of the firefly lantern
(Nathanson, 1986
). Octopamine
is known to exert its physiological actions through a number of G-protein
coupled receptors associated to adenylate cyclases
(Walker et al., 1996
;
Roeder, 1999
). In the nervous
system of the marine snail Aplysia, for instance, an octopamine
receptor positively coupled to an adenylate cyclase has been identified
(Li et al., 1994
). In the
three ophiuroid species of the present survey, it was shown by Vanderlinden et
al. (2003
) that the cAMP
pathway is involved in bioluminescence control. The results of the present
study for A. filiformis therefore support the hypothesis that
octopamine receptors might be present in the photocyte membrane of this
species and stimulate an adenylate cyclase, leading to an increase of cAMP
levels inside the photocyte. A similar pathway could be involved in A.
filiformis and O. californica for tryptamine stimulation, but
cannot be postulated for O. aranea since neither tryptamine nor
octopamine triggered any luminescence in this species.
Cyclic AMP activates protein kinase A, which is involved in the regulation
of receptors and the opening and closing of ion channels. It can, among other
effects, increase Ca2+ influx
(Kennedy, 1994). A previous
study has, indeed, shown that calcium movements are required in the
photogenesis of all three ophiuroid species
(Dewael and Mallefet, 2002b
).
In the absence of extracellular calcium, luminescence is strongly inhibited.
Eventually, the intracellular increase of Ca2+ concentration would
lead to the triggering of the light reaction, through a mechanism not yet
understood. Moreover, calcium could also act on octopamine release from nerve
terminals, since when lobster nerves are depolarised, octopamine is liberated
by a Ca2+-dependent process
(Axelrod and Saavedra, 1977
).
Our results obtained with octopamine stimulation on A. filiformis arm
segments and with tryptamine stimulation on A. filiformis and O.
californica arm segments, in Ca2+-free ASW, highlight the
necessity for extracellular Ca2+. As a matter of fact, almost no
luminescence remained when arm segments were stimulated with octopamine and
tryptamine in the absence of Ca2+. Although, some very weak
luminescence could still be observed in Ca2+-free ASW following
octopamine, tryptamine and KCl stimulation, this observation may be due to the
intracellular calcium stores that most excitable cells usually maintain
(Triggle, 1989
), even in the
absence of extracellular calcium. Moreover, some calcium could originate from
the preparation itself since it is part of most echinoderms' framework
(Hernandez et al., 1987
).
Furthermore, the combination of 103 mol
l1 taurine, which has been shown to trigger a very weak
luminescence in A. filiformis (0.74% of KCl control;
Dewael and Mallefet, 2002a), +
109 mol l1 octopamine increases light
production (52% of KCl control) compared with octopamine administered on its
own (1% of KCl control), suggesting a synergic effect of those two
transmitters. Finally, since acetylcholine is known to act as a
neurotransmitter involved in A. filiformis luminescence control
(Dewael and Mallefet; 2002a
),
we tested the effects of tryptamine and octopamine combined with ACh. The
results show that only the combination of all three drugs potentiates light
emission compared to luminescence induced by Ach alone. These observations
might imply either a modulatory effect of both tryptamine and octopamine on
Ach, or that all these substances, including taurine, act as neurotransmitters
working in synergy to trigger photogenesis.
In conclusion, this study shows that tryptamine and octopamine might be
involved in the luminescence control of some ophiuroid species. In A.
filiformis, both tryptamine and octopamine trigger photogenesis and the
combinations of octopamine + taurine as well as octopamine + tryptamine + ACh
increase luminescence. In O. californica, tryptamine in synergy with
acetylcholine and taurine, induces light production. In O. aranea, on
the other hand, neither tryptamine nor octopamine seem to be involved in
photogenesis. In this latter species, none of the neurotransmitters tested so
far trigger light emission; further experiments will be done in order to
clarify the luminescence control of O. aranea. These experiments,
once more, confirm that the control mechanisms of photogenesis differ between
ophiuroid species, as shown in other studies
(Dewael and Mallefet, 2002a;
Vanderlinden et al., 2003
).
Our results show for the first time that tryptamine and octopamine may be
proper neurotransmitters in Echinoderms.
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Acknowledgments |
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