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PubMed1988

Hippocampal serotonin mediates hypoactivity in dietarily obese hamsters: a possible manifestation of aging?

To determine whether endogenous opiates mediate hyperactivity in food restricted hamsters and serotonergic fibers innervating the hippocampus mediate hypoactivity in obese hamsters, food restriction and high-fat diet supplementation were used to produce significant body fat changes (8 vs. 21%). The levels and pattern of spontaneous running were examined after IP saline or naloxone HCl (20 mg/kg) and following the infusion of vehicle and 5,7-dihydroxytryptamine creatine sulfate (4 micrograms/2 microliters) into rostromedial septum of mature female hamsters. Septum-medial preoptic area (POA), hippocampus, hypothalamus, and cortex were dissected from the three groups as well as from two additional groups of hamsters receiving vehicle or neurotoxin. Concentrations of serotonin, norepinephrine, and dopamine were measured in these tissues by HPLC method. Fat-fed hamsters were hypoactive relative to food-restricted hamsters. Naloxone had no significant effect on running behavior. Serotonin neurotoxin increased the running activity of fat-fed hamsters to the level displayed by control hamsters by increasing the number of runs, the total activity level, the speed of running and by decreasing the duration of pauses. Neurotoxin led to selective deletion of serotonin in the hippocampus (77%) and parietal cortex (50%). Serotonergic fibers innervating the hippocampus thus appear to mediate the hypoactivity that is induced by dietary obesity in mature hamsters. Since serotonin mediates some other manifestations of aging, and slow weight increases characterize mid-portion of hamster life span, we hypothesize that serotonergic mediation of hypoactivity is another manifestation of aging.

5,7-Dihydroxytryptamine↗

PubMed1984

Effect of GM1 ganglioside on neonatally neurotoxin induced degeneration of serotonin neurons in the rat brain.

The effect of exogenous GM1 ganglioside on the 5,7-dihydroxytryptamine (5,7-HT; a selective serotonin neurotoxin) induced alteration of the postnatal development of central 5-hydroxytryptamine (5-HT; serotonin) neurons has been investigated using neuro-chemical and immunocytochemical techniques. Neonatal 5,7-HT (50 mg/kg s.c.) treatment is known to lead to a marked and a permanent degeneration of distant 5-HT nerve terminal projections (e.g. in cerebral cortex, hippocampus and spinal cord), while projections close to the 5-HT perikarya in the mesencephalon and pons-medulla increase their nerve density. These regional alterations are reflected by decreases and increases, respectively, of endogenous 5-HT, [3H]5-HT uptake in vitro and number of 5-HT nerve terminals demonstrated by immunocytochemistry. Treatment of newborn rats with GM1 (4 X 30 mg/kg s.c.; 24 h interval) had no significant effect on the postnatal development of 5-HT neurons. GM1 administration had furthermore no effect on the 5,7-HT induced alteration of the regional 5-HT levels and [3H]5-HT uptake in the cerebral cortex acutely, indicating that GM1 did not significantly interfere with the primary neurodegenerative actions of 5,7-HT. At the age of 1 month a clear counteracting effect of GM1 was observed, in particular of the 5,7-HT induced 5-HT denervations. The 5-HT levels in the frontal and occipital cortex were reduced to 25 and 20% of control after 5,7-HT alone, while these values were 70 and 40%, respectively, after 5,7-HT and GM1 treatment. A similar antagonizing effect of GM1 was found in the frontal cortex when measuring [3H]5-HT uptake. GM1 treatment also caused a minor reduction of the 5,7-HT induced increase of the 5-HT levels in striatum and mesencephalon. Quantitation of 5-HT nerve terminal density in sections processed for 5-HT immunocytochemistry using an automatic image analysis system showed markedly more nerve terminals in the frontal and occipital cortex after 5,7-HT + GM1 compared to 5,7-HT treatment alone. Minor counteracting effects of GM1 were noted in the hippocampus and spinal cord (thoracic-lumbar) as evaluated by chemical 5-HT assay, although substantial counteracting effects were observed locally in these areas by quantitative immunocytochemistry.(ABSTRACT TRUNCATED AT 400 WORDS)

5,7-Dihydroxytryptamine↗

PubMed1988

Effects of neonatal spinal cord serotonin depletion on opiate-induced analgesia in tests of thermal and mechanical pain.

There is considerable evidence that serotonin (5-HT) is involved in the analgesic actions of various opiates. However, it is less clear which opioid receptor types interact with these descending systems and whether the various monoaminergic pathways are specific for different types of nociceptive signals. In the present study we lesioned the spinal cord serotonin pathways by neonatal spinal injections of 5,7-dihydroxytryptamine (5,7-DHT) and tested the analgesic effects of morphine and ketocyclazocine one and two weeks later using both mechanical and thermal noxious stimuli. The treatment depleted spinal cord serotonin by more than 90% while not affecting norepinephrine levels. The effects of morphine were greatly attenuated in the depleted animals when the thermal noxious stimulus was applied. The analgesic actions of morphine were only slightly affected when the mechanical stimulus was applied. The effects of ketocyclazocine were not reduced by the treatment. The results further buttress the conclusion that at least part of morphine's analgesic effects are mediated by descending serotonin systems and that these systems are primarily effective against a thermal stimulus. The data suggest that non-5-HT brainstem system(s) are involved in morphine-induced analgesia to a mechanical noxious stimulus.

5,7-Dihydroxytryptamine↗

PubMed1989

Brainstem serotonergic hyperinnervation modifies behavioral supersensitivity to 5-hydroxytryptophan in the rat.

Rat pups were injected intracisternally (i.c.) or intraperitoneally (i.p.) with 5,7-dihydroxytryptamine (5,7-DHT) or saline and challenged 2 and 14 weeks later with the 5-HT precursor 5-hydroxytryptophan (5-HTP), which evokes behavioral supersensitivity in adult rats, 5,7-DHT induced transient postinjection convulsions in rats injected i.c. but not i.p. Rats with either type of 5,7-DHT lesions displayed supersensitive behavioral responses to 5-HTP. However, rats lesioned by i.p. injections exhibited significantly greater shaking behavior (+1445%) in response to 5-HTP than their i.c. counterparts, who instead showed more forepaw myoclonus (+250%) and head weaving (+270%), the core features of the 5-HT syndrome. Differences in 5-HT syndrome behaviors were already present 2 weeks after lesioning, whereas the difference in shaking behavior was not. After 14 weeks, 5-HT was selectively depleted (-43 to -92%) in hippocampus, spinal cord, and frontal cortex, and differences between i.c. and i.p. 5,7-DHT routes were insignificant except in frontal cortex. Brainstem 5-HT concentrations were significantly increased (+35%) after i.p. 5,7-DHT injections in contrast to reduction (-89%) after i.c. 5,7-DHT; 5-hydroxyindole acetic acid/5-hydroxytryptamine (5-HIAA/5-HT) ratios were decreased (-20%) with either route. These data suggest that brainstem 5-HT hyperinnervation following i.p. 5,7-DHT injection modifies the functional consequences of injury in abating the 5-HT syndrome, but does not result in complete recovery since shaking behavior is enhanced. Loss of presynaptically mediated autoregulation or receptor dysregulation may play a major role in behavioral supersensitivity induced by 5-HTP in rats with 5,7-DHT lesions. To the extent that the 5-HT syndrome is mediated by 5-HT1A receptors and shaking behavior by 5-HT2 sites, differential responses to injury of 5-HT1A and 5-HT2 receptors may contribute to these behavioral differences.

5,7-Dihydroxytryptamine↗

PubMed1983

Uptake of serotonin and norepinephrine in hypothalamic and limbic brain regions during the estrous cycle and the effect of neurotoxin lesions on estrous cyclicity.

The temporal pattern of hypothalamic and limbic aminergic activity during the estrous cycle has been measured by changes in the serotonergic and noradrenergic neuronal uptake during the regular estrous cycle. Significant changes (p = 0.006, 0.01) in the uptake of 3H 5-HT and 3H NE were recorded in the suprachiasmatic nuclei (SCN) at 1200 hours on proestrus. Significant changes (p = 0.01, 0.018) in the uptake of 3H 5-HT in the preoptic area (POA) were found at 1200 hours on both diestrus and proestrus while median eminence (ME) 5-HT showed a significant increase only during proestrus (p = 0.001). In the amygdala (AMYG) 3H 5-HT uptake was significantly different at 1200 hours on diestrus and proestrus while 3H NE uptake was significant (p = 0.001) at 1200 hours only during proestrus. The plasma proestrous luteinizing hormone surge occurred at 1700 hours. The serotonin neurotoxin, 5,7-dihydroxytryptamine, was stereotaxically injected through a 30 gauge needle in concentrations of 5-10 micrograms/microliters/minute for 1 minute in various nuclear regions. In the SCN 4 or 5 day estrous cyclicity was interrupted by diestrus for average periods of up to 15 days; in the POA for periods of 10 days; in the ME for periods of 13 days; and in the AMYG for periods of up to 6 days. Sham injections of 5% ascorbic acid had no effect on cyclicity and following these periods of acyclicity rats resumed normal cycles. These lesion effects and patterns of uptake suggest a common timing mechanism utilizing serotonergic raphe systems for neuroendocrine control. Lesions with 5,7-DHT in all four brain regions disrupt cyclicity, but the greatest delays occur in the SCN and ME regions which are particularly critical to intrinsic neuroendocrine rhythms. Patterns of increase in reuptake capacity in all 4 regions occur 3 hours prior to the critical period for the plasma LH surge and may be an important mechanism for many types of neuroendocrine events including ovulation.

5,7-Dihydroxytryptamine↗

PubMedDate not supplied

Effects of 6-hydroxydopamine or 5,7-dihydroxy-tryptamine on the development of physical dependence on ethanol.

Infant rats, treated intracisternally with 6-hydroxydopamine or 5,7-dihydroxytryptamine, alone or in combination with desmethylimipramine or pargyline, at 5 to 7 days of age, had significant specific depletions of brain norepinephrine, dopamine, both of these amines, or serotonin at 2.5 months of age. Despite apparent long-term depletions of brain biogenic amines, susceptibility to audiogenically-induced seizures following chronic ethanol withdrawal in these animals was similar to that of controls. Amine-depleted rats also displayed spontaneous withdrawal-induced tremors, spastic motor activity and irritability. The interpretation of these preliminary findings with regard to the proposed role of the biogenic amines in the development of physical dependence on ethanol is discussed.

5,7-Dihydroxytryptamine↗

PubMedDate not supplied

Role of serotonin in tolerance to ethanol and barbiturates: evidence for a specific vs. non-specific concept of tolerance.

The results of our recent investigations have suggested that tolerance and cross-tolerance development to motor-impairing and hypothermic effects of ethanol was slowed when brain serotonin (5-HT) was extensively depleted by treatment with p-chlorophenylalanine (p-CPA). These findings have been extended by the observation that p-PCA also slowed the development of tolerance to motor-impairing effects of barbital whether tolerance was tested repeatedly in the same animal or in separate subgroups being tested only once. Additional support was provided by the demonstration that intracerebral injection of 5,7-dihydroxytryptamine (-DHT), which is known to deplete 5-HT markedly, also slowed the development of tolerance to motor-impairing and hypothermic effects of ethanol. In addition, when brain 5-HT level was elevated by administration of L-tryptophan, the rate of tolerance development to ethanol, as measured by motor impairment and hypothermia, was accelerated. In contrast to 5,7-DHT, intracerebral injection of 5,6-DHT was surprisingly found to accelerate the development of tolerance to ethanol. Upon further investigation, however, it was determined that the 5,6-DHT treatment depleted brain 5-HT levels by only 20% and, in addition, resulted in the development of supersensitivity. These results further confirm and extend the generality of our observations that 5-HT may be involved in the development of tolerance and cross-tolerance to sedatives. The possibility of a non-specific vs. specific effect of the serotoninergic system (as well as other aminergic systems) in tolerance and neuroplasticity deserves further investigation. The possible significance of these findings and the role of 5-HT (and noradrenaline) in the mechanism of tolerance are discussed in terms of analogy to enzyme or receptor mechanism.

5,6-Dihydroxytryptamine↗

PubMed1989

Characterization of the inducible serotonin-sensitive dihydroalprenolol binding sites with low affinity for isoproterenol.

The previous findings that the inducible [3H]-dihydroalprenolol (DHA) binding sites with low affinity for isoproterenol (RL) could be regulated by serotonin (5-HT) in vitro and by 5-hydroxytryptophan and the 5-HT uptake inhibitor fluoxetine in vivo, prompted the present pharmacologic characterization of these receptor sites, using nonlinear regression analysis of competition binding curves. If isoproterenol was used as the displacing agent, lesioning with 5,7-dihydroxytryptamine selectively increased [3H]-DHA binding sites with low micromolar affinity. By contrast, if 5-HT was used as the displacing agent, the receptor population with high agonist affinity showed a fourfold increase whereas the density of [3H]-DHA sites with low micromolar affinity for 5-HT was not altered. Neither the 5-HT1A agonist, 8-OH-DPAT, nor mianserin, a 5-HT2 and 5-HT1C antagonist, altered the induced RL receptor population, whereas the selective 5-HT1B agonist CGS-12066B reduced the increase in the RL receptor population with a potency equal to that of 5-HT. These results strengthen the notion that the [3H]-DHA sites with low agonist affinity for isoproterenol represent 5-HT1B receptors induced following a reduction of serotonergic neuronal function.

5,7-Dihydroxytryptamine↗

PubMed1982

Serotonin analog selectively ablates indentified neurons in the leech embryo.

Exposure of embryonic leeches to 5,7-dihydroxytryptamine a cytotoxic analog of the monoamine neurotransmitter serotonin, results in the selective ablation of serotonin-containing neurons in the ventral nerve cord. Other neurons appear to be unaffected by this treatment, including those that contain another monoamine neurotransmitter, dopamine. Embryos with ablations continue to develop into juvenile leeches, but as juveniles they are unable to make normal swimming movements. However, normal swimming movements can be instated in such leeches by injecting them with serotonin.

5,7-Dihydroxytryptamine↗

PubMed1982

New dopaminergic and indoleamine-accumulating cells in the growth zone of goldfish retinas after neurotoxic destruction.

Juvenile goldfish were allowed to grow for 3 months after dopaminergic or indoleamine-accumulating cells in their retinas had been destroyed by intravitreal injection of 6-hydroxydopamine or 5,7-dihydroxytryptamine, respectively. New cells of each type were found growing in concentric rings at the margin of the retina. To compensate for the loss of dopaminergic innervation in retinas treated with 6-hydroxydopamine, cells in the growth zone appeared to proliferate at a higher rate than those in untreated retinas and long processes were extended into the retina by the first dopaminergic cells to appear.

5,6-Dihydroxytryptamine↗

PubMed1991

Intestinal motility changes in rats after enteric serotonergic neuron destruction.

The myenteric plexus consists of several subpopulations of morphologically and chemically distinct neurons known to contain a variety of peptides and amines, one of which is serotonin (5-hydroxytryptamine). These neurons are considered essential for nerve-to-nerve transmission. In the present study, we investigated the effect of 5,6- and 5,7-dihydroxytryptamine (5,6-DHT; 5,7-DHT), indoleamine neurotoxins that selectively and irreversibly injure the serotonergic neurons of the myenteric plexus. Treatment with 5,6-, or 5,7-DHT caused marked disruption of the activity front of the migrating myoelectric complex (MMC), increased its duration, and decreased its propagation velocity. At higher doses, 5,7-DHT also reduced the slow-wave frequency. Immunohistochemical techniques showed that tissue from rats treated with 5,7-DHT was depleted of serotonin-like immunoreactivity within the myenteric plexus neurons. Reserpine also caused motility and immunohistochemical changes similar to those induced by the two neurotoxins. Therefore, destruction of enteric serotonergic neurons disrupts the MMC. These studies support the cellular concepts that serotonergic neurons function as interneurons in the myenteric plexus, modulating and processing the neural stimuli, and that serotonin is an important neurotransmitter in the small intestine.

5,6-Dihydroxytryptamine↗

PubMed1987

Serotonin and kindling development.

The inhibitory effect of serotonin on the kindling model of epilepsy was investigated in the adult rat. Specific neurotoxins such as 5-6 or 5-7 dihydroxytryptamine were used to destroy serotoninergic neurons before kindling sessions, and an immunocytochemical control revealed, at the end of the experiments, the location and the extent of the lesions. The destruction of serotoninergic terminals in the epileptic focus (olfactory bulb or amygdala) facilitated the initial development of kindling obtained by stimulations of these structures. Lesions of pontis, centralis and dorsalis nuclei of the raphe enhanced the rate of olfactory bulb kindling. Finally, we transplanted foetal raphe cells into the olfactory bulb of adult rats before olfactory bulb kindling. The presence of viable grafts, controlled by immunocytochemistry, was associated with an increase of afterdischarge threshold in the olfactory bulb. All these results confirm the inhibitory function of serotonin on kindling development and demonstrate that serotoninergic neurons exert an important control both on local excitability and on the progressive establishment of kindling phenomena.

5,6-Dihydroxytryptamine↗

PubMed1981

Failure to produce blood pressure changes following pharmacological or surgical depletion of brain serotonin in the spontaneously hypertensive rat.

Spontaneously hypertensive (SH) and normotensive (Wistar-Kyoto, WKY) rats were examined for blood pressure changes following depletion of CNS serotonin (5-HT) by 3 separate techniques: (1) p-chlorophenylalanine, (2) 5,7-dihydroxytryptamine, and (3) a lesion of the dorsal and median raphe nuclei. All of these procedures failed to alter blood pressure in either hypertensive or normotensive rats, despite marked reductions (75-85%) in forebrain 5-HT. Moreover, treatment of 10 day-old hypertensive rat pups with intracisternal injections of 5,7-DHT (10 microgram) failed to alter the development of hypertension despite a 75-80% decrease in spinal cord 5-HT. These findings, which show that 5-HT depletion does not alter blood pressure in the SH or the WKY rat, do not lend support to the idea that 5-HT is involved in the regulation of blood pressure or in the development and maintenance of hypertension in the SH rat.

5,7-Dihydroxytryptamine↗

PubMedDate not supplied

[Effect of the local administration of 5,7-DHT and 6-OHDA into the neocortex on the learning and exploratory behavior of rats in an open field].

On Wistar rats characteristics were studied of investigating behaviour in the open field, of learning of conditioned food-reinforced reaction and also of BA and their metabolites content in various brain structures under local intracerebral injections of specific neurotoxins; 6-hydroxydopamine (6-OHDA) and 5,7-dihydroxytryptamine (5,7-DHT), abolishing correspondingly catecholaminergic and serotoninergic terminals. Bilateral injection of 6-OHDA in the neocortex led to a weakening of rats investigating activity in the open field and to an increase of the time of fulfillment of the forming of conditioned food-reinforced reaction. Administration of 5,7-DHT was accompanied by an increase of the investigating behaviour in the open field and a reduction of the duration of the forming of conditioned reaction. Administration of 6-OHDA to the neocortex caused a lowering of catecholamines level in the frontal area of the neocortex and the hippocampus. Analogous administration of 5,7-DHT elicited simultaneously with a deep level lowering of 5-HT and its metabolite in these structures, a change of catecholamines content which testifies to a lesser specificity of the neurotoxin 5,7-DHT in comparison with 6-OHDA. Structures lesion of serotoninergic and catecholaminergic systems of the frontal cortex and the hippocampus brought about by a local administration of 6-OHDA and 5,7-DHT in the neocortex was accompanied by differently directed changes in animals behaviour.

5,7-Dihydroxytryptamine↗

PubMedDate not supplied

Morphology of ventricular wall surfaces following neurotoxin induced degeneration of supraependymal afferents.

Following intraventricular injection of 5,7-dihydroxytryptamine in rats and survival periods up to 25 weeks, the supraependymal serotonergic axon plexus in the lateral and fourth ventricle, except for the plexus upon the hippocampal fimbria in some cases, showed no evidence of regenerative capacities. This contrasts with many reports on regeneration of intraparenchymal serotonergic fibre systems in the mammalian brain following mechanical or neurotoxin-induced experimental degeneration. The supraependymal plexus appears to be critically involved in maintainance of normal ependymal integrity in that following its experimentally induced death many ependymal cells exhibit various pathological alterations in all regions examined. Degeneration of this plexus is also associated with heavy phagocytotic reactions. Morphology, distribution and possible origins of supraependymal macrophages are briefly discussed.

5,7-Dihydroxytryptamine↗

PubMed1981

Serotonin neurotoxins: recent advances in the mode of administration and molecular mechanism of action.

1. Slow infusion of 5,7-DHT into the left lateral ventricle of nomifensine pretreated, pentobarbitone anaesthetized rats produces moderate, asymmetric regional forebrain 5-HT depletions 24 h after the injection; rapid pulse injection of 5,7-DHT results in more extensive and almost symmetric 5-HT reductions. By the eighth day, both injection procedures cause a comparable pattern of 5-HT depletion throughout the CNS. RAdioactivity distribution patterns (following 14C-5,7-DHT) correlate with the characteristics of 5-HT depletions. The type of anaesthetic used (pentobarbitone; pentobarbitone plus ketamine; ether) has little, if any, influence on the long-term 5-HT reductions in the rat CNS. 2. In forebrain regions, near the ventricle, nomifensine does not totally protect catecholamine fibre systems when pentobarbitone is used as the anaesthetic. However, optimum selectivity is provided by a combination of DMI and nomifensine in animals anaesthetized with a combination of pentobarbitone and ketamine. 3. Reaction of 5,6- and 5,7-DHT with oxygen is essential for these drugs to act as neurotoxins. Both drugs interact with the electron transfer chain of mitochondria (at the site of complex III) resulting in accelerated formation of reactive quinoidal intermediates. Metabolism of 5,7-DHT by MAO contributes to the overall in vivo neurotoxicity of this m-substituted dihydroxytryptamine.

5,7-Dihydroxytryptamine↗

PubMed1998

FMRFamide-related peptides, partial serotonin depletion, and osmoregulation in Helisoma duryi (Mollusca: Pulmonata).

Serotonergic neurons were studied by specific histological methods, and neurons containing Phe-Met-Arg-Phe-NH2 (FMRFamide)-related heptapeptides were identified with an antiserum specific for these substances in the central nervous system of the freshwater snail Helisoma duryi. Serotonergic neurons and their axons are present in all of the ganglia (paired buccal, cerebral, pedal, pleural, parietal, and single visceral) and major nerves of the central nervous system. Large neurons containing FMRFamide-related peptide immunoreactivity are located in the left parietal and visceral ganglia, whereas a few small neurons are located in the cerebral and pedal ganglia. Both serotonergic and FMRFamide-related peptide-immunoreactive dendrites and varicosities were observed in the kidney. A second antiserum with high affinity for FMRFamide-related heptapeptides was used to measure the levels of the immunoreactive material in various tissues, and such material was found in every tissue analyzed. When snails were exposed to a medium isosmotic to their hemolymph, the levels of immunoreactive FMRFamide-related peptides increased in the hemolymph, central nervous system, mantle, and kidney. Injection of dihydroxytryptamine, which is known to deplete serotonin content in the snail, also reduced the levels of FMRFamide-related-immunoreactive material in the above tissues. Therefore, serotonin may influence the levels of FMRFamide-related peptides in tissues by regulating the rate of their synthesis, axonal transport, or release. Both serotonin and FMRFamide-related peptides could be involved in osmoregulation.

5,6-Dihydroxytryptamine↗

PubMed1996

Increased serotonin in the developing superior colliculus does not alter the number or distribution of retinotectal ganglion cells.

Administration of a single subcutaneous dose of 5,7-dihydroxytryptamine (5,7-DHT) to newborn hamsters results in a significant increase in the density of serotoninergic (5-HT) fibers in the superficial layers of the superior colliculus (SC) and marked abnormalities in both the crossed and uncrossed retinotectal projections when these animals reach adulthood (R. Rhoades, C. Bennett-Clarke, R. Lane, M. Leslie, and R. Mooney, 1993, J. Comp. Neurol. 334:397-409). The present study was undertaken to determine whether changes in the retinotectal projection of 5,7-DHT-treated animals were associated with alterations in the number or distribution of retinal ganglion cells in these animals. Nissl staining of retinae from normal adult and 5,7-DHT-treated hamsters revealed no differences between them in the number or average diameter of cells in the retinal ganglion cell layer. Retrograde labeling with horseradish peroxidase (HRP) demonstrated no effect of 5,7-DHT treatment on the number or distribution of ipsilaterally or contralaterally projecting ganglion cells. Neonatal 5,7-DHT administration also had no effect on the distribution of soma diameters for HRP-labeled retinal ganglion cells. Electron microscopic analysis demonstrated no significant difference between the number of optic nerve fibers in the normal and 5,7-DHT-treated hamsters. The results are consistent with the conclusion that the effect of 5,7-DHT on the retinotectal projection may primarily be a function of this toxin, or the increase in 5-HT it induces, on the terminal arbors of retinotectal axons rather than on their parent cells.

5,7-Dihydroxytryptamine↗