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PubMed1993

Synaptic contacts of serotonin-like immunoreactive and 5,7-dihydroxytryptamine-accumulating neurons in the anuran retina.

The synapses of serotonin-like immunoreactive retinal neurons were studied in Bufo marinus and Xenopus laevis and those of 5,7-dihydroxytryptamine-labelled cells in Xenopus. Immunoreactivity to serotonin was mostly confined to amacrine cells. Synapses formed by profiles of labelled cells were almost uniformly distributed in the inner plexiform layer in both species. Interamacrine synapses were the most frequent, and in some cases two labelled amacrine cell profiles made a gap junction. Some of the labelled amacrine cells synapsed on to presumed ganglion cell dendrites and onto bipolar cell terminals. Labelled bipolar cell terminals synapsed on to non-labelled amacrine cell dendrites and received inputs both from labelled and non-labelled amacrine cells. Labelled bipolar cell profiles were not observed in the outer plexiform layer. After preloading and photoconversion of 5,7-dihydroxytryptamine in the Xenopus retina, labelled bipolar cell dendrites in the outer plexiform layer were observed to be postsynaptic to cone pedicles and less frequently to rods and horizontal cells. In the inner plexiform layer, synapse types formed by labelled bipolar cells were similar to those with serotonin immunoreactivity. The frequency of synapses formed by 5,7-dihydroxytryptamine-labelled amacrine cells increased, compared with serotonin immunocytochemistry. Labelled amacrine cells synapsed mostly with non-labelled amacrine cells, although the ratio of contacts formed by two labelled profiles increased. Synapses from labelled amacrine cell dendrites to non-labelled bipolar cell terminals and from non-labelled bipolar cell terminals to labelled amacrine cell profiles increased in number, while those from labelled amacrine cells to presumed ganglion cell dendrites decreased. The quantitative data obtained by the two approaches enabled us to propose different neuronal circuits for serotonin-synthesizing and -accumulating neurons of the Xenopus retina.

5,7-Dihydroxytryptamine↗

PubMed1996

Testicular injection of 5,6-dihydroxytryptamine or vasectomy interferes with the local stimulatory effect of oxytocin on testicular steroidogenesis in immature rats.

Previous studies indicated that in immature rats testicular administration of oxytocin stimulates testicular steroidogenesis. In the present study, testicular treatment with oxytocin (50 ng) was combined with pharmacological or surgical denervation of the testis in hemigonadectomized immature rats. For denervation 5,6-dihydroxytryptamine (160 micrograms/testis), a substance that destroys serotoninergic neuronal elements, was injected intratesticularly or vasectomy was performed, which also includes transection of the inferior testicular nerve. In 9-day-old animals both vasectomy and pretreatment of the testis with 5,6-dihydroxytryptamine prevented the oxytocin-induced rise in serum testosterone concentration. In addition, intratesticular injection of oxytocin combined with vasectomy resulted in a significant increase in in vitro basal testosterone secretion of the testis. A similar effect was not observed in the 5,6-dihydroxytryptamine-pretreated group receiving oxytocin. The results indicate that testicular innervation is involved in the control of local peptide effects, and data further suggest a differential role of these neural elements in intratesticular regulatory processes.

5,6-Dihydroxytryptamine↗

PubMed1976

Alcohol intake in the rat after lowering brain 5-hydroxtryptamine content by electrolytic midbrain raphé lesions, 5, 6-dihydroxytryptamine or p-chlorophenylalanine.

Voluntary alcohol consumption was measured in male albino rats after selectively lowering their brain 5-hydroxytryptamine concentration (an AA strain of rats was used, selectively outbred for its high alcohol consumption). The brain 5-hydroxytryptamine concentration was reduced using three different techniques: electrocoagulation of the dorsal and median raphé nuclei of the midbrain; injection of 75 mug of 5,6-dihydroxytryptamine into the lateral cerebral ventricle; and oral administration of 300 mg/kg/day p-chlorophenylalanine as a 0.5 per cent carboxymethylcellulose suspension, for 12 days. The first two methods did not markedly affect alcohol consumption despite a sizable decrease in the brain 5-hydroxytryptamine level: 69 per cent in the raphé-lesioned group and 31 per cent in the 5,6-dihydroxytryptamine-treated group. Intraperitoneal injection of 50 mg/kg L-5-hydroxytryptophan on five successive days resulted in a non-significant decrease in alcohol consumption by the 5,6-dihydroxytryptamine-treated rats. p-Chlorophenylalanine did reduce significantly alcohol drinking but it had a greater effect in increasing water intake, producing a net rise in total fluid consumption. The reduction in alcohol consumption, therefore, was probably an indirect result of the treatment. These findings raise doubts about the previously suggested relationships between brain serotonin depletion and alcohol drinking.

5,6-Dihydroxytryptamine↗

PubMed1977

Ultrastructural effects of 6-hydroxy-dopamine and 5, 6-dihydroxytryptamine on the central nervous system of fresh-water mussel, Anodonta cygnea L.

Ultrastructural effects of 6-hydroxydopamine and 5, 6-dihydroxytryptamine treatments were investigated in the central nervous system of fresh-water mussel. Two days after the treatments, the following characteristic find-structural alterations could be observed in the neuropil of the ganglia: frequent occurrence of multilamellar bodies, lysosomatic structures and elongated tubular forms; shrinking of varicose axon profiles with an enchancement of the density of the axoplasm and clumping of its content; abnormal swelling of certain axons in the neuropil. This degenerative process was accompanied by an intense phagocytosis. The damages evoked by the employed "false transmitters" in the mussel ganglia were, in general, similar to those found in vertebrates. Statistical analysis of the vesicle population of ganglia suggests the intragranular uptake of 6-hydroxydopamine and 5, 6-dihydroxytryptamine and, in addition, the role of dense-core vesicles of different types in the storage of both serotonin and catecholamines. Perikarya composing the cortical layer of the ganglia were not affected by the "false transmitters". This shows that different parts of a mussel neuron are differently sensitive to 6-hydroxydopamine and 5, 6-dihydroxytryptamine.

5,6-Dihydroxytryptamine↗

PubMed1982

Effects of compounds structurally related to 5,6-dihydroxytryptamine on behavior and brain biogenic amines in the rat.

A variety of analogues of the serotonin neurotoxin, 5,6-dihydroxytryptamine were administered to rats by injection into the lateral ventricle of the brain. Each compound evoked a unique pattern of behavioral effects. Only 5,6-dihydroxytryptamine lowered brain 5HT levels, while both 5,6-dihydroxytryptamine and its benzo[b]thiophene analogue caused a transient lowering of brain NE.

5,6-Dihydroxytryptamine↗

PubMed1978

Evaluation of the cytotoxicity of dihydroxytryptamines and 5-hydroxytryptamine antagonists as cytotoxic agents in dimethylhydrazine-induced adenocarcinomata.

The cytotoxicity of 5,6-dihydroxytryptamine (5,6-DHT), 5,7-dihydroxytryptamine (5,7-DHT), bromolysergic acid diethylamide (BOL), methysergide, and cyproheptadine, and also of 5,6-DHT together with either BOL, methysergide, or cyproheptadine in dimethylhydrazine-induced (DMH) carcinomata of rat colon was evaluated by estimating the percentage of necrotic cells in histological sections of tissues taken 15 h after injection of each of the drugs. In addition, the influence of methysergide and cyproheptadine on the tumour cell mitotic rate was estimated by means of a stathmokinetic technique. Both 5,6-DHT and 5,7-DHT were cytotoxic at each dose tested and for each of these agents the percentage of necrotic cells was directly correlated with the dose of drug used. BOL was not found to be cytotoxic to the colonic carcinomata, whereas both methysergide and cyproheptadine did cause detectable tumour cell necrosis. Methysergide was also found to accelerate tumour cell proliferation, whereas cyproheptadine did not. BOL competitively inhibited the cytotoxicity of 5,6-DHT and neither methysergide nor cyproheptadine potentiated the effect of 5,6 DHT.

5,6-Dihydroxytryptamine↗

PubMed1985

Serotonin turnover and supersensitivity after neonatal 5,7-dihydroxytryptamine.

Adult awake rats which received neonatal pargyline and 5,7-dihydroxytryptamine to severely reduce CNS serotonin terminals and perikarya have a reduced rate of accumulation of brain stem 5-hydroxytryptophan after Ro-44602. The rate of accumulation in the cerebral cortex and spinal cord were near normal when adult, even though serotonin and 5-hydroxyindoleacetic acid were sharply reduced in these regions. The respiratory response to 5-methoxy N,N-dimethyl-tryptamine was much more pronounced in pargyline-5,7-dihydroxytryptamine treated rats than in controls. If supersensitivity in serotonin receptors only develops in areas with decreased transmitter turnover, the site of action of serotonin agonists to depress respiration would seem to reside in the brain stem region. The results also suggest that compensatory changes in turnover do not develop to a similar degree in all CNS areas with altered serotonin content.

5,7-Dihydroxytryptamine↗

PubMed1988

Drug-induced place preference in rats with 5,7-dihydroxytryptamine lesions of the nucleus accumbens.

The conditioned place preference (CPP) paradigm was used to determine a role for serotonin in the nucleus accumbens in the mediation of the rewarding properties of D-amphetamine morphine and diazepam. The effect of these drugs on CPP was examined in controls and in animals with 5,7-dihydroxytryptamine lesions of the nucleus accumbans. The results from control animals confirmed that D-amphetamine (1.5 mg/kg, i.p.), morphine (2.0 mg/kg, i.p.) and diazepam (1.0 mg/kg, i.p.) produced place preference for a distinctive environment that had previously been paired with injections of the drug. In animals with 80% reduction of 5-hydroxytryptamine content of the nucleus accumbens, D-amphetamine CPP was unchanged and morphine CPP was attenuated compared with controls. Diazepam CPP was not apparent in animals with the lesion. In separate experiments, characteristic behavioural effects of the drugs under study were examined in control and in animals with lesion. The results showed a tendency for increased amphetamine hyperlocomotion, enhanced morphine activity and analgesia and decreased diazepam anti-anxiety effect in animals with lesions. Thus, the 5,7-dihydroxytryptamine lesions of the nucleus accumbens differently influenced the CPP induced by the drugs studied and, with the exception of diazepam, the various behavioural effects elicited by each drug. The findings suggest that serotonin-containing neurones of the nucleus accumbens are a component of the neural circuitry that mediates the rewarding properties of morphine, probably of diazepam, but not of D-amphetamine.

5,7-Dihydroxytryptamine↗

PubMed1990

The distribution of serotonin immunoreactivity in the rat locus ceruleus after intraventricular injections of either 5,6- or 5,7-dihydroxytryptamine with special reference to serotonin synthesis.

The localization of serotonin-immunoreactivity (5-HT-IR) in the locus ceruleus (LC) of rats was studied by the peroxidase-anti-peroxidase method using a purified antibody obtained from a rabbit. Antibody production was performed according to the method of Grota and Brown (1974). The antibody was applied to serial cryostat sections with alternate counterstaining by cresyl violet, after intraventricular injections of 5,6-dihydroxytryptamine or 5,7-dihydroxytryptamine prior to treatment with pargyline and a precursor of 5-HT. The majority of LC neurons were immunopositive, and more than half of all LC neurons clearly showed 5-HT-IR. Although core cells were the most predominant, all types of neurons were immunopositive, and randomly scattered throughout the LC. The uptake inhibitor, Lilly 110140, administered in sufficient amounts prior to an injection of pargyline, did not reduce 5-HT-IR within the LC. The results suggest that LC neurons receive 5-hydroxytryptophan (5-HTP) through an afferent vascular-neuronal channel and/or by diffusion from blood capillaries much more than 5-HT itself. We consider from these results that all types of LC neurons throughout the nucleus are masked 5-HT cells, and that the majority of LC neurons utilize blood-borne 5-HTP as an immediate precursor for intraneuronal 5-HT synthesis.

5,6-Dihydroxytryptamine↗

PubMed1980

Raphe lesions and 5,7-dihydroxytryptamine induce grooming reflexes in adrenalectomized cats.

Grooming reflexes are induced by frontal neocortical, pontile, or spinal lesions in dogs and cats. In intact cats, the combined treatments of adrenalectomy and para-chlorophenylalanine administration induce grooming reflexes. Two other ways of depleting serotonin (with 5,7-dihydroxytryptamine and raphe lesions) were combined with adrenalectomy in the present study as further tests that serotonin and glucocorticoid hormones are the critical factors in the induction of grooming reflexes. Because the deficit in serotonin is confined to the superior colliculi in cats with frontal and pontile lesions, 5,7-dihydroxytryptamine (5,7-DHT) was injected directly into the superior colliculi at eight sites, 2 microgram/site (1 microliter at .5 microliter/min). Electrolytic dc lesions of the dorsal and superior central raphe nuclei were made in another group, and then both groups were adrenalectomized. There were three control groups: (a) a group with vehicle injections in the superior colliculi and laporatomies, (b) a group with 5,7-DHT injections in the superior colliculi, and (c) a group with the raphe lesions. Large receptive fields for grooming reflexes occurred only in the groups with combined treatments. Thus the mechanism of induction of grooming reflexes by central nervous system lesions involves independent changes in a hormonal and a neurotransmitter system which combine to effect the change in behavior.

5,7-Dihydroxytryptamine↗

PubMed1983

Effects of reserpine, alpha-methyl-p-tyrosine, p-chlorophenylalanine and 5,7-dihydroxytryptamine on the hippocampal kindling effect in rats.

The role of the brain monoamines in the development of hippocampal kindling was studied. Reserpine markedly facilitated the formation of hippocampal kindling. The high amplitude spike waves in the amygdala and reticular formation appeared earlier in the reserpine treated rats than in the saline injected rats. alpha-Methyl-p-tyrosine did not have any effect on the formation of hippocampal kindling. Systemic injection of p-chlorophenylalanine and intraventricular injection of 5,7-dihydroxytryptamine also did not have any effect on the formation of hippocampal kindling. Progressive changes of afterdischarge elicited by hippocampal stimulation in the alpha-methyl-p-tyrosine, p-chlorophenylalanine and 5,7-dihydroxytryptamine treated rats are the same as those in the saline injected rats. These results indicate that the decrease in both catecholamines and serotonin levels caused a marked facilitation of the hippocampal kindling formation, but the separate decrease in either catecholamines or serotonin did not produce a significant effect.

5,7-Dihydroxytryptamine↗

PubMed1988

[Effect of the intracisternal administration of the neurotoxins 6-hydroxydopamine and 5,7-dihydroxytryptamine on the formation of the passive avoidance reaction and the biogenic amine level in the brain of rats].

In Wistar rats, intracisternal administration of 6-hydroxydopamine caused a 3.0-3.5-fold decrease in noradrenaline and dopamine levels whereas 5,7-dihydroxytryptamine led to a 2.5-fold reduction of the serotonin content in the hypothalamus. The degeneration of serotoninergic neurons produced by 5,7-dihydroxytryptamine did not affect passive avoidance response while the lesion of catecholaminergic neurons with 6-hydroxydopamine disturbed it. Participation of the brain monoaminergic system in the mechanisms of conditioning is discussed.

5,7-Dihydroxytryptamine↗

PubMed1975

Specific effect of 5,6-dihydroxytryptamine on the monoamine fluorophore of the frog's gustatory cells.

A specific formaldehyde-induced yellow fluorescence, suggesting the presence of serotonin-like monoamine has been demonstrated in the gustatory cells of the frog. The fungiform papillae of frogs were examined fluorescence-histochemically after intraperitoneal injection of 5,6-dihydroxytryptamine. The results indicated that the fluorophore of gustatory cells was affected selectively by the drug injection: the yellow fluorescence was transiently enhanced 3 hours after the drug injection, thereafter being reduced rapidly. The effect of 5,6-dihydroxytryptamine was long-lasting with the reduction of the yellow fluorophore persisting at least for the experimental duration of 14 days. A single injection of 6-hydroxydopamine induced a complete depletion of noradrenaline fluorescence from adrenergic nerve terminals, while the fluorescence of gustatory cells was not affected by a high dose of the drug. The present results with pharmacologic treatments further support the view that the gustatory cell of the frog contains a serotonin-like monoamine.

5,6-Dihydroxytryptamine↗

PubMed1987

Morphological changes induced in turtle retinal neurons by exposure to 6-hydroxydopamine and 5,6-dihydroxytryptamine.

Following intraocular injection of the dopamine neurotoxin 6-hydroxydopamine (10-50 micrograms on two successive days in a Ringer vehicle containing ascorbate and pargyline) and an incubation period of 1 to 18 days, degeneration was noted in presumptive amacrine cells in the retina of the turtle, Pseudemys scripta elegans. Injection of vehicle alone produced no effect. Affected perikarya initially showed swollen mitochondria, lysosomes and distended cisternae. At later stages the cells took on a darkened appearance. In contrast, affected amacrine processes in the inner plexiform layer became markedly distended and lost their cytoplasmic contents, resulting in empty, very swollen profiles. No degeneration was noted distal to the affected cell bodies, i.e. the affected cells were not interplexiform neurons. Cells lesioned by 6-hydroxydopamine were shown to accumulate [3H]dopamine. Intraocular administration of 5,6-dihydroxytryptamine (a single dose of 10-40 micrograms in the same vehicle) followed by 4-6 days incubation resulted in a marked darkening of certain bipolar cell axon terminals, cell bodies and Landolt's clubs. The toxic effects of 5,6-dihydroxytryptamine were blocked by zimelidine, a serotonin uptake blocker. Thus, these two neurotoxins have different targets in the turtle retina. At the highest dose tested, however, 6-hydroxydopamine did produce degenerative changes in the presumed serotonergic bipolar cell.

5,6-Dihydroxytryptamine↗

PubMed1985

Up-regulation of serotonergic binding sites labeled by [3H]WB4101 following fimbrial transection and 5,7-dihydroxytryptamine-induced lesions.

Lesions of the serotonergic afferents to the hippocampus, by fimbrial transection or by 5,7-dihydroxytryptamine treatment, produce an increase in the Bmax of [3H]WB4101 to its nanomolar affinity binding site, with no effect on its picomolar affinity binding site or on [3H]prazosin binding. The nanomolar site is serotonergic as the serotonergic agonists, serotonin and 8-hydroxydipropylaminotetraline (8-OH-DPAT) have nanomolar affinity for [3H]WB4101 binding when studied in the presence of a prazosin mask (30 nM) of the alpha-1 component of [3H]WB4101 binding. The serotonin receptor antagonists metergoline, lysergic acid diethylamide and lisuride also have high nanomolar affinities while ketanserin, yohimbine, prazosin and noradrenergic agonists have affinities in the micromolar range. Fimbrial transection or 5,7-dihydroxytryptamine injections produced 32% and 44% increases in the Bmax of [3H]WB4101 binding in the presence of a prazosin mask. Serotonin competition for [3H]WB4101 binding was identical in control and experimental tissue from each lesion experiment. Although specific binding of [3H]WB4101 was increased, there was no change in the affinities or the percentages of the two binding components for serotonin competition with [3H]WB4101. These data suggest that removal of the serotonergic input to the hippocampus produces an increase in the Bmax of serotonin receptor binding sites labeled by [3H]WB4101.

5,7-Dihydroxytryptamine↗

PubMed1994

Differential effects of 5,7-dihydroxytryptamine-induced serotoninergic degeneration of 5-HT1A receptors and 5-HT uptake sites in the rat brain.

The time-course of 5,7-dihydroxytryptamine-induced lesions (2, 5 and 14 days after i.c.v. injection of 150 micrograms) and the effects of acute reserpine treatment (10 mg/kg, i.p., one or 5 days before scheduled death), were evaluated by autoradiography of [3H]paroxetine binding sites in the rat brain. Reserpine had no significant effect on [3H]paroxetine binding, indicating that the depletion of serotonin is not sufficient per se to alter the serotonin uptake sites in any region. Two days after the 5,7-dihydroxytryptamine lesion, [3H]paroxetine binding was already decreased in the majority of brain regions. In the caudate putamen these binding sites were significantly decreased only 14 days after the lesion, whereas the ventral tegmental area (or the enclosed median forebrain bundle), the dorsal raphe (mainly the ventral portion) and the median raphe maintained their high density of serotonin uptake sites even after 14 days. Results were similar using [3H]citalopram as ligand for the serotonin uptake sites, in the brains of rats lesioned 5 days before death; an exception was the ventral portion of the dorsal raphe, where there was a significant increase with [3H]paroxetine and a decrease with [3H]citalopram binding. In adjacent sections of the same brains we also measured [3H]8-OH-DPAT binding, confirming that it completely disappears in the dorsal raphe after the lesion. Thus, considering the extent of serotonin cell body degeneration, there appears to be a paradoxical mismatch between the excessive loss of [3H]8-OH-DPAT binding and the resistance of [3H]citalopram or [3H]paroxetine binding in the dorsal raphe, suggesting that the two binding sites may undergo adaptive regulation in surviving neurons.

5,7-Dihydroxytryptamine↗

PubMed1990

Further insights into the oxidation chemistry and biochemistry of the serotonergic neurotoxin 5,6-dihydroxytryptamine.

The neurodegenerative properties of the serotonergic neurotoxin 5,6-dihydroxytryptamine (5,6-DHT) are widely believed to result from its autoxidation in the central nervous system. The autoxidation chemistry of 5,6-DHT has been studied in aqueous solution at pH 7.2. The reaction is initiated by direct oxidation of the indolamine by molecular oxygen with resultant formation of the corresponding o-quinone 1 and H2O2. A rapid nucleophilic attack by 5,6-DHT on 1 leads to 2,7'-bis(5,6-dihydroxytryptamine) (6) which is more rapidly autoxidized than 5,6-DHT to give the corresponding diquinone 7 along with 2 mol of H2O2. The accumulation of 6 in the reaction solution during the autoxidation of 5,6-DHT despite its more rapid autoxidation indicates that diquinone 7 chemically oxidizes 5,6-DHT (2 mol) to quinone 1 so that an autocatalytic cycle is established. The H2O2 formed as a byproduct of these autoxidation reactions can undergo Fenton chemistry catalyzed by trace transition metal ion contaminants with resultant formation of the hydroxyl radical, HO., which directly oxidizes 5,6-DHT to a radical intermediate (9a/9b). This radical is directly attacked by O2 to yield quinone 1 and superoxide radical anion, O2.-, which further facilitates Fenton chemistry by reducing, inter alia, Fe3+ to Fe2+. A minor side reaction of 1 with water leads to formation of at least two trihydroxytryptamines. Diquinone 7 ultimately reacts with 6, 5,6-DHT, and perhaps trihydroxytryptamines, leading via a sequence of coupling and oxidation reactions to a black indolic melanin polymer. Enzymes such as tyrosinase, ceruloplasmin, and peroxidase and rat brain mitochondria catalyze the oxidation of 5,6-DHT to form dimer 7 and, ultimately, indolic melanin. The role of the autoxidation and the enzyme-mediated and mitochondria-promoted oxidations of 5,6-DHT in expressing the neurodegenerative properties of the indolamine are discussed.

5,6-Dihydroxytryptamine↗

PubMedDate not supplied

The cardiovascular effects of intraventricular 5,6-dihydroxytryptamine in conscious hypertensive rats.

1. Conscious experimental hypertensive rats injected intraventricularly with 5,6-dihydroxytryptamine (50 microgram) responded with a rapid and long-lasting (4 days) fall in blood pressure and this was accompanied by a bradycardia of similar duration. 2. The acute actions of 5,6-dihydroxytryptamine on the cardiovascular system were not modified by pretreatment with bromolysergide (0.5 mg/kg, i.p.), methysergide (2.5 mg/kg, i.p.) or intraventricular phentolamine (200 microgram). 3. The results suggest that central serotonergic neurones play an important role in the regulation of blood pressure. However, the site of action remains to be investigated.

5,6-Dihydroxytryptamine↗