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At least 19 recordsLinked to original sources
PubMed1976

Cerebral arterial spasm. Part 4: in vitro effects of temperature, serotonin analogues, large nonphysiological concentrations of serotonin, and extracellular calcium and magnesium on serotonin-induced contractions of the canine basilar artery.

In vitro experiments were performed using a small volume chamber to study serotonin-induced contractions of the canine basilar artery. Temperature was found to have a profound effect on the artery's response to serotonin. Raising the temperature to 40 degrees C (104 degrees F) increased the maximum response by 20% and lowering the temperature by 10 degrees C caused a 40% reduction in the maximum contraction. Cumulative log-dose response curves for analogues of serotonin demonstrated a high degree of specificity for the serotonin receptor and large nonphysiological concentrations of serotonin caused relaxation of the contracted artery. Extracellular calcium was shown to be an absolute requirement for serotonin-induced contractions. Extracellular magnesium, in contrast, was shown to inhibit serotonin-induced contractions.

Animals↗
PubMed1978

Release of endogenous serotonin from two identified serotonin-containing neurones and the physiological role of serotonin re-uptake.

1. The amounts of endogenous serotonin (5-HT) released into the medium by the cerebro-buccal ganglionic ring of Aplysia californica incubated in artificial sea water (ASW) were measured. The rate of spontaneous 5-HT release varied between 0.4 and 1.2 p-mole per hour, which is less than 1% of the total 5-HT present in this preparation.2. Direct stimulation of the ordinarily silent 5-HT-containing giant cerebral neurones resulted in a 80-100% increase of the 5-HT released, but only when the 5-HT uptake was blocked by chlorimipramine (1-10 muM).3. High K(+) media (50 mM) also caused a significant increase in the amount of 5-HT released from the preparation provided that chlorimipramine (1-10 muM) was present in the incubation fluid.4. Co(2+) ions (10-30 mM) added to the incubating medium blocked the spontaneous leak of endogenous 5-HT as well as the release, in the presence of chlorimipramine, evoked either by stimulation of the 5-HT-giant cerebral neurones or high K(+)-media.5. In the presence of chlorimipramine or desmethylimipramine, the duration and/or the amplitude of the excitatory or the inhibitory synaptic potentials evoked in the buccal neurones by the stimulation of the 5-HT giant cerebral neurones were markedly enhanced.6. These results strongly support the idea that 5-HT is the synaptic transmitter released at the excitatory and inhibitory junctions established by the 5-HT giant cerebral neurones in the ipsilateral buccal ganglia. In addition, they underline the role of amine re-uptake in the physiological inactivation of 5-HT as a transmitter.

Action Potentials↗
PubMed1978

Effect of 1-(m-trifluoromethylphenyl)-piperazine on 3H-serotonin binding to membranes from rat brain in vitro and on serotonin turnover in rat brain in vivo.

1-(m-Trifluoromethylphenyl)-piperazine inhibited the specific binding of tritiated serotonin to membranes from rat brain in vitro at lower concentrations than did quipazine or MK-212 (6-chloro-2-[1-piperazinyl]-pyrazine). In rats 1-(m-trifluoromethylphenyl)-piperazine decreased the concentration of 5-hydroxyindoleacetic acid (5-HIAA) without altering the concentration of serotonin in whole brain. The decrease in 5-HIAA was apparently due to a decrease in serotonin turnover, since 1-(m-trifluoromethylphenyl)-piperazine caused a slower decline in serotonin concentration after synthesis inhibition by alpha-propyldopacetamide and a slower accumulation of 5-HIAA after probenecid injection to block its efflux from brain. The decrease in serotonin turnover is an expected result of stimulating serotonin receptors in brain and has earlier been reported to occur with quipazine. Thus all of the results are compatible with the idea that 1-(m-trifluoromethylphenyl)-piperazine acts as a serotonin receptor agonist in rat brain.

Animals↗
PubMed1976

Is the serotonin binding protein (SBP) a soluble storage form for serotonin?

The binding of serotonin to a soluble, high affinity binding protein (SBP) present in synaptosomes and assoicated with serotonergic tracts, has now been studied for the effect of drugs and, in particular, drugs interacting with contractile proteins. Vincristine, vinblastine, and cytochalasin B were found to cause 50% inhibition of serotonin binding to SBP at 1.5 X 10(-6)M, 7.5 X 10(-6)M and 50 X 10(-6)M, respectively. Colchicine did not affect the binding at 1 X 10(-3)M. When vinblastine was injected intraventricularly, the binding capacity of SBP isolated from brain 20 and 26 hours after injection was decreased 42% and 60% respectively. It is concluded that SBP is an actin-like contractile protein, distinct from microtubulin, and not associated with membranes. The storage of serotonin through binding to a protein with such properties suggests that this compartment is in some way involved in the translocation or transfer of serotonin from one part of the cell to another.

Animals↗
PubMed1977

[On the mode of action of serotonin in the isolated atrium of the hamster. I. Serotonin: amine of mixed action (author's transl)].

5-hydroxytryptamine (serotonin) produces a positive chronotropic effect in the isolated atrium of the hamster. The characterization of this effect using reserpine pretreatment, propranolol, pargyline, 6-hydroxydopamine or the combination of some of those drugs enable us to conclude that serotonin is an amine of mixed action in the isolated atrium of the hamster, that is, its positive chronotropic effect has a direct component, which is obtained with lower concentrations of agonist and an indirect component through the liberation of endogenous noradrenaline from the sympathetic nerve terminals. The highest concentrations of serotonin are responsible of that component. Pargyline potentiates the indirect component of 5-HT, because inhibition of intraneuronal monoamine oxidase (MAO) avoids the degradation of the noradrenaline released, but it does not potentiate the direct component, indicating that postsynaptic cardiac MAO has little importance in the metabolism of serotonin administered exogenously.

Animals↗
PubMed1977

Serotonin and dopamine as neurotransmitters in mytilus: block of serotonin receptors by an organic mercurial.

The effects of mersalyl, bromo-LSD (BOL) and methysergide (UML) on the relaxation of catch by certain indole and catechol derivatives were studied in the anterior byssus retractor muscle of Mytilus. Mersalyl antagonized relaxation in response to serotonin whereas BOL and UML were less effective. Two other indole derivatives, ergotamine and gramine, were also blocked by mersalyl; BOL and UML antagonized relaxation in response to dopamine more effectively than did mersalyl. Two other catechols, epinephrine and norepinephrine, were also blocked more effectively by BOL and UML than by mersaly. Relaxation in response to neural stimulation was blocked more effectively by mersalyl than by BOL. The blocking action of mersalyl on neural relaxation reversed very poorly after washing the drug, but complete reversal was induced by brief exposure to dithiothreitol. It is concluded that the evidence supports an hypothesis that the transmitter released by relaxing nerves is serotonin. It is suggested that mersalyl blocks serotonin by combining with a sulfhydryl group at or near the site on the receptor to which the indole nitrogen attaches.

Acetylcholine↗
PubMed1979

Corticosteroidogenesis by isolated human adrenal cells: effect of serotonin and serotonin antagonists.

The direct effect of serotonin and antiserotonin agents on adrenal steroid biosynthesis was studied in isolated adrenal cells derived from patients with Cushing's syndrome. The results indicate that serotonin increases corticosterone production, while the serotonin antagonists cyproheptadine and methysergide depress adrenal steroid - particularly cortisol and aldosterone - biosynthesis.

Adrenal Cortex↗
PubMed1977

A comparative analysis of methods suitable for detection of platelet alloantibodies: inhibition of 14C-serotonin uptake, 14C-serotonin release and microcomplement fixation.

Three HLA-specific antisera were comparatively analyzed by platelet microcomplement fixation and 14C-serotonin uptake and/or 14C-serotonin release studies with platelets. In general, there was a good correlation of HLA antibody specificity exhibited in all 3 test systems. Quantitative differences in the response of platelets to HLA antisera were observed and accounted for by differences in antigen density and different types of antibodies involved. Platelet autoantibodies could not be detected by means of 14C-serotonin release from platelets in plasma.

Antibody Specificity↗
PubMedDate not supplied

[Blood serotonin level in sciatica and the serotonin theory of migraine pathogenesis].

The blood serotonin level was determined by the fluorescent method of Ashcroft in 13 patients with sciatic pains during the pains and after the disappearance. The serotonin level was usually higher at the time of pains. In the discussion the author reminds that serotonin level falls during a migrainous attack and points out that the results of the present study confirm the specificity of sertonin level fall in migraine.

Adult↗
PubMed1979

Reduction of whole blood serotonin in depressed patients treated with a new, selective serotonin-uptake inhibitor, femoxetine.

Femoxetine, a phenylpiperidine derivative with potent serotonin (5-HT)-uptake inhibitory properties, was investigated in 12 depressive patients for its clinical effect as well as its effect on 5-HT concentration in whole blood. The global evaluation after 6 weeks showed a good effect in six patients. The 5-HT concentration was found to be reduced from a mean value of 0.21 to about 0.05 micrograms/ml, indicating a total depletion of 5-HT from the thrombocytes. The steady-state concentrations of femoxetine resulted in reduction of 5-HT to the same level in all patients. No correlation between degree of 5-HT reduction and therapeutic effect was found.

Anisoles↗
PubMedDate not supplied

The effect of serotonin receptor blocking agents--cyproheptadine and danitracen--on serotonin turnover in the rat brain.

Cyproheptadine (CPH), 0.5 mg/kg ip, did not affect the cerebral serotonin (5-HT) level, but elevated the level of 5-hydroxyindoleacetic acid (5-HIAA). Danitracen (DN), 1 mg/kg ip, depressed the cerebral 5-HT level and elevated the 5-HIAA level, but at a dose 10 mg/kg did not affect the levels of either the amine, or its metabolite. Both CPH and DN, 1 mg/kg, significantly potentiated the disappearance of 5-HT after administration of p-chlorophenylalanine. DN, in a low dose, accelerated the disappearance of 5-HT after inhibition of 5-HT synthesis by alpha-propyldopacetamide. The rate of accumulation of 5-HIAA after probenecid, was increased only by CPH. CPH did not affect the 5-HT accumulation after pargyline, while DN depressed its accumulation. The results of experiments on the levels of 5-HT and 5-HIAA, and on the rate of disappearance of 5-HT after inhibition of tryptophan decarboxylase suggest that CPH and DN increase the 5-HT turnover. The results of studies on the turnover rate of 5-HT after administration of probenecid and parygline do not corroborate fully this assumption. Possibly, this discrepancy may depend on differences in the action of 5-HT in various brain areas and interaction of serotoninolytics tested with effects of the MAO inhibitor.

Amides↗
PubMed1978

Effect of p-chlorophenylalanine on cerebral serotonin binding, serotonin concentration and motor activity in the rat.

The effect of p-chlorophenylalanine (PCPA) on the specific binding of 3H-serotonin (5-HT) was investigated in crude membrane preparations of the rat forebrain. The level of cerebral 5-HT and 5-hydroxyindoleacetic acid were concomitantly determined. A single dose of PCPA (300 mg/kg i.p.) increased specific binding at a low concentration of 3H-5-HT within 24 h by more than 100%. The time course of the elevation of specific binding was mirrored by the reduction in the 5-HT level. However, 8--10 days after drug administration, specific binding was close to the control level, while 5-HT was still significantly reduced. A Scatchard analysis revealed that the apparent affinity was significantly increased (KD reduced) during the initial period after PCPA administration, whereas the number of binding sites (BMax) was little changed. In contrast, after reported injections of PCPA (3 injections of 300 mg/kg at 6--8 day intervals, or 100 mg/kg/day for up to 12 days) leading to a prolonged 5-HT depletion, BMax was significantly increased, while KD tended to be restored towards the baseline level. Daily injections of PCPA (100 mg/kg) for 12 days resulted in a transitory increase in day-time motor activity with a maximum on drug day 3, and in a persistent reduction of night-time activity. It is concluded that the initial PCPA-induced decrease in KD was due to a reduced competition for binding sites by the endogenous 5-HT, whereas the increase of BMax after a prolonged 5-HT depletion may reflect a 5-HT receptor supersensitivity.

Animals↗
PubMed1978

Effects of serotonin, of its biosynthetic precursors and of the anti-serotonin agent metergoline on the release of glucagon and insulin from rat pancreas.

We have evaluated the effect of serotonin (5-HT) and of its biosynthetic precursors 5-Hydroxytryptophan (5-HTP) and tryptophan (TRP) on the release of immunoreactive glucagon (IRG) and insulin (IRI) from isolated islets and pieces of pancrease of the rat. In isolated islets, 5-HT inhibited the IRI response to a high glucose concentration (3.0 mg/ml), without affecting the IRG response to either a low (0.5 mg/ml) or a high glucose concentration; TRP stimulated the IRG and IRI response to the low glucose concentration, while 5-HTP was ineffective. When pieces of pancreas were used, 5-HT and 5-HTP inhibited IRG response to both glucose concentrations, while IRI release was inhibited only by 5-HT. The anti-5-HT agent metergoline enhanced the release of IRG and IRI by pieces of pancreas at both glucose concentrations. The results indicate that exogenous and endogenous 5-HT inhibit basal as well as glucose-mediated IRG and IRI release; that isolated islets are less sensitive than pieces of pancreas to the inhibitory effect of 5-HT and that TRP acts as an amino acid and not as a precursor of 5-HT.

5-Hydroxytryptophan↗
PubMed1978

Participation of serotonin in the phasic release of luteinizing hormone. II. Effects of lesions of serotonin-containing pathways in the central nervous system.

Circadian LH variations were measured in castrated, estradiol-implanted female rats bearing lesions of the raphe nuclei, in which most serotonin (5-HT) containing ascending projections originate, or mediopontine transections interrupting such projections before they enter the hypothalamus. Previous data indicated that pharmacological blockade of 5-HT biosynthesis abolishes the rhythmic pattern of LH secretion; the present study was intended to check whether surgical depletion of hypothalamic 5-HT had a similar effect and whether such abolition could be correlated with hypothalamic or forebrain endogenous concentrations of the amine and of its metabolite, 5-hydroxyindoleacetic acid (5-HIAA). Maximal inhibition of hypothalamic 5-HT and 5-HIAA concentrations were obtained after complete basal mediopontine transections and after lesions of the medial and the dorsal raphe nuclei; under these conditions, the daily variations in plasma LH were reduced by more than 70%. Smaller lesions, even when they completely destroyed the medial raphe, were much less effective. A good correlation was observed between the amplitude of the LH cycle and the extent of hypothalamic, but not of forebrain, 5-HT and 5-HIAA depletion. However, and in contrast to the results of pharmacological 5-HT inhibition, the cyclic pattern of LH secretion could not be totally abolished by any of these surgical procedures. It is concluded that the dorsal raphe contributes to the regulation of rhythmic LH secretion in castrated female rats bearing estradiol implants by modulating the amplitude of this circadian cycle rather than by generating the rhythmic pattern itself.

Animals↗
PubMed1978

Participation of serotonin in thyrotropin release. I. Evidence for the action of serotonin on thyrotropin releasing hormone release.

Injection of serotonin (5-HT) into the third ventricle of the rat resulted in a rapid increase of serum TSH; a significant effect was observed 5 min after injection, whereas the maximal effect appeared 10 min after the injection of 1 microgram 5-HT. This stimulating effect of 5-HT was completely prevented by pretreatment with cyproheptadine, a blocker of 5-HT receptors, whereas fluphenazine, a dopamine receptor blocker, was unable to block it. Third venticle injection of 5-HT in rats bearing anterior hypothalamic lesions (which did not affect the suprachiasmatic nucleus or the medio-basal hypothalamus) also induced an increase of serum TSH similar to that observed in normal rats despite the fact that these animals show a lower basal TSH. In vitro, the addition of 5-HT to an incubation medium containing one hemi-anterior pituitary did not modify medium TSH, whereas 5-HT addition induced an increase of medium TSH in the system containing one hemi-anterior pituitary and two hypothalami. We conclude that 5-HT acts on TSH function probably through a stimulation of TRH release.

Animals↗
PubMed1979

Participation of serotonin in thyrotropin release. II. Evidence for the action of serotonin on the phasic release of thyrotropin.

During a 12-h light 12-h dark schedule (lights off at 1900 h), male Sprague-Dawley rats show a circadian rhythm of plasma TSH with a zenith near midday. The participation of serotonin (5HT) in the phasic release of TSH was studied using both pharmacological and surgical-stereotaxical approaches. Animals treated with parachlorophenylalanine methyl ester (pCPA), an inhibitor of 5HT synthesis (one or two injections of 250 mg/kg each) showed a reduction or a disappearance of the diurnal peak of TSH, respectively. Additional treatment by 5-hydroxytryptophan, a precursor of 5HT, completely, restored the diurnal TSH peak. Treatment with 5,6-dihydroxytryptamine creatine sulfate, a neurotoxin which selectively destroys 5HT terminals, also induced alterations of the diurnal peak of TSH. There were no major modifications observed in the low nocturnal levels of TSH in rats treated with pCPA, 5-hydroxytryptophan, or 5,6-dihydroxytryptamine. The major serotoninergic innervation of the hypothalamus originates from the raphe dorsalis or centralis; destruction of these two nuclei caused a quasiabolition of the diurnal TSH peak (only a low amplitude TSH circadian rhythm persisted). Hypothalamic 5HT content was measured in the majority of these experiments; the greatest depletions (near 90%) were observed after two injections of pCPA or in rats bearing raphe lesions. We conclude that the diurnal peak of TSH, observed during the physiological circadian rhythm, is serotoninergic dependent.

5,6-Dihydroxytryptamine↗
PubMed1979

Re-evaluation of the uptake of desoxyfructo-serotonin by human platelets, and of its effect on the uptake of serotonin.

Employing C14-glucose and C14-serotonin (5HT) as precursors, we have synthesized desoxyfructo-5HT [1-desoxy-1-(5-hydroxytryptamine)-D-fructose] labelled either in the sugar or 5HT moieties, and examined the uptake of the labelled substrate by washed human platelets. Desoxyfructo-5HT appears to interact with the 5HT uptake site, effectively inhibiting the uptake of H3-5HT. However, our data indicate that contrary to published reports, the entry of desoxyfructo-5HT into platelet vesicles or cytoplasm is negligible.

Biotransformation↗