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PubMed2003

[Serotonin dysfunctions in the background of the seven deadly sins].

The symbolic characters of the Seven Deadly Sins can be traced from time to time in the cultural history of human mankind, being directly specified in certain artistic products. Such are, among others, the painting entitled "The Seven Deadly Sins and the Four Lost Things" by Hieronymus Bosch and the poems Divina Commedia and The Foerie Queene by Dante Alighieri and Edmund Spenser, respectively. However, there are several paragraphs referring to these behaviours of the Seven Deadly Sins in the Bible and in the dramas of William Shakespeare. The objective of the present review is to propose that dysfunctions in the central serotonergic system might be involved in the neurobiology of these 'sinful' behaviour patterns. Evidences indicate that behaviour traits such as Accidia (Sloth), Luxuria (Lust, Lechery), Superbia (Pride), Ira (Wrath, Anger), Invidia (Envy), Avaritia (Greed, Avarice), and Gula (Gluttony) can relate to the functional alterations of serotonin in the brain. Results of biochemical and molecular genetic (polymorphism) studies on the human serotonergic system (receptor, transporter, enzyme), findings of functional imaging techniques, effects of depletion (or supplementation) of the serotonin precursor tryptophan, data of challenge probe investigations directed to testing central serotonergic functions, alterations in the peripheral serotonin measures (platelet), and the changes in the CSF 5-hydroxy-indoleacetic acid content indicate such serotonergic involvement. Furthermore, results of animal experiments on behaviour change (aggressive, dominant or submissive, appetite, alcohol preference) attributed to serotonin status modification and the clinically evidenced therapeutic efficacy of pharmacological interventions, based on the modulation and perturbation of the serotonergic system (e.g. selective serotonin reuptake inhibitors), in treating the 'sinful' behaviour forms and analogous pathological states reaching the severity of psychiatric disorders (depression, sexual disturbances, social phobia, impulsivity-aggression, obsessive-compulsive and related spectrum disorders, paranoid jealousy, eating disorders) all strongly suggest the possibility that brain serotonin dysfunctions might underlie the neurophysiology of the Seven Deadly Sins.

Behavior↗
PubMed1992

Mechanisms by which cancer chemotherapeutic drugs induce emesis.

Because the area postrema seems essential for chemotherapy-induced vomiting, both circulating and/or neurally mediated stimuli in this area could trigger the emetic response. In our laboratories results of cross-circulation and direct intracerebroventricular infusion experiments in dogs do not support a role for circulating substances. The large increases in serum vasopressin induced by cisplatin were not blocked by inhibitors of the angiotensin-converting enzyme. In the ferret inhibition of serotonin synthesis with p-chloro-phenylalanine, administration of selective antagonists of 5-hydroxy-tryptamine3 (5-HT3) receptors, or visceral deafferentation inhibited the emetic response evoked by cisplatin or high-dose cyclophosphamide. The results suggest that serotonin plays an important role and that peripheral neural mechanisms are involved in the emetic response. The strong antiemetic efficacy of selective 5-HT3 antagonists also has been confirmed in humans. In cancer patients high-dose cisplatin increased the plasma and urinary levels of 5-hydroxy-indoleacetic acid (5-HIAA), but did not affect platelet and free plasma serotonin. The changes in 5-HIAA levels paralleled the onset and development of vomiting. No evidence of serotonin depletion has been obtained after high-dose cisplatin. Dacarbazine, another strongly emetogenic agent, increased urinary 5-HIAA; however, only small increases in 5-HIAA were produced with low-dose cisplatin or cyclophosphamide-containing regimens. Thus, emetogenicity appears to be directly related to the ability of the cytotoxic agent to release serotonin. In humans, antiemetics such as ondansetron, metoclopramide, and dexamethasone did not effect high-dose cisplatin-induced increases in serotonin metabolism. Therefore, these antiemetics seem not to affect the amount of serotonin released. The mechanism by which chemotherapeutic drugs induce serotonin release is unknown; however, release may occur by direct cytotoxicity on the gastrointestinal mucosa, including the enterochromaffin cells. Delayed emesis appears to be mediated by 5-HT3-independent mechanisms. It is proposed that emesis that develops despite high-dose ondansetron (residual emesis) should be considered delayed emesis. Residual and delayed episodes of emesis have similar time courses, are characterized by very mild emetic episodes and poor response to 5-HT3 antagonists, and are not associated with increases in serotonin metabolism.

Animals↗
PubMed2006

[Endogenous nociceptin level in ischemic stroke: connection to serotonin system].

Particular role of the heptadecapeptide nociceptin (orphanin FQ), the endogenous agonist of the NOP receptor, has been widely demonstrated in the regulation of pain sensation and anxiety-related behavior. In our best knowledge this is the first study reporting plasma nociceptin levels in 26 acute stroke and 6 transiens ischemic attack (TIA) patients. We have found significantly elevated plasma nociceptin levels in all the three groups of patients studied (stroke influencing the carotis or the lacunar region and TIA). We suggest that elevated plasma nociceptin level is the consequence of stroke as in the group of patients recovered from previous stroke was found similar the control value. Plasma serotonin level was found non-significantly decreased in patients with stroke influencing the lacunar region and TIA patients. However the plasma 5-hydroxy-indoleacetic acid (5HIAA) levels were found significantly elevated in patient groups with stroke influencing both the carotis and the lacunar regions. Data may serve as further evidence for the serotonergic dysregulation in stroke.

Acute Disease↗
PubMed1991

[Treatment with octreotide (SMS 201-995) in a case of intestinal carcinoid tumor].

Over the past few years the usefulness of some somatostatin's analogues in the treatment of intestinal tract endocrine tumors has been demonstrated. Notwithstanding, the results obtained are variable. The case of a carcinoid tumor with a hepatic metastasis is presented and its clinical as well as its biochemical and its morphological results are evaluated after treatment with octreotide over a seven months period. It is important to highlight the great clinical improvement obtained at the beginning of treatment. Treatment was not effective in the control of tumor progression. After the injection of such a drug, a decrease in serotonin and 5-hydroxy-indoleacetic acid serum levels was observed as well as a reduction in the urinary metabolite. It is concluded that octreotide is very useful for the symptomatic treatment of carcinoid syndrome.

Aged↗
PubMedDate not supplied

Effects of indeloxazine hydrochloride on behavioral and biochemical changes in the chronic phase of focal cerebral ischemia in rats.

The effects of a new cerebral activator, indeloxazine hydrochloride, on behavioral, electroencephalographic and biochemical changes were investigated during the chronic phase in rats subjected to left middle cerebral artery occlusion. Disturbance of the one-trial passive avoidance task and neurological deficits were present for 14 days after middle cerebral artery occlusion, while no significant changes in spontaneous motor activity and electroencephalogram in the cerebral cortex were observed. Significant decreases in the content of serotonin and norepinephrine in the frontal cortex, of norepinephrine and 3-methoxy-4-hydroxy-phenylethylglycol in the hippocampus, and of 3-methoxy-4-hydroxy-phenylethylglycol in the corpus striatum on the occluded side were observed on day 14 after surgery. Oral administration of the test drug was started from day 7 after surgery and was repeated once a day for 8 days. Indeloxazine (10 or 20 mg/kg) significantly prolonged the latency of step-through in the passive avoidance test and desynchronized the spontaneous electroencephalogram without affecting neurological deficits. Indeloxazine (10 or 30 mg/kg) caused significant increases in serotonin and decreases of 5-hydroxy-indoleacetic acid in the bilateral frontal cortex and hippocampus and contralateral corpus striatum. Indeloxazine (30 mg/kg) increased norepinephrine in the contralateral frontal cortex and bilateral hippocampus and decreased 3-methoxy-4-hydroxy-phenylethylglycol in the contralateral hippocampus. Thus, we found that indeloxazine ameliorated cerebral function in the chronic ischemic model. From the present results, it is suggested that the pharmacological action of indeloxazine may be attributable to its enhancing action on central monoaminergic systems.

Animals↗
PubMed1977

Influence of dibutyryl cyclic AMP on the level of catecholamines and 5-hydroxytryptamine in discrete areas of rat brain.

Dibutyrul cyclic AMP (dbcAMP) was injected intracerebroventricularly into rats in doses of 50, 100 or 200 microgram. Noradrenaline (NA), dopamine (DA), 5-hydroxytryptamine (5-HT) or 5-hydroxy indoleacetic acid (5-HIAA) concentrations were measured spectrophotofluorimetrically in discrete brain areas: cortex, hypothalamus, striatum, hippocampus with nucleus amygdala and nucleus accumbens (limbic system) and pons with medulla oblongata. DbcAMP (in each dosage administered) decreased, NA content of cortex and of pons with medulla oblongata. NA content in the hypothalamus and striatum was decreased only after the largest dose of dbcAMP. In the limbic system NA concentration was diminished after a dose of 100 or 200 microgram of dbcAMP. There was a decrease in DA level measured in the striatum alone after a dose of 100 microgram of dbcAMP. 5-HT concentration was increased in the striatum and the pons with medulla oblongata after each dose level of dbcAMP; in the cortex after a dose of 50 and 100 microgram; and in the hypothalamus after a dose of 200 microgram. 5-HIAA level was increased in the striatum, limbic system, pons with medulla oblongata after all doses of dbcAMP. We conclude that dbcAMP affects presynaptic central catecholaminergic and serotoninergic neurons in an opposite, manner, although discrete brain areas have a different susceptibility to dbcAMP action. These findings provide some explanation for the behavioural effects of dbcAMP.

Animals↗
PubMed1976

Analysis for indole compounds in urine by high-performance liquid chromatography with fluorometric detection.

We describe a chromatographic system involving a high-performance chemically-bonded reverse-phase column and fluorescence detection for measurement of indoles in urine. We controlled retention and selectivity by optimizing the methanol content and pH of the mobile phase. Six reference indoles were separated in less than 20 min; three 5-hydroxyindoles were eluted in less than 7 min. About 5-15 ng of aqueous solutions of these compounds can be detected. The combination of selectivity (from use of the chromatographic column) and fluorescence detection permitted analysis for five of the six indoles after a single urine-deproteinization step.

5-Hydroxytryptophan↗
PubMed1986

Inhibition of monoamine oxidase by viloxazine in rats.

Biochemical and pharmacological investigations about the effect of the antidepressant drug viloxazine (Vivalan) on catecholamine metabolism in rats led to the following results: Viloxazine exerts a dose and time dependent inhibition of monoamine oxidase activity of brain and liver mitochondrial fraction and tissue homogenates of hypothalamus, heart, liver, and adrenal glands, both in vitro and after oral and parenteral administration in vivo. Consequently, an increase in catecholamine concentrations in brain of rats could be observed after pretreatment with viloxazine. In addition brain serotonin concentrations rose and 5-hydroxy-indoleacetic acid was diminished. However, characterization of inhibition of monoamine oxidase activity by viloxazine in vitro revealed: Compared to the specific inhibitors clorgyline for MAO-A- and pargyline for MAO-B-activity, viloxazine was a very weak inhibitor both for MAO-A and MAO-B in vitro. The type of inhibition was competitive and reversible. From the presented results and the results obtained by other laboratories it is concluded that inhibition of monoamine oxidase activity by viloxazine, although clearly demonstrated in animal experiments, may not be the only mechanism for an antidepressant action of the drug in man.

Animals↗
PubMedDate not supplied

[Features of indoleamine metabolism in adolescent girls with delayed sexual development].

Indolamine metabolism was studied in 203 patients with retarded sexual development of different genesis and in 116 girls of the same age. Considerable disorders in the level of serotonin and the products of its metabolism: 5-oxy-indoleacetic acid and melatonin, a hormone synthesized by the pineal gland--were found in abnormal sexual maturation. The nature of revealed changes depended, to a large extent, on genesis of disease which could be used for differential diagnosis of different forms of retarded sexual development. Possible involvement of indolamines in pathogenetic mechanisms ensuring the formation of a pathological process, was discussed.

Adolescent↗