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Results for “5,6-Dihydroxytryptamine”

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At least 37 records · Page 2Linked to original sources
PubMed1975

Microspectrofluorimetric analysis of the formaldehyde induced fluorescence in midbrain raphe neurons.

The formaldehyde induced fluorescence in perikarya localized in the midbrain rephe nuclei was investigated using the Falck-Hillarp technique in combination with qualitative (spectral analysis) and quantitative microspectorfluorimetry. The spectral evidence obtained after various pharmacological and lesion experiments with the neurotoxic compounds 5,6-dihydroxytryptamine and 5,7-dihydroxytryptamine, strongly favours the view that the vast majority of the perikarya in the cell groups B-7, B-8 and B-9 (according to Dahlström and Fuxe) are 5-hydroxytryptamine neurons, defined as structures capable of synthesizing, metabolizing, and storing 5-hydroxytryptamine. The spectral data indicate that the 5-hydroxytryptamine neurons might contain in addition to 5-hydroxytryptamine another indolealkylamine, possibly tryptamine, in low concentrations. The perikarya were shown to be able to take up and accumulate exogenously administered 6-hydroxytryptamine provided that monoamine oxidase was inhibited. Quantitative microfluorimetric analysis disclosed that the tryptophan hydroxylase inhibitor p-chlorophenylalanine was unable to block effectively this enzyme in the 5-hydroxytryptamine perikarya, although acutely a partial blockade was observed. The 5-hydroxytryptamineerogenously to the action of p-chlorophenylalanine and this might be associated with different states of neuronal activity. The difference in potency of p-chlorophenylalanine as regards tryptophan hydroxylase inhibition in perikarya and in nerve terminals may be related to different properties of tryptophan hydroxylase in various parts of the neuron and/or to a high turnover of the enzyme in the perikarya.

5-Hydroxytryptophan↗
PubMed1975

Serotonin content in the central nervous system of rats and cholinergic tremor.

Oxotremorine did not alter the level of 5-HT and 5-hydroxyindoleacetic acid in different brain regions. The content of 5-HT in the striatum was diminished by electrolytic lesions of the raphe system, by microinjection of the selective depletor 5,6-dihydroxytryptamine into the raphe system and inhibition of synthesis by pCPA or pCAM. The intensity of oxotremorine-induced tremor was reduced only in some experimental groups without clear-cut correlation to the decreased 5-HT levels. In pCPA-pretreated animals resoring of 5-HT concentration by intrastriatal microinjection of 5-HT and ip administration of 5-HT did not reestablish tremor intensity. There is no evidence that cholinergic tremor is triggered indirectly and depends upon an intact 5-HT system.

Animals↗
PubMed1978

Serotonin neurons of the midbrain raphe: ascending projections.

The ascending projections of serotonin neurons of the midbrain raphe were analyzed in the rat using the autoradiographic tracing method. Axons of raphe serotonin neurons ascend in the ventral tegmental area and enter the medial forebrain bundle. A number of fibers leave the major group to ascend along the fasciculus retroflexus. Some fibers enter the habenula but the majority turn rostrally in the internal medullary lamina of the thalamus to innervate dorsal thalamus. Two additional large projections leave the medial forebrain bundle in the hypothalamus; the ansa peduncularis-ventral amygdaloid bundle system turns laterally through the internal capsule into the striatal complex, amygdala and the external capsule to reach lateral and posterior cortex, and another system of fibers turns medially to innervate medial hypothalamus and median eminence and form a contrelateral projection via the supraoptic commissures. Rostrally the major group in the medial forebrain bundle divides into several components: fibers entering the stria medullaris to terminate in thalamus; fibers entering the stria terminalis to terminate in the amygdala; fibers traversing the fornix to the hippocampus; fibers running through septum to enter the cingulum and terminate in dorsal and medial cortex and in hippocampus; fibers entering the external capsule to innervate rostral and lateral cortex; and fibers continuing forward in the medial olfactory stria to terminate in the anterior olfactory nucleus and olfactory bulb.

5,6-Dihydroxytryptamine↗
PubMed1979

The antinociceptive effect of intracerebroventricularly administered prostaglandin E1 in the rat.

It is generally accepted that prostaglandins (PGs) are nociceptive substances. However, earlier studies from this laboratory indicated that morphine analgesia, in the rat, was not only serotonin mediated, but involved PGs as well. Several PG synthesis inhibitors were shown to inhibit morphine analgesia and PGE1 was shown to potentiate the antinociceptive effect of morphine. Intraperitoneal administration of PGE1, but not PGE2 and PGF2alpha, elicited antinociceptive effect per se, by the radiant heat method. The present study was undertaken to confirm the antinociceptive action of PGE1, after intracerebroventricular administration, against nociceptive impulses induced by radiant heat, pressure, and high frequency electric current. PGE1 produced a dose-dependent antinociceptive effect by the radiant heat and pressure methods. It potentiated the antinociceptive action of morphine by the electrical stimulation method. The antinociceptive action of PGE1 was not evident in 5,6-dihydroxytryptamine-pretreated rats, suggesting that this effect is serotonin mediated. The present study thus confirms the antinociceptive action of PGE1 and suggests that, unlike its peripheral action, the central action of PGE1 results in suppression of nociceptive responses which may be serotonin mediated.

5,6-Dihydroxytryptamine↗
PubMed1975

Studies on the experimental production of endomyocardial fibrosis and cardiomegaly of unknown origin by dietary means.

Three groups of rats were kept on diets similar to those eaten by indigenous inhabitants in parts of Africa where CUO and EMF are commonly found, for 30 months. Many of the animals on a tryptophan-deficient diet developed CUO whereas those on a tryptophan-deficient diet which contained a 5-HT content also developed lesions similar to EMF. The third group of rats, which ate a diet similar to this second group but supplemented by a high-protein intake, did not develop any cardiac lesions.

5,6-Dihydroxytryptamine↗
PubMedDate not supplied

Response to electric shock in rats: effects of selective midbrain raphe lesions.

The forebrain serotonin (5-HT) concentrations of rats with lesions in the median (M; n equal to 5), dorsal (D; n equal to 5), and both (DM; n equal to 6) midbrain raphe nuclei were, respectively, 22, 48, and 70% lower than in control animals (n equal to 10). The lesion and control groups, however, did not evidence differences in pain sensitivity as measured by the flinch-jump technique. On the other hand, of the animals tested, those with M (n equal to 3) and DM (n equal to 4) lesions required more trials than controls (n equal to 6) to acquire a one-way avoidance response. D lesion rats (n equal to 2) did not differ from controls in one-way avoidance learning, except in terms of prolonged escape latencies during the first three trials. The previously reported increased sensitivity to painful stimuli subsequent to medial forebrain bundle lesions or para-chlorophenylalanine administration, therefore, does not appear to be due exclusively to disruption of ascending 5-HT fibers originating in the dorsal and median raphe nuclei. The effects of midbrain raphe lesions of avoidance learning, furthermore, depend on lesion locus, and are not due to either hypo- or hyperalgesia.

5,6-Dihydroxytryptamine↗
PubMed1976

Effect of harmine and brain lesions on apomorphine induced motor activity.

Application of harmine (10 mg/kg IP) 30 min before apomorphine decreased the motoric effects of the latter. Following harmine an increase in 5-HT and a decrease in 5-HIAA in different brain regions have been found. Injection of 5,6-DHT into nucleus medianus raphe 7 days before the experiment caused a significant increase of the apomorphine effect. Harmine pretreatment reduced this escessive motility as well as additional lesion of the substantia nigra with 6-OH-DA. Lesion induced by 6-OH-DA alone was without significant effect on the hypermotility following apomorphine. Application of PCPA 3 days before testing elicited an increase of apomorphine-induced hypermotolity which could be abolished by preceding harmine application. The experiments demonstrate the inhibitory effect of the central serotoninergic system on the apomorphine syndrome as well as the serotoninergic-dopaminergic interaction in hypermotility.

5,6-Dihydroxytryptamine↗
PubMed1979

Role of putative neurotransmitters in prolactin, GH and LH response to acute immobilization stress in male rats.

Immobilization for 30 min induced a significant rise of prolactin (Prl), a significant reduction of growth hormone (GH), and no modification of plasma luteinizing hormone (LH) values in male rats. Depletion of brain catecholamine stores increased Prl and decreased LH levels while GH secretion was not affected. Blockade of beta-adrenergic receptors reduced GH and increased LH values. Plasma GH levels were also drastically reduced by depletion of brain serotonin (SER) levels and by atropine, and were increased by blockade of the H1 histamine (HIS) receptor. The anti-gamma-aminobutyric acid (GABA) agent picrotoxin significantly reduced Prl and GH plasma levels. Depletion of brain catecholamine stores or blockade of beta-adrenergic receptors antagonized the restraint-induced rise of plasma Prl values, while the decrease of GH elicited by stress was not modified by any pharmacological manipulation. These results indicate that although several putative neurotransmitters (PN) of the central nervous system (CNS) are implicated in the modulation of baseline levels of Prl, GH and LH, only the stress-induced activation of Prl secretion appears to be mediated by a PN, namely through a noradrenergic, beta-adrenergic route.

5,6-Dihydroxytryptamine↗
PubMed1976

Stimulatory role for brain serotoninergic system on prolactin secretion in the male rat.

Systemic administration of parachlorophenylalanine (PCPA, 100 mg/kg sc on alternate days X two times), a blocker of serotonin (5-HT) synthesis, considerably decreased brain 5-HT and plasma prolactin (PRL) levels in young male rats. Intraventricular (IVT) administration of 5,7-dihydroxytryptamine (5,7-DHT, 200 mug/20 mul), a neurotoxic drug which destroys 5-HT nerve terminals, induced, 3, 12, and 30 days after treatment, a marked depletion of brain 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) and considerably reduced plasma PRL levels at each time interval. Feeding of rat for up to 4 days with a tryptophan (TP)-deficient diet, caused a depletion of brain 5-HT and 5-HIAA contents and did not modify plasma PRL levels. Addition of TP (2 g/kg of diet) to the TP-deficient diet resulted in increased brain 5-HT and 5-HIAA contents and significantly increased PRL levels. These data provide evidence for the role of the 5-HT system in the maintenance of tonic PRL secretion.

5,6-Dihydroxytryptamine↗