SEARCH · PubMed Health

Results for “Dihydroxytryptamines”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 469 records · Page 26Linked to original sources

PubMed1988

Selective depletion of dopamine, octopamine, and 5-hydroxytryptamine in the nervous tissue of the cockroach (Periplaneta americana).

High-performance liquid chromatography with electrochemical detection was used to measure the concentrations of 3,4-dihydroxyphenylethylamine (dopamine), 5-hydroxytryptamine (5-HT), p-hydroxyphenylethanolamine (octopamine), alpha-methyl-p-tyrosine, and tryptophan in the cerebral ganglia of cockroaches (Periplaneta americana) after peripheral administration of alpha-methyl-p-tyrosine and alpha-methyltryptophan. In addition, the levels of dopamine, 5-HT, octopamine, alpha-methyl-p-tyrosine, and tryptophan were determined after injection of alpha-methyl-p-tyrosine, 6-hydroxydopamine, or 5,7-dihydroxytryptamine directly into the cerebral ganglia by means of microinjection needles. Peripheral administration of alpha-methyl-p-tyrosine (400-1,600 micrograms/insect) caused a reduction in dopamine and 5-HT concentrations in cockroach cerebral ganglia, although the reduction in dopamine concentrations was more pronounced. Peripheral injections of alpha-methyl-p-tyrosine also reduced octopamine levels in the cerebral ganglia. Peripheral injection of alpha-methyltryptophan (400-1,600 micrograms/insect) caused a marked reduction in 5-HT and tryptophan concentrations in cockroach cerebral ganglia without altering dopamine or octopamine concentrations. Central injections of alpha-methyl-p-tyrosine (80 micrograms/insect) reduced dopamine concentrations in the cerebral ganglia. However, neither 6-hydroxydopamine (20 micrograms/insect) nor 5,7-dihydroxytryptamine (20 micrograms/insect) caused reductions in amine levels when applied near or directly into the cerebral ganglia. The results suggest that specific lesions of aminergic neurons in insects by either 6-hydroxydopamine or 5,7-dihydroxytryptamine are impractical. The specific, long-lasting depletion of 5-HT by alpha-methyltryptophan suggests that this chemical may be useful in elucidating the functions of 5-HT in insects.

5,7-Dihydroxytryptamine↗

PubMed1978

A 5-hydroxytryptamine-like mode of anorectic action for 6-chloro-2-[1-piperazinyl]-pyrazine (MK-212).

The mechanism of the reduction in food consumption elicited by 6-chloro-2-[1-piperazinyl]-pyrazine (MK-212) administered systemically was investigated in the rat. (+/-)-Fenfluramine and (+)-amphetamine were included in some studies for comparative purposes. 2 Pretreatment with methergoline, a 5-hydroxytryptamine (5-HT) antagonist, reduced the magnitude of the anorectic effect of 1.5 and 3 mg/kg of MK-212, while the anti-5-HT agents, cyproheptadine and cinanserin, were likewise effective against the 3 mg/kg dose. 3 Xylamidine, an antagonist of 5-HT that penetrates poorly into the central nervous system, completely blocked the decrease in food intake caused by 5-HT administered peripherally, while not antagonizing an equianorectic dose of MK-212. 4 Reduction of brain 5-HT by intraventricular injection of 5,6-dihydroxytryptamine, intraperitoneal administration of p-chloroamphetamine or placement of a lesion in the region of the median raphé nucleus diminished the anorectic response to 3 mg/kg of MK-212. The anorectic effect of amphetamine was reduced by p-chloroamphetamine or lesion in the raphé, but not by 5,6-dihydroxytryptamine. The decrease in food consumption produced by 1.5 mg/kg of MK-212 was antagonized by prior treatment with p-chloroamphetamine, but not by 5,6-dihydroxytryptamine. 5 Haloperidol, which blocks receptors for dopamine, antagonized the anorexigenic effect of amphetamine, but was ineffective in offsetting the action of MK-212, 3 mg/kg. 6 Pretreatment with chlorimipramine to inhibit the 5-hydroxytryptaminergic uptake mechanism did not affect the anorectic response to 3 mg/kg of MK-212, whereas the response to fenfluramine was diminished. 7 The results indicate that the anorectic action of MK-212 involves a 5-HT-like component which is more evident at the higher dose level of the compound. The anorexigenic property of MK-212 may depend, at least partly, upon the integrity of 5-HT-containing neurones in the central nervous system.

5,6-Dihydroxytryptamine↗

PubMed1987

Sodium-dependent [3H]imipramine binding in rat hippocampus and its relationship to serotonin uptake.

The relationship of [3H]imipramine recognition sites and serotonergic function was investigated by simultaneously determining the desipramine-defined and sodium-dependent components of [3H]imipramine binding and the serotonin levels and uptake in hippocampus of rats without and with selective lesion of serotonergic neurons with 5,7-dihydroxytryptamine. In control rats, the desipramine-defined [3H]imipramine binding to hippocampal membranes showed a high affinity (Kd = 2 nM) and low affinity (Kd = 31 nM) component. In contrast, the Scatchard analysis of sodium-dependent binding revealed a single class of sites of high affinity (Kd = 1.5 nM). Displacement of sodium-dependent [3H]imipramine binding by cold imipramine resulted in a steep curve best fitted to a one-site model. Sodium-dependent binding of [3H]imipramine at 4 nM concentration represented only about 38% of desipramine-defined binding. 5,7-Dihydroxytryptamine treatment resulted in marked reduction of hippocampal serotonin concentration and uptake without any changes in norepinephrine levels. Virtually only the low affinity component of desipramine-defined [3H]imipramine binding was detected by Scatchard analysis in 5,7-dihydroxytryptamine lesioned rats. The desipramine-defined "specific" [3H]imipramine binding in hippocampi of lesioned rats was decreased by 46%, whereas the sodium-dependent binding was only 18% of that seen in controls. Desipramine-defined specific binding in absence of sodium was not altered by lesion to serotonergic neurons. The results suggest that desipramine-defined specific [3H]imipramine binding may not be appropriate for studying the role of imipramine sites in relation to serotonin neuronal uptake and that determination of sodium-dependent binding components of both [3H]imipramine binding and serotonin uptake should be used in future studies.

5,7-Dihydroxytryptamine↗

PubMed1990

Development of renovascular hypertension after central serotonin depletion.

The participation of the central serotonergic system in the development of two-kidney, two clip (2K2C) Goldblatt renovascular hypertension in the rat has been examined. Half of the rats were treated with desmethylimipramine intraperitoneally and 5,7-dihydroxytryptamine intracisternally; the other half received only desmethylimipramine and the 5,7-dihydroxytryptamine vehicle. Two days later, a silver clip was placed in both renal arteries in half of the rats of each group. A sham operation was performed in the remaining rats. Blood pressure was recorded during the 5 weeks after treatment. At the end of the experiment, blood and cerebrospinal fluid samples were obtained. The brain was dissected into several areas and kept frozen. Norepinephrine, serotonin, angiotensinogen, and renin-like concentration were evaluated in the brain areas. Plasma renin activity and angiotensinogen concentration in the plasma and cerebrospinal fluid were estimated. In the sham-operated groups, blood pressure was lower in the treated than in the control rats. The curve of blood pressure increase, as well as the final blood pressure, was similar in the treated and control 2K2C rats. Serotonin was significantly depleted by the 5,7-dihydroxytryptamine treatment in all brain areas. Treatment did not induce any changes in central norepinephrine concentration. Plasma renin activity was diminished in the treated sham-operated rats. These data indicate that the central serotonin depletion does not prevent the development of hypertension and confirm the role of the amine in normal blood pressure regulation. On the other hand, the peripheral renin-angiotensin system might participate in the development of high blood pressure in serotonin-depleted animals.

5,7-Dihydroxytryptamine↗

PubMed1981

Pharmacological evidence for a role of brain serotonin in the maintenance of plasma renin activity in unanesthetized rats.

To determine whether serotonin is involved in the regulation of renin secretion in unanesthetized rats, plasma renin activity was measured in animals treated with the serotonin-depleting drugs p-chlorophenylalanine and 5,7-dihydroxytryptamine, with the serotonin releasing drug p-chloroamphetamine and with the serotonin agonist quipazine. Plasma corticosterone was also measured. p-Chlorophenylalanine decreased plasma renin activity and p-chlorophenylalanine plus 5-hydroxytryptophan increased plasma renin activity. Plasma renin activity was also reduced in rats that had received intraventricular 5,7-dihydroxytryptamine after pretreatment with desmethylimipramine. p-Chlorophenylalanine and 5,7-dihydroxytryptamine did not change plasma corticosterone concentration. p-Chloroamphetamine and quipazine produced dose-dependent increases in plasma renin activity and plasma corticosterone. The increase in plasma renin activity produce by quipazine was more rapid than that produced by p-chloroamphetamine. The effects of p-chloroamphetamine on plasma renin activity and plasma corticosterone were prevented by prior administration of p-chlorophenylalanine. The renin stimulating effect of p-chloroamphetamine was unaffected by adrenalectomy. L-Tryptophan failed to increase plasma renin activity. The data support the hypothesis that in rats release of serotonin within the central nervous system increases renin secretion and corticosterone secretion and that the increase in renin is independent of the increase in corticosterone.

5,7-Dihydroxytryptamine↗

PubMed1982

Electron microscopy of aminergic retinal neurons.

The synaptic connections of the dopaminergic retinal neurons of Cynomolgus monkeys and rabbits were studied in the electron microscope. In the Cynomolgus monkeys, a labelling method with 5,6-dihydroxytryptamine was used, whereas an autoradiographic technique with a monoamine oxidase inhibitor and (3H)-dopamine was used in the rabbits. The labelling method with 5,6-dihydroxytryptamine altered the normal ultrastructure of the dopaminergic neurons, but their synaptic structures were still easily recognized. The autoradiographic method left the ultrastructure of the labelled neurons unchanged, and large dense-cored vesicles could therefore be seen to be associated with the dopaminergic neurons in the rabbits. Other morphological characteristics could also be seen. The distribution of dopaminergic perikarya in the inner nuclear layer and dopaminergic processes in the inner plexiform layer was consistent with that of amacrine cells in both Cynomolgus monkeys and rabbits. Furthermore, the dopaminergic processes had output synapses of the conventional kind characteristic of amacrine cells. In both animals, the dopaminergic processes were presynaptic to amacrine cell bodies and both pre- and postsynaptic to other amacrine cell processes. The number of output synapses was larger than the number of input synapses. Serial and convergent synaptic arrangements were common. The synaptic organization of the indoleamine-accumulating neurons in the retinae of rabbits, cats, goldfish and carp were also investigated in the electron microscope. The neurons were labelled with 5,6-dihydroxytryptamine after the otherwise interfering dopaminergic processes had been destroyed. The indoleamine-accumulating neurons of the three species had a distribution of perikarya and processes like that of amacrine cells. They also had synapses of the conventional kind. In the rabbit and the cat, the indoleamine-accumulating processes had mainly reciprocal synapses with rod bipolar terminals in the innermost part of the inner plexiform layer. They were, however, also also pre- and postsynaptic to other amacrine cells, and in the cat, they had synaptic contacts with cone bipolar cells and the dendrites of ganglion cells. The indoleamine-accumulating neurons of the goldfish and carp were mainly pre- and postsynaptic to other amacrine cells, even if contacts with bipolar terminals were also seen. In the retinae of goldfish and carp, a subset of indoleamine-accumulating processes were discovered in the middle part of the inner plexiform layer that had a previously not recognized type of conventional output synapse with two postsynaptic elements. This synapse was called a branched conventional synapse. It was found and investigated in the retinae of normal goldfish and carp. Its presynaptic structures were found to be similar to those seen in certain conventional synapses with presynaptic "globular clusters" and only one postsynaptic element.

Animals↗

PubMed1979

Evaluation of the non-specific effects of catecholamine and serotonin neurotoxins by injection into the medial forebrain bundle of the rat.

Low doses of 6-hydroxydopamine (6-OHDA), 5,6-dihydroxytryptamine (5,6-DHT) and 5,7-dihydroxytryptamine (5,7-DHT) that have previously been shown to produce behavioral change following intracerebral infusion were injected into the medial forebrain bundle of the rat. This site contains serotonin (5-HT), norepinephrine (NE), and dopamine (DA) fibers whose anatomical locations have been described. Damage to these fiber systems was quantified by measuring depletion of telencephalic 5-HT, NE and DA. The effects of infusions of 6-OHDA, 5,6-DHT and 5,7-DHT were compared to the effects of unequivocally non-specific electrolytic lesions and copper sulfate infusions. Survival time was varied to evaluate the amount of regeneration that could be expected over periods from 8 to 60 days. Amine levels were found to be stable over the time period examined. With the doses used, evidence was found to support the position that non-specific damage caused by general cytotoxic effects of 6-OHDA and 5,7-DHT is minimized sufficiently to permit the acquisition of useful data on the function of central catecholamine and indoleamine systems.

5,6-Dihydroxytryptamine↗

PubMed1978

Model of central chemical 'serotoninectomy' in mice.

The influence of 5,7-dihydroxytryptamine (5,7-DHT) and 5,6-dihydroxytryptamine (5,6-DHT) on the level of noradrenaline (NA), dopamine (DA), 5-hydroxytryptamine (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA) in discrete brain areas of mice was studied. Moreover, the level of free and total acetylcholine (Ach) in the whole brain was measured. The behaviour of animals was also observed. 5,7-DHT caused a relatively specific short-term decrease of 5-HT and 5-HIAA level in discrete areas of mice brain with the decrease of DA level in the striatum. This substance seems to produce a relatively specific disruption of central 5-HT neurons in mice. 5,7-DHT is an unspecific neurotoxic drug for mouse brain. Both substances did not affect the gross behaviour of mice.

5,6-Dihydroxytryptamine↗

PubMed1989

Serotonin depletion modifies the pigeon electroretinogram.

Significant amounts of endogenous serotonin have been detected in the retina of many nonmammalian vertebrates. In the pigeon retina, serotonin-like immunoreactivity has been localized within a subpopulation of bipolar and amacrine cells, and serotonin-containing terminals have been found to be segregated in different laminae of the inner plexiform layer. In the current experiments 5,7-dihydroxytryptamine was injected intravitreally in the pigeon eye in order to examine the effect of serotonin depletion on the functional activity of the retina. The physiological modifications induced by the serotonin depletion were examined by recording electroretinographic responses to light flashes of different intensity under conditions of light and dark adaptation. Our results show that 5,7-dihydroxytryptamine treatment selectively increases b-wave amplitude and modifies the function relating b-wave amplitude to Log flash intensity without affecting the peak latency and the amplitude of oscillatory potentials. These results can be interpreted in terms of a possible inhibitory role of serotonin on b-wave generators.

5,7-Dihydroxytryptamine↗

PubMed1979

Serotoninergic synapses on ependymal and hypendymal cells of the rat subcommissural organ.

The nervous input to the subcommissural organ (SCO) of the rat has been investigated with Falck-Hillarp fluorescence histochemistry and electron microscopical techniques. Previous fluorescence histochemical observations of a dense plexus of serotoninergic nerve fibres in relation to the basal SCO were confirmed. Electron microscopically, unmyelinated fine varicose axons ranging in size from 0.1--0.6 micrometer were observed to penetrate into the SCO hypendyma. Boutons and presynaptic varicosities filled with a diversity of round and elongated clear vesicles, and occasional large dense cored vesicles establish asymmetric (Gray's type I) synaptic contacts with the basal processes and somata of the SCO ependymal and hypendymal cells. A typical varicosity in synaptic contact with an SCO cell contains a population of approximately 85% clear, elongated vesicles 45 X 60 nm in diameter, 15% clear, round vesicles 50 nm in diameter, and 1--2% large dense cored vesicles with a vesicle diameter of about 85 nm and a dense core diameter of 50--55 nm. The mean length of the postsynaptic membrane specialization was found to be 0.5 micrometer. Experiments with specific neurotoxic drugs revealed that the nerve terminals in synaptic contact with the SCO cells are identical to the fibres of the serotoninergic plexus identified fluorescence histochemically. Thus, an intraventricular injection of either 5,6-dihydroxytryptamine or 5,7-dihydroxytryptamine induced typical degenerative changes in most of the boutons in synaptic contact with the SCO cells, and also a disappearance of the yellow fluorescent nerve plexus. It is concluded that the SCO of the rat receives a dense plexus of serotonin-containing nerve fibres which form typical synaptic contacts with the specialized ependymal cells of the SCO and that these fibres may constitute the only direct nervous input to the organ. The degeneration of the serotoninergic synapses elicited a long-lasting, pronounced increase in the secretory activity of the SCO. Despite long survival times after the treatment with neurotoxic drugs, we found no evidence of regenerative restitution of the serotoninergic innervation nor normalization of the secretory activity of the SCO. The observed inverse relationship between secretory activity and serotoninergic innervation is in line with previous observations which indicate that the 5-hydroxytryptamine input to the SCO ependymal and hypendymal cells exerts a powerful inhibition on their protein synthetic machinary.

5,6-Dihydroxytryptamine↗

PubMed1996

Neurotoxicity of free-radical-mediated serotonin neurotoxin in cultured embryonic chick brain neurons.

Exposure of serotonin (5-HT) to oxygen-derived free-radical-generating system, xanthine oxidase-hypoxanthine or to a Fenton reaction results in the formation of the neurotoxin, tryptamine-4,5-dione. In cultured embryonic chick brain neurons, incubation of tryptamine-4,5-dione or its ethyl carbonate derivative resulted in a dose-dependent neurotoxicity (1-100 microM). The addition of sulfhydryl compound, glutathione at 2 or 10 microM significantly enhanced the toxicity induced by 10 microM tryptamine-4,5-dione. On the contrary, glutathione at 10 microM decreased the neurotoxic effect caused by 10 microM 5,6- and 5,7-dihydroxytryptamine in the cultured neurons. The toxicity resulted from 5,6- and 5,7-dihydroxytryptamine could be fully prevented by a 5-HT uptake inhibitor, fluoxetine. However, the toxicity caused by tryptamine-4,5-dione and glutathione conjugate could not be blocked by fluoxetine (10 or 100 microM) or by a glutathione transferase inhibitor, boric acid/serine. The results indicate a different molecular mechanism among 5-HT derived neurotoxins and suggest that tryptamine-4,5-dione and/or its glutathione conjugate would cause neuronal damage, if they are formed in vivo.

5,6-Dihydroxytryptamine↗

PubMed1982

Selective neurotoxin lesions of the lateral septum: changes in social and aggressive behaviours.

Bilateral microinjection of 5,7-dihydroxytryptamine into the lateral septum resulted in a behavioural profile in the Social Interaction test of anxiety similar to that seen after chronically-administered benzodiazepines. In contrast, bilateral microinjection of 6-hydroxydopamine into this locus did not alter the profile of rats tested in this model. In a colony-intruder model of aggression, the 5,7-dihydroxytryptamine lesioned rats showed decreased dominance, while the 6-hydroxydopamine lesioned rats showed increased dominance and reduced subordination. The results suggest that lateral septal 5-hydroxytryptamine, but not catecholamines, is important in the control of anxiety, whereas both lateral septal 5-hydroxytryptamine and catecholamines are involved in the control of aggression.

5,7-Dihydroxytryptamine↗

PubMedDate not supplied

Cardiovascular effects of intracisternal 6-hydroxydopamine and of subsequent lesions of the ventrolateral medulla coinciding with the Al group of noradrenaline cells in the rabbit.

The acute cardiovascular effects of intracisternal injections of 6-hydroxydopamine (6-OHDA), 5,6-dihydroxytryptamine and 5,7-dihydroxytryptamine and the degree of neurotransmitter depletion achieved by such injections were studied. The two different vehicles used--0.2% ascorbic acid in 0.9% NaCl, or 0.9% NaCl--had little effect on the cardiovascular response to 6-OHDA injections but had a striking effect on levels of noradrenaline (NA) subsequently measured in the thoracic spinal cord. 6-OHDA (600 micrograms kg-1 free base) dissolved in normal saline depleted spinal cord NA to less than 1% of control levels whereas the same dose of 6-OHDA dissolved in ascorbate saline only depleted spinal cord NA to 24% of control levels. The degree of depletion of NA in medulla, pons and hypothalamus was similar in the two groups. Ascorbic acid also appeared to contribute to the non-specific toxicity of intracisternal injections of 6-OHDA. The hypertension and bradycardia that followed lesions of the ventrolateral medulla coinciding with the A1 group of noradrenergic cells (Al lesions) were attenuated in animals in which spinal cord NA had been depleted to 2% of control using 6-OHDA in normal saline. However, pretreatment with 6-OHDA in ascorbate saline, which only reduced spinal cord NA to 23% of control, had no effect on the cardiovascular response to Al lesions. It seems likely that the effects of Al lesions are mediated, at least in part, by NA projections descending within the spinal cord.

5,6-Dihydroxytryptamine↗

PubMed2002

Monoamine neurotoxins-induced apoptosis in lymphocytes by a common oxidative stress mechanism: involvement of hydrogen peroxide (H(2)O(2)), caspase-3, and nuclear factor kappa-B (NF-kappaB), p53, c-Jun transcription factors.

The destruction of dopaminergic and serotonergic nerve cells by selective 6-hydroxydopamine (6-OHDA), 5,6-dihydroxytryptamine (5,6-DHT) and 5,7-dihydroxytryptamine (5,7-DHT), respectively, is a commonly used tool to investigate the mapping of neuronal pathways, elucidation of function and to mimic human neurodegenerative disease such as Parkinson's and Alzheimer's diseases. Despite intense investigations, a complete picture of the precise molecular cascade leading to cell death in a single cellular model is still lacking. In this study, we provide evidence that 6-OHDA, 5,6- and 5,7-DHT toxins-induced apoptosis in peripheral blood lymphocytes cells in a concentration-dependent fashion by a common oxidative mechanism involving: (1) the oxidation of toxins into quinones and production of the by-product hydrogen peroxide, reflected by desipramine-a monoamine uptake blocker-and antioxidants inhibition, (2) activation and/or translocation of nuclear factor-kappaB, p53 and c-Jun transcription factors, showed by immunocytochemical diaminobenzidine-positive stained nuclei, (3) caspase-3 activation, reflected by caspase Ac-DEVD-CHO inhibition, (4) mRNA and protein synthesis de novo according to cycloheximide and actinomycin D cell death inhibition. These results are consistent with the notion that uptake and intracellular autoxidation of those toxins precede the apoptotic process and that once H(2)O(2) is generated, it is able to trigger a specific cell death signalisation. Thus, taken together these results, we present an ordered cascade of the major molecular events leading peripheral blood lymphocytes to apoptosis. These results may contribute to explain the importance of H(2)O(2) as a second messenger of death signal in some degenerative diseases linked to oxidative stress stimuli.

5,6-Dihydroxytryptamine↗

PubMed1980

Serotoninergic mechanisms of beta-endorphin- and clonidine-induced analgesia in rats.

Both beta-endorphin and clonidine proved to have statistically significant analgesic activity (increase in latency to hind-paw lick in hot plate test) in rats. Furthermore, the pain inhibition induced by beta-endorphin and clonidine could be antagonized by prior treatment of animals with either naloxone (a narcotic antagonist) or the depletors of central serotonin pathways such as 5,6-dihydroxytryptamine, 5,7-dihydroxytryptamine and p-chlorophenylalanine have not effect on latency to hind-paw lick. The data indicate that serotoninergic activity in the brain plays a role in the elaboration or modulation of beta-endorphin and clonidine analgesia in rats.

5,6-Dihydroxytryptamine↗

PubMed1981

Innervation of the intestine in the bivalve mollusc Chione stutchburyi.

The innervation of the gut of the venerid bivalve mollusc, Chione stutchburyi, has been examined by fluorescence histochemistry, electron microscopy and autoradiography. Specific green and yellow varicose fluorescent fibres indicate the presence of dopaminergic and serotonergic axons, respectively. Three different types of axons can be distinguished by the morphological characteristics of their vesicles. Type I axons contain predominantly small granular vesicles (average diameter 65 nm), Type II axons possess large granular vesicles (average diameter 100 nm) and Type III axons contain large opaque vesicles (average diameter 150 nm). The granular vesicles in both Types I and II axons react positively to dichromate, and their granularity is reduced by reserpine indicating that they are monoaminergic. Only Type I axons accumulate tritiated dopamine and are selectively damaged by 6-hydroxydopamine. It is concluded that Type I axons are dopaminergic. Type II axons are serotonergic: they alone take up tritiated 5-hydroxytryptamine, and 5,7-dihydroxytryptamine selectively causes degenerative changes in these axons. Type III axons contain an unidentified neurotransmitter substance. The large opaque vesicles of these axons do not react to dichromate and are unaffected by reserpine, 6-hydroxydopamine or 5,7-dihydroxytryptamine.

5,7-Dihydroxytryptamine↗

PubMed1989

Paraventricular nucleus neuronal responses following electrical stimulation of the midbrain dorsal raphe: evidence for cotransmission.

In order to determine the responses of paraventricular nucleus neurones following activation of central serotonergic pathways, single unit activity was recorded and responses following electrical stimulation of the midbrain dorsal raphe nucleus were examined. Excitation was recorded from approximately 50% of the cells, independent of whether they were antidromically identified as projecting to the median eminence or unidentified. Approximately 20% of cells were inhibited by the stimulation, the majority of these being unidentified. Parachlorophenylalanine-induced inhibition of serotonin synthesis reduced hypothalamic serotonin levels by 77% and caused a significant reduction in the proportion of cells excited by the stimulation, whereas the inhibitory responses were not affected. Intracerebroventricular administration of the serotonergic neurotoxin, 5,7-dihydroxytryptamine, which caused similar reductions in hypothalamic serotonin content (77%), reduced still further the proportion of excitatory responses and also reduced the proportion of cells inhibited by the stimulation. The data obtained suggest that serotonin acts as an excitatory neurotransmitter in the paraventricular nucleus; this is discussed particularly with respect to the regulation of the hypothalamo-hypophysial-adrenocortical axis. The loss of inhibitory responses in 5,7-dihydroxytryptamine treated, as opposed to the parachlorophenylalanine treated, animals suggests that the serotonergic fibers innervating the recorded cells may contain a cosecreted substance that may have important physiological actions in the control of neuronal activity in the region recorded.

5,7-Dihydroxytryptamine↗

PubMed1978

Bulbospinal tryptaminergic neurones. A search for the role of bulbospinal tryptaminergic neurones in the control of sympathetic activity.

1. The possible role of bulbospinal tryptaminergic neurones in the control of sympathetic activity has been investigated in anaesthetised cats. 2. Depletion of spinal cord stores of 5-hydroxytryptamine was achieved by systemic administration of p-chlorophenylalanine or by intraspinal microinjections of 5,6-dihydroxytryptamine. 3. Blood pressure was little changed by these treatments, neither was the pattern of ongoing activity in sympathetic nerves (arterial pulse rhythmicity and respiratory modulation), the influence of pulmonary afferent nerves on this activity (determined by an airway occlusion technique), the sympatho-inhibitory influence of the carotid sinus baroreceptors, nor the sympatho-inhibitory or -excitatory influences of somatic afferent nerves. 4. Since both p-chlorophenylalanine and 5,6-dihydroxytryptamine treatment caused extensive disruption of the bulbospinal tryptaminergic neurones, it was concluded that these play no significant role in the mediation of the responses tested in anaesthetised cats in the present study.

5,6-Dihydroxytryptamine↗