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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↗

PubMed2001

Altered respiratory motor drive after spinal cord injury: supraspinal and bilateral effects of a unilateral lesion.

Because some bulbospinal respiratory premotor neurons have bilateral projections to the phrenic nuclei, we investigated whether changes in contralateral phrenic motoneuron function would occur after unilateral axotomy via C(2) hemisection. Phrenic neurograms were recorded under baseline conditions and during hypercapnic and hypoxic challenge in C(2) hemisected, normal, and sham-operated rats at 1 and 2 months after injury. The rats were anesthetized, vagotomized, and mechanically ventilated. No group differences were seen in contralateral neurograms at 1 month after injury. At 2 months, however, there was a statistically significant decrease in respiratory rate (RR) at normocapnia, an elevated RR during hypoxia, and an attenuated increase in phrenic neurogram amplitude during hypercapnia in the C(2)-hemisected animals. To test whether C(2) hemisection had induced a supraspinal change in respiratory motor drive, we recorded ipsilateral and contralateral hypoglossal neurograms during hypercapnia. As with the phrenic motor function data, no change in hypoglossal output was evident until 2 months had elapsed when hypoglossal amplitudes were significantly decreased bilaterally. Last, the influence of serotonin-containing neurons on the injury-induced change in phrenic motoneuron function was examined in rats treated with the serotonin neurotoxin, 5,7-dihydroxytryptamine. Pretreatment with 5,7-dihydroxytryptamine prevented the effects of C(2) hemisection on contralateral phrenic neurogram amplitude and normalized the change in RR during hypoxia. The results of this study show novel neuroplastic changes in segmental and brainstem respiratory motor output after C(2) hemisection that coincided with the spontaneous recovery of some ipsilateral phrenic function. Some of these effects may be modulated by serotonin-containing neurons.

5,7-Dihydroxytryptamine↗

PubMed1975

Alcohol drinking in the rat after destruction of serotonergic and catecholaminergic neurons in the brain.

Rats were offered solutions of ethyl alcohol that were increased in strength from 3-30% concentration over a 12 day interval. Then, 50 mug 5,6-dihydroxytryptamine (5,6-DHT), 200 mug 6-hydroxydopamine (6-OHDA), or 100 mug 5, 7-dihydroxytryptamine (5,7-DHT) were injected acutely into the lateral cerebral ventricle in a 20 mul volume. The selection of ethyl alcohol was enhanced following the lesioning of serotonergic neurons by 5,6-DHT in terms of preference-aversion curves as well as the gm/kg intakes. Conversely, a similar destruction of dopamine and norepinephrine containing neurons by 6-OHDA marked suppressed alcohol preference and the overall intake of this fluid. 5,7-DHT had an intermediary effect of alcohol intake. These findings support the concept that the selection or rejection of alcohol may depend on an imbalance in the neuronal activity of either monoaminergic system in the brain of the rat.

5,6-Dihydroxytryptamine↗

PubMed1991

Cocaine-induced elevation of plasma adrenocorticotropin hormone and corticosterone is mediated by serotonergic neurons.

We investigated the hypothesis that cocaine-induced elevations of plasma adrenocorticotropin hormone (ACTH) and corticosterone are mediated by brain serotonin (5-HT) neurons. Adult male rats were pretreated with the 5-HT depleting agent p-chlorophenylalanine, the 5-HT neurotoxin 5,7-dihydroxytryptamine, the partial 5-HT1A agonist 8-(2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl)-8- azaspirol[4,5]-decane-7,9-dione (BMY 7378) or the 5-HT1C/2 antagonist ritanserin. The effects of cocaine (2-15 mg/kg, i.p.) on plasma ACTH and corticosterone were then examined. Cocaine dose-dependently increased ACTH and corticosterone concentration. This increase was prevented by 5-HT depletion with PCPA and by destruction of 5-HT neurons with i.c.v. injections of 5,7-dihydroxytryptamine. The cocaine-induced elevation of ACTH and corticosterone was not significantly modified by administration of the partial 5-HT1A agonist BMY 7378, suggesting that 5-HT1A receptors probably do not mediate ACTH and corticosterone secretion. However, pretreatment with the 5-HT2/5-HT1C antagonist ritanserin virtually eliminated the cocaine-induced elevation of corticosterone. To determine whether these effects of cocaine are centrally mediated, conscious rats received cocaine injections into the cerebral ventricle through chronically implanted cannulas. Plasma ACTH concentrations were dose-dependently increased, whereas low doses (50 micrograms/kg, i.c.v.) produced a maximal increase in corticosterone concentration. These data indicate that the cocaine-induced stimulation of ACTH and corticosterone secretion is mediated by 5-HT neurons in brain, and furthermore, that 5-HT2 or 5-HT1C receptors are responsible for this effect.

5,7-Dihydroxytryptamine↗

PubMed1979

[Effect of intracerebroventricular injection of 6-hydroxydopamine and 5,6-dyhydroxytryptamine on the phasic secretion of luteinizing hormone (author's transl)].

In ovariectomized rats carrying an estradiol sylastic implant the effect of the intraventricular administration of the serotonin neurotoxin 5,6-dihydroxytryptamine and of the norepinephrine neurotoxin 6-hydroxydopamine on the circadian secretion of the luteinizing hormone (LH) was studied. The decrease of 5-HT after injection of 5,6-dihydroxytryptamine reduced the a.m. and p.m. values and suppressed the phasic rhythm of LH. The diminution of noradrenaline after administration of 6-hydroxydopamine increased the a.m. and did not alter the p.m. values, resulting in a partial abolition of the rhythm.

Animals↗

PubMed1983

Synaptic organization of the indoleamine-accumulating neurons in the cyprinid retina.

The distribution and synaptic connections of the indoleamine-accumulating neurons in the retinae of the goldfish and carp were studied by means of fluorescence and electron microscopy. The indoleamine-accumulating neurons were visualized after intravitreal injection and uptake of the indoleamine 5,6-dihydroxytryptamine. This labeling procedure produced a characteristic yellow fluorescence of the indoleamine-accumulating neurons and also characteristic ultrastructural changes in these cells. To avoid interference from the dopaminergic neurons of the retina, their processes were either removed by prior treatment with 5-hydroxydopamine or prevented from taking up 5,6-dihydroxytryptamine by the simultaneous injection of the catecholamine alpha-methyl-noradrenaline. Fluorescence-microscopic studies confirmed earlier reports that the indoleamine-accumulating perikarya and processes are distributed similar to those of amacrine cells. The indoleamine-accumulating processes ramify in three bands in the inner plexiform layer, the outermost one being the densest. Electron-microscopic investigations showed the indoleamine-accumulating neurons to have synapses of the conventional type, similar to amacrine cells. Their main synaptic contacts are with other amacrine cells, but synapses with bipolar cell terminals are also present. Both the distribution of the indoleamine-accumulating processes and their synaptic arrangement in the cyprinid retina differ from those found in mammalian retinae investigated previously.

5,6-Dihydroxytryptamine↗

PubMed1981

Serotoninergic control of punished behavior: effects of intra-raphe microinjections of chlordiazepoxide, GABA and 5-HT on behavioral suppression in rats.

The effects of intra dorsalis raphe microinjections of chlordiazepoxide, GABA and 5-HT were studied on a model of behavioral suppression in rats. The suppression of responding for food was elicited by a 10 min presentation of a signal previously associated with the delivery of electric foot shocks. Microinjections of chlordiazepoxide, GABA and 5-HT (0.2 microliters) performed in awake hand-held rats reduced the behavioral suppression. Chlordiazepoxide and 5-HT acted in a synergistic way, while such a synergy could not be obtained when chlordiazepoxide and GABA were coadministered. Moreover, the effects of intra-raphe chloridazepoxide no longer appeared in rats given intra dorsalis raphe 5-7 dihydroxytryptamine (3 micrograms in 0.4 microliters) 3 weeks before testing. All these results further support the hypothesis of the involvement of 5-HT neurons both in punishment-induced inhibition and in the antipunishment activity of benzodiazepines. No evidence was obtained suggesting a GABAergic mediation for the functional interaction of chlordiazepoxide with 5-HT neurons in this experimental model. Since high 3H-flunitrazepam binding was found at the raphe dorsalis level, and since a 30% decrease in the number of intra-raphe 3H-flunitrazepam binding sites was detected after intra-raphe 5-7 dihydroxytryptamine, it is possible that intra-raphe chlordiazepoxide controls 5-HT neurons partly through some benzodiazepine binding sites located on 5-HT cells.

5,7-Dihydroxytryptamine↗

PubMed1980

Studies on the mechanism of shock. Central serotoninergic neuron activity after trauma in the rat.

An attempt has been made to assess the effect of injury (limb ischaemia, scald) on the central serotoninergic system of the rat by studying the effect of these injuries on the tryptophan concentration, the tryptophan hydroxylase activity and the metabolism of serotonin in the hypothalamus, mid-brain and hind-brain. The effects of a serotonin uptake inhibitor and an antagonist on the survival time and mortality rate after limb ischaemia have been examined as well as the effects of central lesions produced by the injection of 5.6- and 5.7-dihydroxytryptamine into a lateral cerebral ventricle and the i.p. injection of (+/-)-4-chloroamphetamine. A few changes indicative of increased activity in the central serotoninergic system were found--an increase in tryptophan hydroxylase activity after 4 h bilateral hind-limb ischaemia, better survival of fed rats pre-treated with 5,6-dihydroxytryptamine--but for the most part the changes were not as great as those produced by starving or exposure to cold. Hence the effect of trauma on this system seems small.

5,6-Dihydroxytryptamine↗

PubMed1994

Selective involvement of central 5-HT2 receptors in the maintenance of tolerance to ethanol by arginine8-vasopressin.

Arginine8-vasopressin (AVP) has been shown repeatedly to affect learning and memory and to maintain tolerance to ethanol if the brain serotonin and catecholamine systems are intact. In the present study, 5,7-dihydroxytryptamine (5,7-DHT) was injected intracerebroventricularly to disrupt serotonergic projections from the raphe to the forebrain. This resulted in a marked decrease in 5-hydroxytryptamine (5-HT) immunoreactivity in the terminal areas of the septum and the hippocampus, but not in the serotonin-containing neuronal cell bodies in the raphe nuclei. In control rats, tolerance to the motor-impairing effects of ethanol lasted for only 5 days after the cessation of ethanol treatment but could be maintained indefinitely for as long as AVP was given. In the 5,7-dihydroxytryptamine-lesioned rats, AVP was unable to maintain the tolerance. Continuous intracerebroventricular infusion of 5-HT restored the ability of AVP to maintain ethanol tolerance in the lesioned rats. A selective 5-HT2 agonist (alpha-methylserotonin) was equally effective, and a 5-HT3 receptor agonist (2-methylserotonin) was slightly less effective, but the 5-HT1A agonist dipropylaminotetralin (8-hydroxy-dipropylaminotetralin) was totally ineffective in this respect. The results indicate selective involvement of brain 5-HT2 and possibly 5-HT3 receptors in mediating AVP maintenance of tolerance to ethanol but do not pinpoint their specific loci or roles.

5,7-Dihydroxytryptamine↗

PubMed1987

Regulation of dihydropyridine calcium antagonist binding sites in the rat hippocampus following neurochemical lesions.

The effects of catecholaminergic, cholinergic, serotonergic, and glutaminergic terminal destruction and neurotransmitter depletion on [3H]nitrendipine binding to rat brain membranes were determined using the neurotoxins 6-hydroxydopamine, 5,7-dihydroxytryptamine, and kainic acid and the neurotransmitter-depleting agent reserpine. Following intracisternal injection of 6-hydroxydopamine there were time-dependent increases (14-23%) in the density but not change in the affinity of hippocampal [3H]nitrendipine binding sites. 6-Hydroxydopamine significantly increased [3H]nitrendipine binding in the hippocampus 4 and 10 days following injection. However, no significant change in binding was observed at 16 and 26 days. [3H]Nitrendipine binding in the cerebral cortex, striatum, cerebellum, and brain stem was unaffected by 6-hydroxydopamine. Neither 5,7-dihydroxytryptamine nor kainic acid affected [3H]nitrendipine binding in the hippocampus and cerebral cortex. Acute and chronic reserpinization also did not affect [3H]nitrendipine binding in the hippocampus and cerebral cortex. These results indicate that dihydropyridine calcium antagonist bindings sites in rat brain are subject to brain region-specific regulation following neurochemical lesions and may be present in their largest densities on postsynaptic membranes.

Adrenergic Fibers↗

PubMed1979

Evidence against serotonin involvement in the tonic component of electrically induced convulsions and in carbamazepine anticonvulsant activity.

Intraventricular injection of 5,7-dihydroxytryptamine, selective destruction of descending serotoninergic neurons by 5,6-dihydroxytryptamine or electrolytic and chemical lesions of the nucleus raphe dorsalis did not affect the electroconvulsive threshold in rats. No effect was observed after the systemic administration of drugs known to increase central serotonin transmission, such as quipazine, m-chlorophenylpiperazine, and moderate doses of d-fenfluramine, whereas p-chlorophenylalanine, an inhibitor of serotonin synthesis, decreased seizure susceptibility. The anticonvulsant activity of carbamazepine was not modified in animals with the same experimental lesions. The results, in relation to the high selectivity of the experimental procedures employed to deplete brain and spinal cord serotonin, do not bear out any involvement of serotonin in the tonic component of electrically induced convulsions or in the action of carbamazepine.

Animals↗

PubMed1992

Effects of p-chloroamphetamine on brain serotonin neurons.

p-Chloroamphetamine (PCA) is a useful pharmacologic tool for selectively increasing brain serotonin function acutely by release of serotonin into the synaptic cleft. PCA produces behavioral, neurochemical and neuroendocrine effects believed due to serotonin release after doses in the range of 0.5-5 mg/kg. At higher doses and at longer times, PCA causes depletion of brain serotonin. The mechanisms of this depletion are not well understood but require the serotonin uptake carrier. Antagonism of PCA-induced depletion of brain serotonin is a useful means of assessing the ability of a compound to block the serotonin uptake carrier on brain serotonin neurons. PCA can also be used as a neurotoxic agent to deplete brain serotonin in functional studies, apparently by destroying some serotonergic nerve terminals. Used in this way, PCA has an advantage over 5,6- and 5,7-dihydroxytryptamines in being effective by systemic injection, and it affects brain serotonergic projections with a different neuroanatomic specificity than the dihydroxytryptamines.

Animals↗

PubMed2004

Effects of fenfluramine on free-operant timing behaviour: evidence for involvement of 5-HT2A receptors.

RATIONALE: Temporal differentiation in the free-operant psychophysical procedure is sensitive to the 5-hydroxytryptamine (5-HT)1A receptor agonist 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT) and the 5-HT2 receptor agonist 2,5-dimethoxy-4-iodo-amphetamine (DOI); both drugs shift the psychophysical curve leftwards, reducing the indifference point, T50. We have examined the effect of the 5-HT releasing agent fenfluramine on temporal differentiation. OBJECTIVE: We examined whether fenfluramine's effect on temporal differentiation can be antagonised by the 5-HT1A receptor antagonist N-[2-(4-[2-methoxy-phenyl]-1-piperazinyl)ethyl]-N-2-pyridinylcyclohexane-carboxamide (WAY-100635) and the 5-HT2A receptor antagonist ketanserin, and compared the effects of fenfluramine, DOI and 8-OH-DPAT in intact rats and rats whose 5-HTergic pathways had been destroyed by 5,7-dihydroxytryptamine. METHODS: Rats were trained under the free-operant psychophysical procedure to press levers A and B in 50-s trials in which reinforcers were provided intermittently for responding on A in the first half, and B in the second half of the trial. Percent responding on B (%B) was recorded in successive 5-s epochs of the trials; logistic psychophysical curves were fitted to the data for derivation of timing indices (T50, time corresponding to %B=50%, and Weber fraction). Experiment 1 examined the effects of acute treatment with fenfluramine, and the interaction between fenfluramine and the 5-HT1A and 5-HT2A receptor antagonists WAY-100635 and ketanserin; experiment 2 compared the effects of fenfluramine, 8-OH-DPAT and DOI in intact rats and rats whose 5-HTergic pathways had been destroyed by intra-raphe injection of 5,7-dihydroxytryptamine. Concentrations of 5-HT and catecholamines in the brain were measured by high-performance liquid chromatography. RESULTS: Experiment 1: fenfluramine (2 mg/kg) reduced T50; this effect was attenuated by ketanserin (1.0 mg/kg) but not by WAY-100635 (100 microg/kg). Experiment 2: 8-OH-DPAT (100 microg/kg) and DOI (250 microg/kg) reduced T50 in both groups; fenfluramine reduced T50 only in the sham-lesioned group. Levels of 5-HT were reduced by 80% in the lesioned group; catecholamine levels were not affected. CONCLUSIONS: The results suggest that fenfluramine affects temporal differentiation via the release of endogenous 5-HT which acts mainly on postsynaptic 5-HT2A receptors.

Animals↗

PubMed1994

Interaction of serotonin- and dopamine-related neurotoxins with "serotonin binding proteins" in bovine frontal cortex.

Binding of [3H]serotonin and [3H]dopamine to serotonin-binding proteins (SBP) from soluble extracts of bovine frontal cortex is increased by Fe2+. This group recently attributed this effect of Fe2+ to its ability to enhance the oxidation of [3H]serotonin and [3H]dopamine in the presence of dissolved molecular oxygen, and to the ability of the formed oxidation products to bind covalently to cysteine residues of SBP. In this study it is shown that the binding of both ligands is potently inhibited by dopamine as well as by several catecholamine-and serotonin-related neurotoxins: adrenochrome, 5,6-dihydroxytryptamine, 5,7-dihydroxytryptamine, 6-hydroxydopamine and 6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline. In contrast, serotonin can only potently inhibit part (36%) of the [3H]dopamine binding, while 1,2,3,4-tetrahydroisoquinoline is only a weak competitor for both ligands. Potent inhibition by the toxins is associated with the presence of electrophilic centres at the aromatic ring, either of the products themselves (adrenochrome) or of their oxidation products (all other competitors). These findings suggest that "SBP" represent an important target for the Fe(2+)-mediated binding of [3H]-serotonin, [3H]dopamine and related neurotoxins.

Adrenochrome↗

PubMed1981

Evidence of the modulatory role of serotonin in acetylcholine release from striatal interneurons.

The release of acetylcholine was studied in isolated striatal slices of the rat. The spontaneous and ouabain-stimulated release of acetylcholine was higher in those slices where serotonergic input was somehow impaired: raphe nuclei lesion or p-chlorophenylalanine pretreatment or 5, 7-dihydroxytryptamine pretreatment resulted in a higher release. L-(m-chlorophenyl)-piperazine, a pure serotonin receptor stimulant and D-fenfluramine, a serotonin releaser significantly reduced the release of acetylcholine evoked by ouabain. Serotonin antagonists (cyproheptadine, mianserine and methysergide) prevented the effect of serotonin agonists. When the serotonergic neurons were destroyed either by p-chlorophenylalanine or by 5, 7-dihydroxytryptamine pretreatment D-fenfluramine had no inhibitory action; however, the effect of L-(m-chlorophenyl)-piperazine was not affected. It is suggested that there is a link between serotonergic and cholinergic neurons in the striatum: serotonin released from raphe-striatal neurons is able to inhibit the release of acetylcholine from striatal interneurons.

Acetylcholine↗

PubMed1983

Separate involvement of the spinal noradrenergic and serotonergic systems in morphine analgesia: the differences in mechanical and thermal algesic tests.

Experiments using 3 analgesic tests, the tail-pinch, hot-plate and tail-flick methods, were done to evaluate the roles of the spinal noradrenergic and serotonergic systems in the production of morphine analgesia in rats. To deplete noradrenaline or serotonin in the spinal cord, 6-hydroxydopamine or 5,6-dihydroxytryptamine was given intrathecally. 6-Hydroxydopamine suppressed the antinociceptive effects of morphine injected systemically or intracerebrally (into the nuclei reticularis gigantocellularis and paragigantocellularis or into the periaqueductal gray matter) in the tail-pinch test, but not significantly in the hot-plate and tail-flick tests. Conversely, 5,6-dihydroxytryptamine suppressed the antinociceptive effects of systemically given morphine in the hot-plate test, but not significantly in the tail-pinch and the tail-flick tests. The results not only provide further evidence for the involvement of the descending inhibitory systems in morphine antinociception, but also show that the extent of participation of the spinal noradrenergic and serotonergic systems in the effects of morphine has to be carefully assessed as different analgesic tests (tail-pinch, tail-flick and hot-plate) yield different results.

Animals↗

PubMed1993

5-HT3 receptors in the rat central nervous system are mainly located on nerve fibres and terminals.

Autoradiographic and membrane binding studies with [3H](R,S)- or [3H](S)-zacopride were performed in combination with lesions using various neurotoxins in an attempt to identify which neuronal cell types are endowed with 5-HT3 receptors in the rat central nervous system. Lesions of noradrenergic (by DSP-4), dopaminergic (by 6-hydroxydopamine) and serotonergic (by 5,7-dihydroxytryptamine) systems had little effect generally on the density of 5-HT3 receptors labelled with [3H](R,S)- or [3H](S)-zacopride in various regions of the brain and the spinal cord. The only exception was the amygdala where a significant loss (approximately -20%) of 5-HT3 receptors labelled by [3H](R,S)-zacopride was associated with the selective lesion of serotonergic fibres by 5,7-dihydroxytryptamine. Microinjection of kainic or ibotenic acid into the dorsal and ventral hippocampus reduced the density of 5-HT1A receptors labelled with [3H]8-OH-DPAT (approximately -45%) as expected from their known location on intrinsic neuronal cell bodies and/or dendrites. In contrast, the same lesion did not affect 5-HT3 receptors, suggesting their location on fibres 'en passage'. At the spinal level, 5-HT3 receptors were found to exist on primary afferent fibres terminating within the superficial layers of the dorsal horn, as shown by the marked reduction in the local autoradiographic labelling by [3H](S)-zacopride after either dorsal rhizotomy (-81%) or neonatal capsaicin treatment (-72%). These data suggest that 5-HT3 receptors in the central nervous system are generally located presynaptically on nerve terminals or fibres of non-monoaminergic neurones.

Animals↗

PubMed1986

Effects of pargyline, reserpine and neurotoxin lesions on [3H]tryptamine binding sites in rat brain.

[3H]Tryptamine binding sites were measured in 4 areas of rat brain following treatment with either pargyline or reserpine for 12 days, or 5 days and 30 days following intraventricular injections of 6-hydroxydopamine or 5,7-dihydroxytryptamine. Pargyline treatment decreased [3H]tryptamine binding in cerebral cortex, hippocampus, striatum and hypothalamus. Reserpine treatment increased binding in the cerebral cortex and hippocampus, but not in the striatum or hypothalamus. Neither 6-hydroxydopamine nor 5,7-dihydroxytryptamine altered [3H]tryptamine binding in any of the 4 brain areas. These results indicate that [3H]tryptamine binding sites in brain may be modified by drugs that can potentially affect tryptamine metabolism, and that the sites are not located on catecholamine or serotonin axons.

Animals↗