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PubMed1995

Effects of dorsal rhizotomy and selective lesion of serotonergic and noradrenergic systems on 5-HT1A, 5-HT1B, and 5-HT3 receptors in the rat spinal cord.

Autoradiographic studies were performed in combination with dorsal rhizotomy or selective lesion of descending serotonergic or noradrenergic systems in an attempt to identify the neuronal cell types endowed with the serotonin 5-HT1A, 5-HT1B and 5-HT3 receptors in the rat spinal cord. Unilateral sectioning of seven dorsal roots (C4-T2) at the cervical level produced a marked decrease (approximately-75%, 10 days after the surgery) in the binding of [125I]iodozacopride to 5-HT3 receptors in the superficial layers of the ipsilateral dorsal horn, further confirming the preferential location of these receptors on primary afferent fibres. In addition, a significant decrease (approximately 20%) in the binding of [3H]8-OH-DPAT to 5-HT1A receptors and of [125I]GTI to 5-HT1B receptors was also observed in the same spinal area in rhizotomized rats, suggesting that a small proportion of these receptors are also located on primary afferent fibres. The labelling of 5-HT1B receptors was significantly decreased (-12%) in the dorsal horn at the cervical (but not the lumbar) level, and that of 5-HT3 receptors was unchanged in the whole spinal cord in rats whose descending serotonergic projections had been destroyed by 5,7-dihydroxytryptamine. Conversely, the labelling of 5-HT1A receptors was significantly increased in the cervical (+13%) and lumbar (+42%) dorsal horn in 5,7-dihydroxytryptamine-lesioned rats. Similarly, [3H]8-OH-DPAT binding to 5-HT1A receptors significantly increased (+26%) in the lumbar (but not the cervical) dorsal horn in rats whose noradrenergic systems had been lesioned by DSP-4. The labelling of 5-HT1B receptors was also increased (+31% at the cervical level; +17% at the lumbar level), whereas that of 5-HT3 receptors remained unchanged in these animals. These data indicate that complex adaptive changes in the expression of 5-HT1A and 5-HT1B receptors occurred in the rat spinal cord following the lesion of descending monoaminergic systems.

5,7-Dihydroxytryptamine↗

PubMed1978

Cell proliferation in dimethylhydrazine-induced colonic adenocarcinomata following cytotoxic drug treatment.

A stathmokinetic technique was used to study cell proliferation in dimethylhydrazine-induced adenocarcinomata of rat colon following treatment with cytotoxic drugs. The rate of cell division was significantly increased three days after treatment with 5,7-dihydroxytryptamine and seven days after treatment with 5-fluorouracil. Acceleration of tumour cell proliferation following 5,7-dihydroxytryptamine treatment was inhibited by treating animals with the antiseritoninergic drug Xylamidine Tosylate. Acceleration of tumour cell proliferation following 5-fluorouracil treatment was inhibited by treating animals either with the antiseritoninergic drug BW501 or with the histamine H2-receptor blocking drug Cimetidine.

5,7-Dihydroxytryptamine↗

PubMed1980

The role of cerebral serotonin in the development of tolerance to centrally administered phenobarbital.

Chronic intracerebroventricular injection of phenobarbital results in the development of tolerance to the depressant effects of the drug. The neurotransmitters involved and the manner in which cerebral neurons adapt to this depressant effect are at present unknown. This study examines whether brain serotonin containing neurons participate in the attenuation of the hypnotic response caused by chronic barbiturate administration. Depletion of serotonin with p-chlorophenylalanine, p-chloroamphetamine and 5,7-dihydroxytryptamine did not affect the initial dose-response curve to the centrally injected barbiturate, but all treatments resulted in significant delays in tolerance development. A negative correlation between the extent of whole brain serotonin remaining and the duration of loss of righting reflex on the last day of the chronic phenobarbital regimen was obtained after pretreatment with p-chlorophenylalanine, p-chloroamphetamine and saline. The sleep times of animals pretreated with 5,7-dihydroxytryptamine did not fit this linear relationship. Treatment with p-chloroamphetamine after cessation of the chronic phenobarbital regimen did not influence the rate of tolerance reversal. Steady state levels of serotonin and the concentration of its metabolite, 5-hydroxyindoleacetic acid, in different brain areas were comparable in controls and tolerant rats when examined at various stages intolerance development. However, tolerant and non-tolerant rats sacrificed at time points immmediately after central phenobarbital injection had different temporal patterns of 5-hydroxyindoleacetic acid elevation in the striatum, hypothalamus and midbrain which were observable only during the loss of righting reflex. The data indicate that cerebral serotonin neurons participate in the attenuation of hypnosis following chronic phenobarbital injections.

Animals↗

PubMed1986

Brainstem localization of a thyrotropin-releasing hormone-induced change in respiratory function.

When rats received microinjections of 100 ng thyrotropin-releasing hormone (TRH) into the medial portions of the nucleus tractus solitarius and 12th nucleus or raphe obscurus, at the level of the obex, a significant decrease in the inspiratory time was found. Examination of TRH immunocytochemistry revealed a high density of TRH-positive nerve terminals in these regions, especially the more caudal aspects. If serotonin was depleted by neonatal 5,7-dihydroxytryptamine treatment, the respiratory response of the adults to TRH appeared potentiated. Even though the neonatal 5,7-dihydroxytryptamine reduces the occurrence of TRH-positive cell bodies, TRH-positive fibers were not appreciably altered. These results are discussed with regard to a possible role of endogenous TRH in the brainstem on rhythmic respiratory activity.

5,7-Dihydroxytryptamine↗

PubMed1985

Involvement of amygdaloid catecholaminergic mechanism in suppressive effects of desipramine and imipramine on duration of immobility in rats forced to swim.

The suppressive effect of systemic injection of desipramine and imipramine on the duration of immobility in rats forced to swim was inhibited by 6-hydroxydopamine given into the medial amygdaloid nucleus as a pretreatment. Pretreatment with 5,7-dihydroxytryptamine given into the medial amygdaloid nucleus had no effect on the immobility-reducing effect of tricyclic antidepressants. The concentrations of catecholamines and serotonin in 6-hydroxydopamine- and 5,7-dihydroxytryptamine-pretreated rats, respectively, were significantly lower than those in the saline-injected rats. These results suggest that the suppressive effect of systemic injection of desipramine and imipramine on the duration of the immobility of rats forced to swim was mediated by the catecholaminergic but not the serotonergic mechanisms in the medial amygdaloid nucleus.

5,7-Dihydroxytryptamine↗

PubMed1987

Tolerance to the serotonin 5-HT1 agonist RU 24969 and effects on dopaminergic behaviour.

The pharmacological responses to intraperitoneal injection of the serotonin (5-HT) 5-HT1 agonist RU 24969 (0.25-5 mg/kg) were studied in rats either after single administrations or after repeated treatment (5 mg/kg per day for 3 days). The following effects were recorded after a single dose: (A) a strong increase in locomotor activity in intact rats and its potentiation after 5,7-dihydroxytryptamine lesion of 5-HT neurons; (B) at a low dose, a potent enhancement of the circling behaviour induced by the dopamine (DA) D2 agonist LY 171555 in 6-hydroxydopamine-lesioned rats; (C) an early reduction (2 h) of 5-hydroxyindole acetic acid levels in the striatum and the nucleus accumbens followed by a late increase (24 h) in the latter structure. The following modifications were observed 24 h after the repeated treatment with RU 24969: (A) the locomotor effect of the drug was strikingly reduced both in intact and 5,7-dihydroxytryptamine-lesioned animals. On the contrary, the locomotion elicited by the DA releaser d-amphetamine, or the 5-HT1A agonist 8-OH-DPAT, was unchanged; (B) the rotation scores of 6-hydroxydopamine-lesioned rats injected with LY 171555 after a low dose of RU 24969, were greatly reduced. Moreover, the circling response was almost abolished in rats treated with the DA agonist alone; (C) the early reduction of 5-hydroxyindole acetic acid levels was antagonized while the late increase was enhanced. It is concluded that both the state of tolerance and the reversal of the action of RU 24969 that followed repeated treatment might be related to down-regulation of a subtype of the 5-HT1 receptor, possibly the 5-HT1B subtype, that would play a critical role in the expression of DA-mediated behaviour, locomotor activity and 5-HT metabolism.

5,7-Dihydroxytryptamine↗

PubMed1991

Role of central serotonergic neurons in the effect of sertraline in rats in the forced swimming test.

Sertraline, administered i.p. in single doses or as three injections in 24 h, significantly reduced the immobility of rats in the forced swimming test at 64 and 100 mumol/kg. The effect of three doses of 64 mumol/kg in 24 h was not modified in animals treated i.p. with metergoline (5 mg/kg) 3 h before testing. I.c.v. administration of 150 micrograms 5,7-dihydroxytryptamine, which depleted brain serotonin, or infusion of 6 micrograms 6-hydroxydopamine in the locus coeruleus, which markedly depleted noradrenaline in terminal regions, was also ineffective. The effect of 64 mumol/kg sertraline, once daily for 7 days, was not modified by i.c.v. 5,7-dihydroxytryptamine. The effect of three doses of 64 mumol/kg sertraline in 24 h was instead completely antagonized by 100 mg/kg sulpiride given 90 min before testing. The exact mechanism of this effect and its relevance for the favourable effects of sertraline in human depression remain to be clarified.

1-Naphthylamine↗

PubMed1983

Effect of specific serotonergic lesions on cholinergic neurons in the hippocampus, cortex and striatum.

Local injection of 5,7-dihydroxytryptamine into the median raphe nucleus of rats pretreated with desipramine decreases the serotonin content of the hippocampus and cortex. The turnover of acetylcholine, as measured by the rate of decline of acetylcholine content after hemicholinium-3, is not affected in the hippocampus or the striatum, but is increased in the cortex by such treatment. Local injection of 5,7-dihydroxytryptamine into the dorsal raphe nucleus of desipramine-treated rats decreases the serotonin content of the hippocampus, cortex, and striatum. The turnover of acetylcholine is increased in the hippocampus and cortex, but not affected in the striatum. Thus, serotonergic neurons from the median raphe nucleus appear to tonically inhibit cholinergic neurons in the cortex, and serotonergic neurons from the dorsal raphe nucleus appear to tonically inhibit cholinergic neurons in the hippocampus and cortex. These serotonergic neurons do not appear to act tonically on striatal cholinergic neurons.

5,6-Dihydroxytryptamine↗

PubMed1985

The role of serotonergic neurons in dorsal raphe, median raphe and anterior hypothalamic pressor mechanisms.

The role of serotonergic neurons in the dorsal raphe and median raphe in the pressor response to electrical stimulation of these areas, and the contribution of these neurons to the pressor response to serotonin (5-HT) in the anterior hypothalamus-preoptic area (AH/PO) have been studied by the use of local injections of 5,7-dihydroxytryptamine (5,7-DHT), a neurotoxin selective for 5-hydroxytryptamine (5-HT). When blood pressure was recorded in urethane-anesthetized rats, selective lesions of 5-HT-containing neurons in the dorsal raphe nucleus reduced by 60% the pressor response to electrical stimulation (50 Hz, 100-150 microA, 0.3 msec pulse duration) of this nucleus. On the other hand, selective lesion of 5-HT-containing neurons in the median raphe nucleus had no effect on the pressor response to electrical stimulation of this area. Injection of 5,7-dihydroxytryptamine into the anterior hypothalamus/preoptic area resulted in an increased pressor response to the injection of 5-HT (5 nmol) into the lesioned area 10 days later. Furthermore, the destruction of 5-HT-containing neurons in the dorsal raphe nucleus resulted in an enhanced pressor response to the injection of 5-HT (5 nmol) into the anterior hypothalamus/preoptic area, while the destruction of 5-HT-containing neurons in the median raphe nucleus had no effect on the pressor response to the injection of 5-HT (5 nmol) into the anterior hypothalamus/preoptic area. Therefore, it appears that 5-HT neurons in the dorsal raphe nucleus are important in the pressor response to electrical stimulation and are involved in a pressor mechanism in the anterior hypothalamus/preoptic area.(ABSTRACT TRUNCATED AT 250 WORDS)

5,7-Dihydroxytryptamine↗

PubMed1987

5-Hydroxytryptamine agonistic action of methysergide and the absence of supersensitivity to 5-HT agonists in spinal flexor reflexes in rats.

The intravenous administration of L-5-hydroxytryptophan (5-HTP), 5-methoxy-N,N-dimethyltryptamine (5-MeODMT), p-chloroamphetamine (PCA), LSD and methysergide to acute spinal rats, transected at C1, stimulated the flexor reflexes induced by electrical stimulation applied to the skin of the toe. The enhancement produced by 5-HTP, 5-MeODMT and PCA, was not antagonized by the prior administration of a dose of LSD or methysergide, although the enhancement produced by 5-MeODMT, LSD and methysergide, but not that produced by 5-HTP and PCA, was antagonized by cyproheptadine. In rats treated with 5,6-dihydroxytryptamine (intracisternal administration, 2 weeks previously) supersensitivity was observed to the effects of 5-HTP, a precursor of 5-HT, while subsensitivity was observed for the effects of PCA, a releaser of 5-HT. However, no supersensitivity was observed for the effects of 5-MeODMT, LSD and methysergide. These results suggest that methysergide may have an agonistic action on the 5-HT receptors in spinal cord and that supersensitivity to 5-HTP in rats treated with 5,6-dihydroxytryptamine was due to the lack of uptake of 5-HT into terminals of descending 5-HT fibres or to the change in 5-HT receptors which were not sensitive to 5-MeODMT, LSD, methysergide or cyproheptadine.

5,6-Dihydroxytryptamine↗

PubMed1989

Lesions to ascending noradrenergic and serotonergic pathways modify antinociception produced by intracerebroventricular administration of morphine.

Ascending noradrenergic and serotonergic pathways were lesioned by injection of 6-hydroxydopamine into the dorsal bundle or 5,7-dihydroxytryptamine into the ventromedial tegmentum respectively, and the antinociceptive effect of morphine, administered by intracerebroventricular injection assessed using the tail-flick test 3-14 days later. Lesions of the dorsal bundle selectively depleted levels of noradrenaline (NA) in the forebrain and increased the antinociceptive effect of morphine early, but not later, in the time course of action. Lesions to the locus coeruleus depleted NA in the forebrain and spinal cord but had no effect on the antinociceptive action of morphine. Lesions of the ventromedial tegmentum selectively depleted 5-hydroxytryptamine (5-HT) in the forebrain and transiently reduced the action of morphine. 5,7-Dihydroxytryptamine given intraventricularly depleted 5-HT in the forebrain and spinal cord and also transiently reduced the antinociceptive effect of morphine. These results indicate that aminergic pathways, projecting to the forebrain, are involved in the suppression of the tail-flick reflex produced by injection of morphine into the lateral ventricle.

5,7-Dihydroxytryptamine↗

PubMed1976

Genetic differences in ethanol drinking of the rat following injection of 6-OHDA, 5,6-DHT or 5,7-DHT into the cerebral ventricles.

The preference characteristics for ethanol of four different strains of rats were determined in a two-choice situation by offering water and ethanol in a concentration which was increased from 3 to 30% over a 12-day test sequence. Using stereotaxic procedures, 50 mug 5,6-dihydroxytryptamine (5,6-DHT), 200 mug 6-hydroxydopamine (6-OHDA) or 100 mug 5,7-dihydroxytryptamine (5,7-DHT) were then injected acutely into the lateral cerebral ventricle in a 20 mul volume. Rats of the Sprague-Dawley strain increased their ethanol preference following the lesioning of the serotonergic system by 5,6-DHT, whereas similar destruction of catecholaminergic neurons by 6-OHDA markedly suppressed ethanol intake; Long-Evans rats displayed a similar trend in ethanol drinking patterns. However, animals of the Holtzman strain manifested the increased drinking after 5,6-DHT, but showed no suppression of drinking following 6-OHDA. The preference of rats of the Wistar strain was unaffected by 5,6-DHT but attenuated by 6-OHDA. 5,7-DHT had little or no effect on ethanol consumption in any of these strains. These findings thus suggest that genetic factors are an important determinant in an animal's response to a drug that affects 5-HT or NE systems in the brain, particularly when ethanol selection is investigated.

5,6-Dihydroxytryptamine↗

PubMed1980

Increased self-administration of d-amphetamine after destruction of 5-hydroxytryptaminergic neurons.

Rats will initiate self-administration of d-amphetamine and achieve a stable injection rate within 7-10 days. Animals injected intraventricularly with 5,7-dihydroxytryptamine, which selectively destroys 5-hydroxytryptamine-containing neurons, consistently self-injected larger amounts of d-amphetamine from the first day of training, but the acquisition of a stable rate of drug self-administration was not altered. Bilateral microinjection of 5,7-dihydroxytryptamine into nucleus accumbens failed to alter either the acquisition of d-amphetamine self-administration or the maintenance of a stable rate of injection.

5,7-Dihydroxytryptamine↗

PubMed1985

Effects of TRH, ethanol, and TRH-ethanol combination on activity in rats with altered monoamine content.

Investigations were undertaken with 5,7-dihydroxytryptamine and 6-hydroxydopamine treated rats to see whether activity changes induced by TRH, ethanol and the TRH-ethanol combination would be affected after reduced monoamine function. In keeping with earlier results, TRH increased activity, ethanol reduced activity and the TRH-ethanol combination produced activity counts greater than those for TRH alone. Neither the 5,7-dihydroxytryptamine-induced reduction of brain serotonin nor the 6-hydroxydopamine treatments which reduced brain catecholamines altered the hyperactivity induced by TRH or the TRH-ethanol combination. While reduction of brain serotonin did not affect the ethanol-induced changes in activity, preferential reduction of dopamine as well as reduction of both norepinephrine and dopamine significantly antagonized this measure of ethanol-induced depression. The reduction of dopamine alone produced the greatest effect on this action of ethanol. It can be concluded from the data that the increased locomotion induced by TRH and the TRH-ethanol combination does not depend upon endogenous monoamines, whereas the sedative effects of ethanol are apparently influenced by alterations in brain catecholamine function.

5,7-Dihydroxytryptamine↗

PubMed1985

Spinal cord substance P mediates bicuculline-induced activation of cardiovascular responses from the ventral medulla.

Substance P (SP) and serotonin are contained in ventral medullary projections to the intermediolateral cell column (IML) of the spinal cord, and both neurotransmitters excite sympathetic preganglionic neurons upon injection into the IML. Since gamma-aminobutyric acid (GABA) in the ventral medulla inhibits, and GABA-receptor antagonists excite sympathetic outflow to the cardiovascular system, experiments were done to determine if SP and serotonin in the spinal cord were responsible for mediating these GABAergic effects. Anesthetized rats were either given intrathecal injections of SP antagonists acutely, or pretreated with intrathecal injections of the serotonin neurotoxin, 5,7-dihydroxytryptamine. The effects of these drugs on mean arterial pressure (MAP) and heart rate (HR), as well as their ability to block the responses to topical application of GABA or the GABA antagonist, bicuculline, at the ventral medulla were assessed. Three SP antagonists (50 micrograms) decreased MAP to 2/3 baseline values, but did not change HR. They also blocked the characteristic increases in MAP and HR elicited by application of bicuculline to the ventral medulla. A lower dose (5 micrograms) of a SP antagonist also decreased MAP and blocked the bicuculline-induced increases in MAP and HR, an effect which was reversed in 1-2 h. Neonatal capsaicin treatment reduced the SP content in the dorsal horns of the thoracic spinal cord, but did not affect the cardiovascular responses to intrathecal injection of SP antagonist nor the blockade of bicuculline-induced responses. Intrathecal injection of 5,7-dihydroxytryptamine two weeks prior to the experiments resulted in 56% depletion of serotonin in the thoracic spinal cord, but did not change either basal MAP and HR, nor the responses to bicuculline and GABA applied to the ventral surface of the medulla. These data provide evidence for a role of spinal cord SP in cardiovascular regulation.

5,7-Dihydroxytryptamine↗

PubMed1992

Effect of the selective lesion of serotoninergic neurons on the regional distribution of 5-HT1A receptor mRNA in the rat brain.

The effects of the selective lesion of serotoninergic neurons by an intra-raphe administration of 5,7-dihydroxytryptamine on the 5-HT1A receptor protein and the 5-HT1A receptor mRNA were examined in various regions of the rat brain using specific antibodies and an antisense riboprobe, respectively. Twenty one days after the treatment, the 5-HT1A receptor protein was no longer detected within the dorsal raphe nucleus but was still present in the hippocampus and entorhinal cortex. Quantitative in situ hybridization showed an 85% decrease in the levels of 5-HT1A receptor mRNA within the dorsal raphe nucleus, but no significant change in the hippocampus, interpeduncular nucleus and entorhinal cortex of 5,7-dihydroxytryptamine-treated rats. These data demonstrate that 5-HT1A receptors are synthesized by serotoninergic neurons in the dorsal raphe nucleus, and by neurons located postsynaptically with regard to serotoninergic projections in other areas. The unchanged levels of 5-HT1A receptor mRNA in the hippocampus, interpeduncular nucleus and entorhinal cortex three weeks after the extensive lesion of serotoninergic neurons are consistent with the absence of 5-HT1A receptor up regulation already reported under this condition.

5,7-Dihydroxytryptamine↗

PubMed1982

Attenuation of induced-anxiety in rats by chlordiazepoxide: role of raphe dorsalis benzodiazepine binding sites and serotoninergic neurons.

In chronically implanted awake rats, microinjections of chlordiazepoxide (5 x 10(-7) M) into the dorsal raphé significantly attenuated the inhibition of lever-pressing for food elicited by a signal of punishment. This effect is abolished by prior application of 5,7-dihydroxytryptamine into the dorsal raphé (3 weeks after the infusion of the neurotoxin, dorsal raphé tryptophan hydroxylase activity was reduced to 25% of control values). Furthermore, the disinhibitory effect of intra raphé chlordiazepoxide can be mimicked or potentiated by intra raphé dorsalis application of serotonin (10(-7) or 10(-8) M, respectively). Further evidence for a crucial interaction between benzodiazepines and serotoninergic processes are provided by in vitro experiments showing that chlordiazepoxide or diazepam (10(-5) M) are able to facilitate the K+-evoked [3H]serotonin release from rat midbrain slices. Finally, a high density of [3H]flunitrazepam binding sites was found in the dorsal (and the median) raphé nucleus, the Kd and Bmax values being not altered by prior infusion of 5,7-dihydroxytryptamine. These in vitro data suggest possible means by which intra raphé (and perhaps peripherally administered) benzodiazepines may affect the activity of serotoninergic neurons and thereby produce their effects on experimental anxiety.

5,7-Dihydroxytryptamine↗

PubMed1987

Regulation of adrenal chromaffin cell development by the central monoaminergic system: differential control of norepinephrine and epinephrine levels and secretory responses.

In the mature rat, reflex sympathetic stimulation by insulin-induced hypoglycemia resulted in profound depletion of adrenal epinephrine, and to a lesser extent, norepinephrine. In the developing rat, insulin evoked little or no secretory response from the adrenals prior to 1 week of age. By 7 days, a moderate depletion of epinephrine was seen and the magnitude of the response increased with age. In contrast, during the first 3 weeks of postnatal life, insulin failed to deplete norepinephrine from the adrenal medulla and in fact, produced an increase. This chiefly resulted from de novo biosynthesis of the amine, as the rise was blocked by alpha-methyl-p-tyrosine. These results suggest that the ontogeny of the two chromaffin cell types (norepinephrine and epinephrine-containing) in the adrenals and the maturation of their secretory responses are under differential regulation. Because descending supraspinal catecholaminergic and serotonergic systems have been implicated to play key roles in regulating adrenomedullary function, the ontogeny of the sympatho-adrenomedullary axis was evaluated after neonatal central lesioning with 6-hydroxydopamine or 5,7-dihydroxytryptamine. 6-Hydroxydopamine resulted in a preferential elevation of epinephrine in the developing adrenals as well as an increase in the responsiveness of the adrenals to reflex stimulation by insulin; the mature secretory pattern was obtained as early as at 4 days postnatally for epinephrine and 9 days for norepinephrine. In contrast, 5,7-dihydroxytryptamine led to a preferential reduction of basal adrenal norepinephrine content.(ABSTRACT TRUNCATED AT 250 WORDS)

5,7-Dihydroxytryptamine↗