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PubMed1992

Serotonergic fibers induce a long-lasting inhibition of monosynaptic reflex in the neonatal rat spinal cord.

The transmitter mechanism of a long-lasting descending inhibition of the monosynaptic reflex was investigated in the isolated spinal cord of the neonatal rat. The monosynaptic reflex elicited by dorsal root stimulation was recorded extracellularly from a lumbar ventral root (L3-L5). Electrical stimulation of the upper thoracic part of the hemisected cord caused an inhibition lasting about 40 s of the monosynaptic reflex. This descending inhibition was markedly attenuated by perfusing the spinal cord with reserpine (1 microM) or 5,7-dihydroxytryptamine (10 microM) for 2-6 h. The perfusion with reserpine (1 microM) for 4 h significantly decreased the contents of 5-hydroxytryptamine, dopamine, and norepinephrine of the neonatal rat spinal cord, whereas the perfusion with 5,7-dihydroxytryptamine (10 microM) for 4 h decreased the contents of 5-hydroxytryptamine and dopamine. The descending inhibition was markedly potentiated by a 5-hydroxytryptamine uptake blocker, citalopram (10 nM), and was blocked by a 5-hydroxytryptamine antagonist, ketanserin (10-100 nM). Application of 5-hydroxytryptamine to the spinal cord induced an inhibition of the monosynaptic reflex, a later part of which was blocked by ketanserin. Ketanserin also moderately blocked inhibitions of the monosynaptic reflex caused by norepinephrine and dopamine. Phentolamine (10 microM) abolished the depressant actions of norepinephrine and dopamine, but did not affect that of 5-hydroxytryptamine or the descending inhibition. These results strongly suggest the involvement of 5-hydroxytryptamine, but not dopamine nor norepinephrine, in the descending inhibition. Besides ketanserin, the descending inhibition was blocked by ritanserin, haloperidol, and pipamperone, which have affinities to 5-hydroxytryptamine2 receptors, and also by spiperone and methiothepin, which are antagonists at both 5-hydroxytryptamine1 and 5-hydroxytryptamine2 receptors (all 1 microM). On the other hand, a 5-hydroxytryptamine1C and 5-hydroxytryptamine2 antagonist, mesulergine (1 microM), and 5-hydroxytryptamine3 antagonists, ICS 205-930 and quipazine (both 1 microM), did not depress either the descending inhibition or the 5-hydroxytryptamine-evoked inhibition of the monosynaptic reflex. The results with these antagonists favor the involvement of 5-hydroxytryptamine2 receptors although the results with mesulergine disagree with this notion. 5-Hydroxytryptamine1 agonists, such as 8-hydroxy-2-(di-n-propylamino)tetralin, buspirone, and 5-carboxyamidotryptamine, and a 5-hydroxytryptamine3 agonist, 2-methyl-5-hydroxytryptamine, induced a long-lasting inhibition of the monosynaptic reflex, which was blocked by ketanserin whereas a 5-hydroxytryptamine2 agonist, S-(+)-alpha-methyl-5-hydroxytryptamine, evoked a biphasic inhibition, in which only the later component was blocked by ketanserin.(ABSTRACT TRUNCATED AT 400 WORDS)

5,7-Dihydroxytryptamine↗

PubMed1994

Postnatal development of the suprachiasmatic nucleus in the rat. Morpho-functional characteristics and time course of tyrosine hydroxylase immunopositive fibers.

According to earlier data, the suprachiasmatic nucleus of neonatal rats is highly innervated by serotonin- and tyrosine hydroxylase-immunopositive fibers [Ugrumov M. V. (1992) Zool. Sci. (Tokyo) 9, 37-45], while the latter were no longer observed in adults. This study has attempted to evaluate the timing of the innervation of the rat suprachiasmatic nucleus by tyrosine hydroxylase-immunopositive fibers, as well as to specify some morpho-functional characteristics of these fibers. According to our semi-quantitative light microscopic immunocytochemical data, few tyrosine hydroxylase-immunopositive fibers were observed in the suprachiasmatic nucleus as early as the second postnatal day. They highly increased in number neonatally reaching a maximum at the 10th postnatal day, and then decreased dramatically in adulthood. These data suggest either the provisional character of the tyrosine hydroxylase-immunopositive fibers themselves or the transient expression of tyrosine hydroxylase within permanent fibers. The tyrosine hydroxylase immunopositivity in the fibers points to their catecholaminergic nature, while the overlapping in the distribution of tyrosine hydroxylase- and serotonin-immunopositive fibers might also suggest the transient expression of tyrosine hydroxylase in serotoninergic neurons. In order to check this hypothesis, the neurotoxins of catecholamine- and serotoninergic neurons, 6-hydroxydopamine and 5,7-dihydroxytryptamine, were intraventricularly injected at the second postnatal day, while their effects were specified by the semi-quantitative immunocytochemistry eight days later. 6-Hydroxydopamine did not modify the content of tyrosine hydroxylase-immunopositive fibers in the suprachiasmatic nucleus. Conversely, the treatment with 5,7-dihydroxytryptamine resulted in a significant increase in the number of the tyrosine hydroxylase-immunopositive fibers, while reducing the amount of the serotoninergic ones.(ABSTRACT TRUNCATED AT 250 WORDS)

5,7-Dihydroxytryptamine↗

PubMed2005

Effect of long-lasting serotonin depletion on environmental enrichment-induced neurogenesis in adult rat hippocampus and spatial learning.

The dentate gyrus of the hippocampal formation produces new neurons throughout adulthood in mammalian species. Several experimental statuses and factors regulating to neurogenesis have been identified in the adult dentate gyrus. For example, exposure to an enriched environment enhances neurogenesis in the dentate gyrus and improves hippocampus-dependent spatial learning. Furthermore, serotonin is known to influence adult neurogenesis, and learning and memory. However, the effects of long-lasting depletion of serotonin over the developing period on neurogenesis have not been investigated. Thus, we examined the influence of long-lasting serotonin depletion on environmental enrichment-induced neurogenesis and spatial memory performance. As reported previously, environmental enrichment significantly increased new neurons in the dentate gyrus. However, there was no improvement of the spatial learning test in adult rats in standard and in environmental enrichment housings. Intracisternal administration of the serotonergic neurotoxin, 5,7-dihydroxytryptamine, on postnatal day 3 apparently reduced serotonin content in the adult hippocampus without regeneration. This experimental depletion of serotonin in the hippocampus of rats housed in an enriched environment had no effect on spatial memory performance, but produced significant decreases in the number of bromodeoxyuridine-labeled new cells in the dentate gyrus. These findings indicate that newly generated cells stimulated by environmental enrichment are not critical for improvements in hippocampus-dependent learning. Furthermore, numbers of bromodeoxyuridine-labeled cells in the dentate gyrus of 5,7-dihydroxytryptamine-injected rats did not differ between 1 day and 4 weeks after bromodeoxyuridine injection. These data suggest that survival of newly generated dentate gyrus cells remains relatively constant under long-lasting serotonin depletion.

5,7-Dihydroxytryptamine↗

PubMed1998

Selective increases in serotonin 5-HT1B/1D and 5-HT2A/2C binding sites in adult rat basal ganglia following lesions of serotonergic neurons.

Quantitative autoradiography was used to examine possible adaptive changes in serotonin 5-HT1B/1D and 5-HT2A/2C receptor binding sites in adult rat basal ganglia, after partial or severe lesions of serotonergic neurons produced by intraraphe injections of variable amounts of 5,7-dihydroxytryptamine. In controls, the 5-HT1B/1D sites labeled with S-CM-G[125I]TNH2 were evenly distributed in the core and the shell of the nucleus accumbens. The density of 5-HT1B/1D sites was higher in the ventral than dorsal part of the striatum and no regional differences were detected along the rostrocaudal axis of the structure. The 5-HT2A/2C sites labeled with [125I]DOI were preferentially distributed in the mediodorsal striatum and higher densities were detected in the shell than core of the nucleus accumbens. Following 5,7-dihydroxytryptamine injections, there were no changes in binding of either receptor subtype after partial lesions entailing 80-90% 5-HT depletions. After severe 5-HT depletions (over 95%), large increases in 5-HT1B/1D binding were observed in the substantia nigra (78%), but no changes took place in the globus pallidus. Increases in 5-HT1B/1D binding were also detected in the shell of the nucleus accumbens (27%). Similar sized increases in 5-HT2A/2C binding (22%) were restricted to the medial striatum. The present results suggest a preferential association between 5-HT1B/1D receptors and the striatonigral neurons containing substance P, as indicated by the striatal distribution of these receptors and their selective increases in the substantia nigra after severe 5-HT deprivation. We recently proposed a similar relationship between the 5-HT4 receptors and the striatopallidal neurons containing met-enkephalin. Moreover, the increases in 5-HT1B/1D binding in the substantia nigra and in the shell of the nucleus accumbens reinforce the view of an implication of this receptor subtype in motor functions. In contrast, the prominent increases in 5-HT2A/2C binding after severe 5-HT deprivation as restricted to the medial region of the striatum and suggest up-regulation of most probably 5-HT2C receptors in a region implicated in cognitive functions.

5,7-Dihydroxytryptamine↗

PubMed1999

Decreased chaos of midbrain dopaminergic neurons after serotonin denervation.

Neuropharmacological investigations aimed at understanding the electrophysiological correlates between drug effect and action potential trains have usually been carried out with the analysis of firing rate and bursting activity. In this study, a selective alteration of neural circuits providing inputs to ventral tegmental area dopaminergic neurons has been produced, and the corresponding electrophysiological correlates have been investigated by nonlinear dynamical analysis. The nonlinear prediction method combined with Gaussian-scaled surrogate data has been used to show the chaotic structure in the time-series corresponding to the electrical activity of ventral tegmental area dopaminergic neurons, extracellularly recorded in vivo. A decrease in chaos of ventral tegmental area dopaminergic neurons was found in a group of rats lesioned with 5,7-dihydroxytryptamine, a neurotoxin which selectively destroys serotonergic terminals. The chaos content of ventral tegmental area dopaminergic neurons in the control group and the decrease of chaos in the lesioned group cannot be explained in terms of standard characteristics of neuronal activity (firing rate, bursting activity). Moreover, in the control group a positive correlation has been found between the density-power-spectrum of the interspike intervals and the chaos content measured by nonlinear prediction S score; this relation was lost in the lesioned group. It is concluded that the impaired serotonergic tone induced by 5,7-dihydroxytryptamine reduces the chaotic behaviour of the dopaminergic cell firing pattern, while retaining many standard interspike interval characteristics. The functional role of this behaviour in a neuronal coding problem context and the implications for the pathophysiology of some mental disorders are discussed.

5,7-Dihydroxytryptamine↗

PubMed2002

Brain structures mediating the suckling stimulus-induced release of prolactin.

Suckling-induced prolactin release is a widely studied neuroendocrine reflex, comprising a neural afferent and a humoral efferent component. The information on the brain structures involved in this reflex is fairly limited. The present studies focused on this question. The following hypothalamic interventions were made in lactating rats and the dams were tested for the suckling-induced prolactin response: (i) unilateral or (ii) bilateral frontal cuts at the level of the anterior and posterior hypothalamus; (iii) administration of 5,7-dihydroxytryptamine or (iv) 6-hydroxydopamine into the hypothalamic paraventricular nucleus (PVN) to destroy serotonergic and catecholaminergic innervation of the cell group, respectively; (v) lesion of the medial subdivision of the PVN; and (vi) horizontal knife cuts below the PVN. Bilateral posterior and bilateral or unilateral anterior frontal cuts caused blockade of the suckling-induced release of prolactin. Likewise, most dams receiving 5,7-dihydroxytryptamine in the PVN did not respond to the suckling stimulus. Immunocytochemistry revealed that, in those rats which did not show a rise in plasma prolactin, there were almost no serotonergic fibres and terminals in the PVN, while in dams which exhibited a response, numerous serotonergic elements were evident. 6-Hydroxydopamine treatment did not cause significant alteration in the prolactin response. Lesion of the medial, largely parvocellular subdivision of the PVN, or horizontal knife cuts below this cell group, blocked the hormone response. The findings demonstrate for the first time that: (i) interruption of the connections between the brain stem and the hypothalamus interferes with the prolactin response to the suckling stimulus; (ii) serotonergic fibres terminating in the hypothalamic PVN are involved in the mediation of the suckling stimulus; and (iii) within the PVN, neurones in the medial, largely parvocellular subdivision of the cell group take part in the transfer of the neural signal, eventually inducing prolactin release.

5,7-Dihydroxytryptamine↗

PubMed2000

NO-mediated cGMP synthesis in cholinergic neurons in the rat forebrain: effects of lesioning dopaminergic or serotonergic pathways on nNOS and cGMP synthesis.

Nitric oxide synthase (NOS) activity and NO-mediated cGMP synthesis were studied in the rat forebrain of control animals and animals which had received a unilateral lesioning of dopaminergic or serotonergic pathways. Lesioning of the dopaminergic innervation using 6-hydroxydopamine resulted in a 50% decrease in NOS activity in the lesioned frontal cortex and caudate putamen. Lesioning of the serotonergic innervation using 5,7-dihydroxytryptamine had no effect on NOS activity. NO-mediated cGMP accumulation in rat forebrain slices was not affected by 6-hydroxydopamine or 5,7, -dihydroxytryptamine lesioning. Using cGMP immunocytochemistry, it was demonstrated that NO-mediated cGMP synthesis was absent from dopaminergic, serotonergic, GABA-ergic and neuronal NOS-containing nerve fibres. A minor colocalization of cGMP immunoreactivity was found in parvalbumin-containing fibres in the cortex. Extensive colocalization between cGMP immunoreactivity and the acetylcholine transporter was found in all cortical areas and in the caudate putamen. There was no effect of the lesions on this colocalization. These results demonstrate NO-mediated cGMP accumulation in cholinergic fibres in the forebrain of the rat and suggest an anterograde signalling function of NO in cholinergic neuronal systems in the cortex and caudate putamen of the rat.

1-Methyl-3-isobutylxanthine↗

PubMed1990

Trypanocidal effects of catecholamines and indolealkylamines.

Catecholamines, indolealkylamines and their analogues are oxidized at neutral or alkaline pH, producing hydrogen peroxide, quinones and free radicals. Several of these amines were tested for trypanocidal effects on Trypanosoma brucei, which possess a well-documented vulnerability to such oxidation products. Dopamine, 5-hydroxydopamine (5-OHDA), 6-hydroxydopamine (6-OHDA), 5-hydroxytryptamine (5-HT), 5,6-dihydroxytryptamine (5,6-DHT) and 5,7-dihydroxytryptamine (5,7-DHT) killed the parasites in vitro, using a fibroblast feeder layer cell culture system, in four to 48 hours at concentrations of 10(-5)-10(-7) M. The 5-OHDA, 6-OHDA, 5,6-DHT and 5,7-DHT were also effective in vivo when tested by intraperitoneal injection of infected mice.

Animals↗

PubMedDate not supplied

Effects of neurotoxin-induced brainstem lesions on the respiratory responses of conscious rats.

Respiration was recorded in unanaesthetized rats breathing air, or CO2 in air, 4-8 days after injection into the rostral brainstem at the level of the dorsal raphe nucleus of either a catecholaminergic neurotoxin, a serotoninergic neurotoxin, or the vehicle (0.5% ascorbic acid) of these drugs. Some rats were pretreated with the noradrenergic neurone protecting agent, desmethylimipramine (DMI). Vehicle injection resulted in an increase in the frequency (f) sensitivity to CO2. In two of four cases, injection of 6-hydroxydopamine caused a similar response but in the remaining cases injections caused increases in inspiratory duration (TI), expiratory duration (TE) and tidal volume (VT) during air-breathing. The serotonergic neurotoxin, 5,7-dihydroxytryptamine, reduced the frequency sensitivity to CO2 significantly. This reduction was not sustained. In all cases air-breathing f was decreased due to a prolongation of TI; in most cases air-breathing VT was increased. The characteristic effect of midline 5,7-dihydroxytryptamine lesions was an increase in the VT sensitivity to CO2. On the basis of the results, it is proposed that noradrenaline is essential to the processes determining basic respiratory rhythm, whereas dopamine and serotonin are important inhibitors in chemoreflex ventilatory patterns.

5,7-Dihydroxytryptamine↗

PubMed2006

The serotonergic inhibition of slowly bursting cells in the intergeniculate leaflet of the rat.

Electrophysiological studies combined with local neurotoxic lesions were conducted on anaesthetized rats in order to determine whether the dorsal raphe nucleus (DRN) inhibits the intergeniculate leaflet (IGL) of the lateral geniculate nucleus by means of innervation by serotonin-containing fibres. In the control animals, electrical stimulation of the DRN induced the long-latency and long-lasting inhibition of the neuronal firing of the IGL cells that are characterized by rhythmic, slow-bursting activity in light conditions. The electrical destruction of the DRN resulted in an increase in the firing rate of the recorded IGL cells, whilst at the same time not affecting the rhythmic, bursting pattern of the activity. In the second group of animals, local neurotoxic lesion of serotonergic fibres was performed by injection of the toxin 5,7-dihydroxytryptamine into the IGL. After 10 days of postoperative recovery, electrophysiological experiments were performed on the toxin-treated rats. In these animals, electrical stimulation as well as electrical lesion of the DRN did not induce any change in the firing of the slowly bursting cells in the 5,7-dihydroxytryptamine-injected IGL. The results obtained provide evidence that inhibition of the IGL slowly bursting cells, by innervation from the dorsal raphe, is mediated by the release of serotonin. Furthermore, the observed serotonergic inhibition of the light-dependent activity of slowly bursting cells can contribute to the neuronal mechanism gating the information that flows through this nucleus to the vestibular, visuomotor, circadian and sleep/arousal systems, with which the IGL is strongly interconnected.

5,7-Dihydroxytryptamine↗

PubMed1981

[3H]Metergoline: a new ligand of serotonin receptors in the rat brain.

A specific binding site for [3H]metergoline characterized by a KD of 0.5-1.0 nM was detected in microsomal and synaptic plasma membranes from various areas of the adult rat brain. Experiments with 5,7-dihydroxytryptamine- and kainic acid-induced lesions indicated that this specific binding site was localized post-synaptically with respect to serotoninergic neurons. The pharmacological characteristics of [3H]metergoline binding to microsomal membranes from the whole forebrain strongly suggest that this ligand labels a class of serotonin receptors. This was particularly obvious in the hippocampus in which serotonin was about 400 times more potent than dopamine and noradrenaline for displacing bound [3H]metergoline. In the striatum, serotonin was only 10 times as potent as dopamine in inhibiting [3H]metergoline binding, suggesting that this ligand may also bind to dopamine receptors. Striking similarities between the binding sites for [3H]metergoline and [3H]serotonin were observed in the hippocampus. Thus, not only the total numbers of binding sites for these two ligands in control rats but also their respective increases following intracerebral 5,7-dihydroxytryptamine treatment were very similar. Therefore, at least in the hippocampus, [3H]metergoline might well be the appropriate ligand for studying the characteristics of the 'antagonist form' of serotonin receptors postulated by Bennett and Snyder.

5,7-Dihydroxytryptamine↗

PubMed1992

Decarboxylation of exogenous L-3,4-dihydroxyphenylalanine in rat striatum as studied by in vivo voltammetry.

An in vivo voltammetric technique was used to determine whether striatal nondopaminergic neurons take up and decarboxylate exogenous L-3,4-dihydroxyphenylalanine (L-DOPA) and release it as dopamine. After the striatal serotonergic neurons of the rat had been destroyed by intraventricular injection of 5,7-dihydroxytryptamine, L-DOPA was administered intraperitoneally. It was found that changes in the dopamine concentration in the striatal extracellular fluid of the rat were the same as those in the nonlesioned rat. L-DOPA was also administered to the rat after the striatal perikarya had been destroyed by the intrastriatal injection of kainate. The striatal dopamine concentrations of the lesioned rat changed in parallel with 5,7-dihydroxytryptamine-lesioned rats, as well as the nonlesioned rats. Moreover, when normal rats were administered L-DOPA, the dopamine concentration was not increased in the cerebellum, where dopamine neurons do not exist. From these observations, it is concluded that exogenous L-DOPA is taken up, decarboxylated to dopamine, and released only in the striatal dopamine neurons.

5,7-Dihydroxytryptamine↗

PubMed1978

Involvement of the periaqueductal grey matter and spinal 5-hydroxytryptaminergic pathways in morphine analgesia: effcts of lesions and 5-hydroxytryptamine depletion.

1 Electrolytic lesions of the periaqueductal grey matter (PAG) were made in rats. The analgesia produced by intraperitoneal injection of morphine (10 and 20 mg/kg), tested by the tail flick and hot plate methods, was substantially reduced in the lesioned rats. Baseline pain thresholds were unaffected by the lesions.2 The lesion effects were not due to damage to the dorsal raphé nucleus. The extent of histologically determined damage to the dorsal raphé and the resulting decrease in striatal 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) concentrations did not correlate with the reduction in morphine analgesia produced by the lesion. Furthermore, microinjections of 5, 6-dihydroxytryptamine (5,6-DHT) into the dorsal raphé nucleus produced a similar fall in 5-HIAA levels but had no effect on morphine analgesia.3 Selective destruction of the periventricular catecholamine system produced by microinjection of 6-hydroxydopamine (6-OHDA) caused a slight decrease in morphine analgesia, thus raising the possibility that catecholamines may be involved in the action of morphine in the PAG.4 5,7-Dihydroxytryptamine-induced lesions of the spinal cord 5-hydroxytryptaminergic pathways reduced cord 5-HT concentration by 70% and markedly attenuated morphine analgesia as determined by the tail flick test.5 These experiments provide additional evidence that the PAG is a major site of action of opiates in producing analgesia. Furthermore, they have demonstrated the probable involvement of spinal 5-hydroxytryptaminergic pathways in the mediation of opiate analgesic effects.

Analgesia↗

PubMed1990

Synaptosomal tryptophan uptake and efflux following lesion of central 5-hydroxytryptaminergic neurones.

1. This study attempted to determine whether the activation of the tryptophan carrier in rat forebrain synaptosomes caused by depolarization or by extracellular sodium depletion occurred exclusively in 5-hydroxytryptaminergic nerve endings. 2. Ascending 5-hydroxytryptaminergic neurones were lesioned either electrolytically or by intraventricular administration of 5,7-dihydroxytryptamine. The extent of the lesion was assessed by comparing the uptake of [3H]-5-hydroxytryptamine (5-HT) in lesioned animals and in sham-operated controls. [3H]-5-HT uptake was reduced by 85.9 +/- 1.63% (mean +/- s.e. mean) in animals receiving electrolytic lesions, and by 87.4 +/- 4.51% in those receiving 5,7-dihydroxytryptamine. 3. The uptake of [3H]-tryptophan by synaptosomes from lesioned animals incubated in standard Na(+)-rich media was slightly lower (278.8 +/- 27.3 pmol mg-1 protein min-1) than that observed in sham-operated controls (360.6 +/- 30.3 pmol mg-1 protein min-1). However, uptake in the absence of extracellular Na+ was increased to a similar extent in both the sham-operated (539 +/- 54.5 pmol mg-1 protein min-1) and lesioned animals (507.2 +/- 42.4 pmol mg-1 protein min-1). 4. The efflux of [3H]-tryptophan in response to extracellular Na+ depletion was similar in sham-operated and lesioned animals. Release expressed as a percentage of tissue [3H]-tryptophan released in response to the pulse of Na(+)-free medium was 6.691 +/- 0.585 (n = 4) in sham-operated controls and 8.195 +/- 0.906 in lesioned animals. 5. The efflux of [3H]-tryptophan in response to K+ depolarization was also unchanged in lesioned animals when compared with sham-operated controls. Release, expressed as described above was, in sham-operated controls 3.76 +/- 0.41 (n = 4) and 4.09 +/- 0.30 in lesioned animals. 6. The results of this study show that the tryptophan carrier which is activated by depolarization or by extracellular Na+ depletion is not located exclusively on 5-hydroxytryptaminergic nerve endings. Moreover the contribution made by 5-hydroxytryptaminergic neurones appears to be only minor.

5,7-Dihydroxytryptamine↗

PubMed1986

Does serotonin play a role in entrance into hibernation?

To study the role of brain serotonin in entrance into hibernation, intraventricular injections of 5,7-dihydroxytryptamine, electrolytic lesions of small parts of the median raphe nucleus, and chemical lesions of the same nucleus were undertaken on the European hamster in winter. All the lesions led to a variable decrease of serotonin levels in all parts of the brain areas examined. However, hibernation was suppressed only in those animals whose serotonergic neurons were destroyed in a small anterior part of the median raphe nucleus. Electrolytic lesions as well as chemical lesions in the other parts of the median raphe nucleus or the 5,7-dihydroxytryptamine injections into lateral ventricles do not prevent hibernation. These data suggest that in the European hamster only a specific group of serotonergic neurons of the median raphe nucleus are involved in the process of entrance into hibernation.

5,7-Dihydroxytryptamine↗

PubMed1996

Brain serotonin depletion attenuates heatstroke-induced cerebral ischemia and cell death in rats.

To explore the importance of brain serotonin (5-hydroxytryptamine) in the heatstroke-induced cerebral ischemia and neuronal injury, we evaluated the effects of heatstroke on brain serotonin release, survival time, cerebral hemodynamic changes, and neuronal cell damage in rats with or without brain serotonin depletion produced by 5,7-dihydroxytryptamine. In vivo voltammetry was used to measure changes in extracellular concentrations of serotonin in the anterior hypothalamus, striatum, and frontal cortex. After the onset of heatstroke, rats without brain serotonin depletion displayed hyperthermia, decreased mean arterial pressure, increased intracranial pressure, decreased cerebral perfusion pressure, decreased cerebral blood flow, increased cerebral serotonin release, and increased cerebral neuronal damage compared with those of normothermic control rats. However, when the cerebral serotonin system was destroyed by 5,7-dihydroxytryptamine, the heatstroke-induced arterial hypotension, intracranial hypertension, ischemic damage to the brain, and elevated cerebral serotonin release were reduced. In addition, the survival time of the heatstroke rats was prolonged after the depletion of brain serotonin. The data indicate that brain serotonin depletion attenuates heatstroke-induced cerebral ischemia and cell death in rats.

5,7-Dihydroxytryptamine↗

PubMed2006

Ventilatory response to hypercapnia and hypoxia after extensive lesion of medullary serotonergic neurons in newborn conscious piglets.

Acute inhibition of serotonergic (5-HT) neurons in the medullary raphé (MR) using a 5-HT(1A) receptor agonist had an age-dependent impact on the "CO(2) response" of piglets (33). Our present study explored the effect of chronic 5-HT neuron lesions in the MR and extra-raphé on the ventilatory response to hypercapnia and hypoxia in piglets, with possible implications on the role of 5-HT in the sudden infant death syndrome. We established four experimental groups. Group 1 (n = 11) did not undergo any treatment. Groups 2, 3, and 4 were injected with either vehicle or the neurotoxin 5,7-dihydroxytryptamine in the cisterna magna during the first week of life (group 2, n = 9; group 4, n = 11) or second week of life (group 3, n = 10). Ventilation was recorded in response to 5% CO(2) (all groups) and 12% O(2) (group 2) during wakefulness and sleep up to postnatal day 25. Surprisingly, the piglets did not reveal changes in their CO(2) sensitivity during early postnatal development. Overall, considerable lesions of 5-HT neurons (up to 65% decrease) in the MR and extra-raphé had no impact on the CO(2) response, regardless of injection time. Postlesion raphé plasticity could explain why we observed no effect. 5,7-Dihydroxytryptamine-treated males, however, did present a lower CO(2) response during sleep. Hypoxia significantly altered the frequency during sleep in lesioned piglets. Further studies are necessary to elucidate the role of plasticity, sex, and 5-HT abnormalities in sudden infant death syndrome.

5,7-Dihydroxytryptamine↗

PubMed1984

Effects of monoamine neurotoxins injected in different brain areas on gonadotropin and androgen secretion in the male.

In order to investigate the relative contribution of the serotoninergic and catecholaminergic innervation of different brain structures to the control of gonadotropin secretion in the male, adult rats were given bilateral injections of the selective neurotoxins, 5,7-dihydroxytryptamine and 6-hydroxydopamine, into the mediobasal hypothalamus, the medial preoptic area, the amygdala, and the medial forebrain bundle. Serum levels of luteinizing hormone (LH), follicle-stimulating hormone, testosterone, pituitary follicle-stimulating hormone, and LH content were measured 15 days later. The medial preoptic area 5,7-dihydroxytryptamine injections were followed by 2- to 3-fold increases of serum LH and testosterone levels and pituitary LH concentration. The 6-hydroxydopamine injections in the medial forebrain bundle resulted in a 60% decrease of pituitary LH content, associated with serum levels of LH and testosterone which were lowered, although not significantly. None of the treatments seemed to influence either serum or pituitary concentrations of follicle-stimulating hormone. These results suggest a hitherto undocumented major function of the serotoninergic innervation of the medial preoptic area in the control of LH secretion in the male and confirm previous reports indicating that some of the catecholaminergic fibers carried by the medial forebrain bundle can be modulatory for LH secretion.

5,6-Dihydroxytryptamine↗