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PubMed1976

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

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

5,6-Dihydroxytryptamine↗

PubMed1986

The effect of altered 5-hydroxytryptamine levels on beta-endorphin content in rat brain.

The purpose of the present study was to examine the effect of altering the concentration of 5-hydroxytryptamine (5-HT) on beta-endorphin (beta-Ep) content in the hypothalamus, thalamus, and periaqueductal gray (PAG)-rostral pons regions of the rat brain. The selective 5-HT reuptake inhibitor, fluoxetine (10 mg/kg), significantly lowered beta-Ep content in the hypothalamus and the PAG. Parachlorophenylalanine, which inhibits 5-HT synthesis, significantly elevated beta-Ep in all brain parts studied. Intracisternal injections of the neurotoxin, 5',7'-dihydroxytryptamine, with desmethylimipramine pretreatment, significantly increased beta-Ep content in the hypothalamus and the PAG. In adrenalectomized rats, fluoxetine significantly decreased beta-Ep levels in the hypothalamus and increased the levels in the PAG. The results indicate that 5-HT may modulate the levels of brain beta-Ep.

5,7-Dihydroxytryptamine↗

PubMed1998

Pretraining infusion of DSP-4 into the amygdala impaired retention in the inhibitory avoidance task: involvement of norepinephrine but not serotonin in memory facilitation.

The present study investigated the involvement of amygdala noradrenergic (NE) and serotonergic (5-HT) systems in memory storage processing. Rats bearing chronic cannulae in the amygdala were trained on a one-trial inhibitory avoidance task and tested for retention 24 hrs later. Five days prior to training, rats received intra-amygdala infusion of vehicle or various doses of N-2-chloroethyl-N-ethyl-2-bromobenzylamine (DSP-4)-a NE-specific neurotoxin when given peripherally. Results showed that pretraining intra-amygdala infusion of 10.0 micrograms or 30.0 micrograms of DSP-4 impaired retention. Further, 30.0 micrograms of DSP-4 also abolished the memory enhancing effect of epinephrine (E) injected peripherally. However, local infusion of DSP-4 depleted not only NE but also 5-HT and DA substantially. Subsequent experiments found that the retention deficit induced by 30.0 micrograms of DSP-4 could be ameliorated by 0.2 microgram NE but not by 5-HT at a wide range of doses infused into the amygdala shortly after training, which ascribed the deficit to depletion of NE. After protecting the 5-HT terminals by a pretreatment of fluoxetine (15.0 mg/kg), pretraining intra-amygdala infusion of 30.0 micrograms DSP-4 shifted the memory-enhancing dose of E from 0.1 mg/kg to 1.0 mg/kg. In contrast, pretraining intra-amygdala infusion of 15.0 micrograms 5,7-dihydroxytryptamine (5,7-DHT) or DSP-4 with a pretreatment of desipramine (DMI, 25.0 mg/kgx2) to protect NE terminals failed to impair retention or attenuate the memory enhancing effect of 0.1 mg/kg E injected peripherally. These findings, taken together, suggest that the memory modulatory effect of peripheral E involved, at least partially, the amygdala NE system.

5,7-Dihydroxytryptamine↗

PubMed2000

Serotonin depletion in vivo inhibits the branching of olfactory projection neurons in the lobster deutocerebrum.

Serotonin depletion during embryogenesis has been shown previously to retard the growth of the olfactory and accessory lobes of the lobster deutocerebrum (Benton et al., 1997). The present study was undertaken to determine whether morphological changes in the interneurons innervating these lobes contribute to this growth retardation. We examined the effects of in vivo serotonin depletion using 5,7-dihydroxytryptamine (5,7-DHT) on the morphology of the olfactory projection neurons, one of two major classes of interneurons that innervate both lobes. Intracellular dye fills of olfactory projection neurons in normal embryos showed that each neuron extensively innervates either the olfactory or accessory lobe before projecting to neuropil regions in the protocerebrum. In embryos injected with 5,7-DHT, however, the deutocerebral arbors of 13.5% of the olfactory projection neurons examined were either markedly reduced compared with normal neurons or absent. Affected neurons also exhibited a number of additional aberrant morphological features suggesting that these neurons represent cells that were affected during their initial morphogenesis. Olfactory projection neurons with aberrant morphologies were also encountered, although less frequently (7.5% of the neurons examined), in control (sham-injected) embryos indicating that the sham injections can affect the development of the brain. This observation provides insights into the nature of effects seen in control embryos in previous experiments (Benton et al., 1997). The results of the present study indicate that in vivo serotonin depletion inhibits the branching of olfactory projection neurons and suggest, therefore, that one of the functions of serotonin during normal development is to promote the ingrowth of these neurons into the deutocerebral neuropils.

5,7-Dihydroxytryptamine↗

PubMed2000

Quantitative autoradiographic mapping of rat brain dopamine D3 binding with [(125)I]7-OH-PIPAT: evidence for the presence of D3 receptors on dopaminergic and nondopaminergic cell bodies and terminals.

The regional distribution and cellular localization of dopamine D3 receptors in the rat brain was examined using quantitative autoradiography. [(125)I]7-OH-PIPAT bound in a saturable and reversible manner and exhibited subnanomolar affinity for a single population of GTP-insensitive sites. The pharmacological profile was characteristic of cloned D3 receptors and nonspecific binding was uniformly low. The highest levels of D3 receptors were measured in the islands of Calleja, nucleus accumbens, ventral pallidum, substantia nigra, and lobules 9 and 10 of the cerebellum. The high specific activity of this ligand also allowed detection of D3 receptors in other regions, including the serotonergic dorsal and median raphe nuclei, indicating that the distribution of this receptor is more widespread than previously appreciated. The cellular localization of D3 receptors in regions containing dopaminergic cells and terminals was examined by discrete injection of neurotoxins. Lesion of dopaminergic neurons with 6-hydroxydopamine produced 50% decreases in [(125)I]7-OH-PIPAT binding in the nucleus accumbens and substantia nigra. Quinolinic acid lesion of neurons originating in the nucleus accumbens also produced approximately 50% decreases in D3 receptors in the nucleus accumbens, substantia nigra, and ventral pallidum. 5, 7-Dihydroxytryptamine lesion of serotonergic cells and processes produced no changes in [(125)I]7-OH-PIPAT binding. These results demonstrate the presence of D3 receptors in several brain regions not previously identified and suggest that D3 receptors are expressed at somatodendritic and terminal levels of both dopaminergic and nondo-paminergic cells within the mesolimbic dopamine system.

5,7-Dihydroxytryptamine↗

PubMed2000

Serotonergic modulation of ethanol-induced electrophysiological depression in young and aged rats.

BACKGROUND: Ethanol (EtOH)-induced electrophysiological depressions in cerebellar Purkinje neurons have been shown to be potentiated by exogenously applied serotonin (5HT). In this study, we determined whether this modulatory action can be activated by endogenous release from presynaptic serotonergic terminals, and whether such a response is altered by age or rat strain. METHODS: Extracellular 5HT levels in cerebellar cortex were measured in real time by in vivo chronoamperometry, by using Nafion-coated carbon fiber electrodes, in anesthetized young (3-5 months old) or aged (18-24 months old) Sprague Dawley and Fischer 344 rats. Some animals were prelesioned with 5,7 dihydroxytryptamine (5,7 DHT). Single unit electrophysiological activity was recorded from cerebellar Purkinje neurons. Serotonin or its presynaptic antagonist methiothepin was applied directly to cerebellar neurons through multibarrel pipettes. RESULTS: Local application of methiothepin dose-dependently induced 5HT overflow in young Sprague Dawley and Fisher 344 rats. Methiothepin-induced 5HT release was decreased significantly in aged or 5,7 DHT-lesioned rats. Local application of methiothepin or 5HT potentiated EtOH-induced electrophysiological depression of Purkinje neurons in young animals of both strains. Methiothepin-potentiated, EtOH-elicited neuronal inhibition was reduced greatly in aged or 5,7 DHT-lesioned rats. Serotonin-facilitated EtOH responses were reduced in the aged Sprague Dawley rats. CONCLUSIONS: EtOH-induced electrophysiological responses in cerebellum can be facilitated by endogenous 5HT release by using a 5HT autoreceptor antagonist. Such actions are attenuated in aged rats perhaps through a presynaptic serotonergic mechanism.

5,7-Dihydroxytryptamine↗

PubMed2001

Endogenous serotonin contributes to a developmental decrease in long-term potentiation in the rat visual cortex.

The primary visual cortex shows synaptic plasticity during a postnatal "critical period," and its plasticity declines with development. Indeed, we found a developmental decrease in the induction of long-term potentiation (LTP) in the rat visual cortex. In visual cortex slices obtained from 2- to 3-week-old rats, tetanic stimulation (100 Hz for 1 sec, twice at an interval of 30 sec) of the white matter reproducibly induced LTP of field potentials in layer II/III. However, in slices from 5-week-old rats, the same tetanic stimulation failed to induce LTP. We hypothesized that endogenous serotonin (5-HT) is responsible for the developmental decrease in visual cortex LTP, because the induction of visual cortex LTP was suppressed by the addition of exogenous 5-HT (10 microm) and because the amount of 5-HT in the visual cortex increased during development. To test this hypothesis, we investigated the effect of methysergide, a 5-HT receptor antagonist, on the induction of visual cortex LTP. When visual cortex slices from 5-week-old rats were perfused with 50 microm methysergide, tetanic stimulation of the white matter induced robust LTP in layer II/III. Furthermore, serotonergic neurons were lesioned by intracerebroventricular injection of 5,7-dihydroxytryptamine (5,7-DHT). LTP was induced in visual cortex slices from 5,7-DHT-treated, 5-week-old rats. These results suggest that the induction of visual cortex LTP in 5-week-old rats is suppressed by endogenous 5-HT. 5-HT may be a factor that determines a critical period for synaptic plasticity in the rat visual cortex.

5,7-Dihydroxytryptamine↗

PubMedDate not supplied

[Influence of neurotensin on behavior of rats with lesions in serotonergic neurons].

After serotonergic lesion by administration of 5,7-dihydroxytryptamine into the dorsalis raphe nucleus, effects of neurotensin microinjections into the caudate nucleus and substantia nigra on rat behavior were compared. Serotonergic lesions resulted in motivated excitement of rats manifested as an increase in the number of intersignal motor reactions during realization and, particularly, extinction of thirst conditioned reflex. Neurotensin microinjections into the caudate nucleus facilitated extinction of the conditioned reflex both in operated and control rats, but such microinjection into the substantia nigra facilitated this process only in operated animals. Neurotensin did not change conditioned reflex realization in both groups of animals but decreased emotional excitement of rats in the "open field". The behavioral effects of neurotensin in operated rats are connected with normalization of motivational and emotional states of animals and may be explained by recovery of interaction between the dopamine- and serotonergic systems. It is suggested that the mechanisms of this normalizing effects of neurotensin at the levels of the caudate nucleus and substantia nigra are different and are associated preferentially with its action either on dopamine- or serotonergic structures.

5,7-Dihydroxytryptamine↗

PubMed1992

[Ultrastructure identification of raphe-spinal serotonergic pain modulating system in rats].

5,6-dihydroxytryptamine was microinjected into the nucleus raphe magus (NRM) of rats. The sections of upper cervical segments were processed for immunoreactive substance P (SP). The degenerated axon terminals and immunoreactive fibers were identified by electron microscopy. The results show that the degenerated axon terminals and immunoreactive positive dendrites and axons were found in the laminae I and II of the dorsal horn. The electron-dense axon terminals were in contact with unlabelled dendrites, some also in contract with immunoreactive dendrites. In lamina II, one of degenerated axon terminals as a center was contacted by several unlabelled axonal boutons. SP labelled terminals were synapsed with unlabelled dendrites and dendritic spine; in addition, unlabelled axo-axonal synapse was found in lamina II. These results suggest that 5-HT axon terminals from NRM directly innervate SP and non-SP neurons in the laminae I and II.

Animals↗

PubMed1992

[Effect of brain serotonin on the arterial pressure and plasma renin in normal and hypertensive rats].

The effects of changes in brain serotonin content after injections of p-chlorophenylalanine (p-CPA), L-5-hydroxytryptophan (L-5HTP) and 5-6-dihydroxytryptamine (5-6DHT) on the mean arterial pressure (MAP), plasma renin activity (PRA) and peripheral levels of atrial natriuretic peptide (ANP) have been studied in normal and hypertensive (2K:1C model) male Wistar rats. The p-CPA (250 mg/kg) and L-5HTP (200 mg/kg) were injected i.p., while 5-6 DHT (15 micrograms/animal in 10 mu/animal vehicle) was injected into lateral brain ventricles. The effects were studied 24 h after the p-CPA injection, 2 h after L-5HTP and 10 or 20 days after 5-6DHT administration. The fall in brain serotonin produced by p-CPA and 5-6DHT did not modify the MAP values in the normal and hypertensive rat model, whereas the increase induced after L-5HTP injection only caused a slight decrease in arterial pressure in normotensive animals. The ARP experimented remarkable rises in the normal and hypertensive rats, these values increasing after L-5HTP and falling after p-CPA and 5-6 DHT injections. Similar changes are detected in the normal group after administration of these substances related to serotoninergic brain activity. The ANP levels rose after renal artery constriction, and they are not affected by the above mentioned substances. Only p-CPA and 5-6DHT reduced a low decrease in the ANP levels 10 days after their administration.(ABSTRACT TRUNCATED AT 250 WORDS)

5,6-Dihydroxytryptamine↗

PubMedDate not supplied

Neonatal 5-hydroxytryptamine depletion induces depressive-like behavior in adult rats.

The influence of neonatal serotonergic lesion on adult behavior in locomotor and depression models was studied in male Wistar rats. When 3-day-old rats were injected intracisternally with 5,7-dihydroxytryptamine (5,7-DHT), a marked depletion of brain 5-HT was observed when animals were killed 3 months after the treatment. Brain catecholamine content was generally not changed by neurotoxin treatment. The behavioral consequence of intracisternal 5,7-DHT administration to developing rats consisted in reduction of adult rats' activity in the forced swimming test. Both desipramine, and, to the lesser extent, fluoxetine, reversed 5,7-DHT-induced immobility of animals.

5,7-Dihydroxytryptamine↗

PubMedDate not supplied

[Delayed effects of neurotensin microinjections into the substantia nigra on conditioned motor reactions of rats with lesions to serotoninergic neurons].

Behavioral effects of neurotensin microinjections into the brain substantia nigra of rats with neurotoxic (5,7-dihydroxytryptamine) lesions of serotoninergic neurons in the dorsal raphe nucleus were studied. It was shown that neurotensin facilitated extinction of conditioned and intertrial reactions to negative (unreinforced) stimuli, but did not change the actualization of positive (with water reward) conditioned signals. Neurotensin-induced effects persisted in subsequent experiments without injections of the peptide. Neurotensin injections reduced the negative emotional states of lesioned animals in the arena during testing conditioned preference. It was concluded that the behavioral effects of neurotensin can be explained by the formation in the lesioned animals of the situational emotional state facilitating adaptive brain functions.

5,7-Dihydroxytryptamine↗

PubMed1977

Studies on membrane receptor sites for serotonin in the brain.

The competitive effect of 5,6-dihydroxytryptamine, morphine and chlorpromazine on the binding of serotonin (5-HT) to rat brain slices was investigated. Ths busynaptosomal localization of the binding of morphine in bovine midbrain preparations was compared to that of 5-HT and found to be considerably higher. The condensation of 5-HT and tryptamine receptor carbonyl groups in brain with phenylisopropylhydrazine was shown in vitro and vivo. Membrane particles labeled with [14C] tryptamine or 5-HT in presence or absence of sodium borohydride (NaBH4) were extracted with chloroform-methanol (C-M) 2:1. The labeled proteolipid precipitated by ether from these extracts showed on electropherograms one single radioautographic spot which was more intense with samples treated with sodium borohydride. In column chromatography, the bound radioactivity peak eluted with the gel void volume, was associated with a protein peak. The eluted, lyophilized material of this fraction was extracted by chloroform methanol (2:1) thus suggesting its proteo-lipid nature.

5,6-Dihydroxytryptamine↗

PubMed1979

Effects of brain serotonin alterations on prostaglandin E1-induced bradycardia in rats.

The vasodepressor and bradycardia responses of saline control, serotonin-depleted and serotonin-potentiated rats to an intravenous dose of prostaglandin E1 (PGE1) were assessed under the urethane anesthesia. Elevation of serotonin concentration in brain with either 5-hydroxytryptophan (a serotonin precursor) or chlorimipramine (an inhibitor of serotonin reuptake), although causing no changes in vasodepressor reuptake), although causing no changes in vasodepressor response, did enhance the PGE1-induced bradycardia in contrast, depleting serotonin concentration in brain with either p-chlorophenylalanine or 5,7-dihydroxytryptamine greatly reduced the PGE1-induced bradycardia without changes in vasodepressor response. Moreover, the reduced PGE1 bradycardia induced by p-chlorophenylalanine treatment was readily reversed by the replacement of the depleted brain serotonin with 5-hydroxytryptophan in combination with a peripheral decarboxylase inhibitor Ro4-4602. The data indicate that brain serotonergic systems play a role in the elaboration or modulation of the PGE1-induced bradycardia. Specifically, brain serotonin seems to facilitate the PGE1-induced bradycardia since its depletion causes a decrease and its potentiation or elevation causes an increase in the PGE1-induced bradycardia.

5,7-Dihydroxytryptamine↗

PubMed1992

Baroreflex changes produced by serotonergic or catecholaminergic lesions in the rat nucleus tractus solitarius.

To distinguish between catecholaminergic and serotonergic mechanisms for baroreflex regulation in the medulla, we compared rats with chemical lesions produced by injecting 6-hydroxydopamine (6-OHDA) or 5,7-dihydroxytryptamine (5,7-DHT) into the nucleus tractus solitarius (NTS) bilaterally at the caudal tip of the area postrema. After 2 weeks, basal blood pressure and heart rate were unaltered, but blood pressure lability, instead of being increased, was slightly reduced. Baroreflex tests in conscious rats showed that although phenylephrine-induced reflex bradycardia was unaffected, nitroprusside-induced reflex tachycardia was enhanced by 5,7-DHT. In anesthetized rats, drug-induced reflex chronotropic responses no longer differed between groups, but attendant decreases or increases in renal nerve activity were consistently reduced by 6-OHDA. On the other hand, upon afferent aortic nerve stimulation, particularly with low current frequencies, bradycardic and sympathoinhibitory responses were enhanced by 5,7-DHT, but the sympathoinhibitory responses were reduced by 6-OHDA. Despite the absence of demonstrable necrosis or cell loss at NTS injection sites, 6-OHDA reduced norepinephrine mainly and serotonin partly, whereas 5-7-DHT reduced serotonin content alone, thereby indicating that chemical lesions had indeed been produced. Because these cardiovascular changes probably reflect differences in catecholaminergic vs. serotonergic baroreflex regulation, our results are generally compatible with the interpretation that baroreflex modulation in the NTS involves catecholaminergic facilitation and serotonergic inhibition.

5,7-Dihydroxytryptamine↗

PubMed1991

The effects of serotonin depletion and raphe grafts on hippocampal electrophysiology and behavior.

The involvement of the serotonergic system in spatial learning and a possible correlation between serotonergic modulation of hippocampal electrical activity and spatial learning were studied in rats. Control, partial septal-lesioned (SL), 5,7-dihydroxytryptamine (5,7-DHT)-injected (DHT), double-lesioned (5,7-DHT and SL; DL), and DL rats that were transplanted with embryonic raphe grafts into the hippocampus (RG) were tested in a spatial task in a water maze and in an active avoidance shuttle-box task. The responses of the dentate gyrus (DG) to perforant-path (PP) stimulation were examined in the same rats, under the following conditions: (1) priming stimulation of the PP (testing feedback inhibition), (2) priming stimulation of the commissural pathway (testing feedforward inhibition), (3) during repeated stimulation of the PP at 7 Hz (frequency potentiation), and (4) following tetanic stimulation [long-term potentiation (LTP)]. DL, but not DHT or SL, treatment severely impaired the performance of rats in both reference- and working-memory tasks in the water maze. This effect was not seen in the shuttle box. The ability of the DG to exhibit LTP, which was reduced in the DHT and SL rats, was apparently similar to controls in the DL group, DL, but not DHT or SL alone, resulted in a reduction of inhibition in the DG. Both the behavioral deficits and the reduction in hippocampal inhibition were ameliorated by intrahippocampal raphe grafts. These results indicate that the serotonergic innervation of the hippocampus plays a role in spatial learning when the septohippocampal neurotransmission systems are disrupted. Furthermore, these results suggest that restoration of modulation of hippocampal inhibition, by raphe grafts, underlies the behavioral recovery observed in these rats.

5,7-Dihydroxytryptamine↗

PubMed1991

Distribution of GAP-43 mRNA in the brain stem of adult rats as evidenced by in situ hybridization: localization within monoaminergic neurons.

Using in situ hybridization, we examined the distribution of the mRNA encoding for the growth-associated protein GAP-43 in the brain stem of adult rats. GAP-43 was expressed at the highest level in the nucleus raphe dorsalis (NDR), nucleus centralis superior (NCS), substantia nigra compacta (SNc), ventral tegmental area (VTA), and locus coeruleus (LC). An intermediate level of signal was detected over the periaque-ductal gray, superior colliculi, and thalamic region, and no significant signal was detected in the substantia nigra pars reticulata and red nucleus. The hybridization signals of GAP-43 mRNA and tryptophan hydroxylase mRNA completely overlapped in the NDR and NCS, and signals for GAP-43 mRNA and tyrosine hydroxylase mRNA overlapped in the SNc, VTA, and LC. The disappearance of the hybridization signal for GAP-43 mRNA after intracerebroventricular injections of the neurotoxins 5,7-dihydroxytryptamine (5,7-DHT) or 6-hydroxydopamine (6-OHDA) indicated that high levels of GAP-43 are synthesized in the serotonergic neurons of the raphe nuclei and in the catecholaminergic neurons of the SNc, VTA, and LC. In light of the role of GAP-43 in axonal outgrowth, modulation of signal transduction, and release of different neurotransmitters in the adult CNS, this phosphoprotein might be involved in the functional plasticity and synaptic transmission of monoaminergic neurons.

5,7-Dihydroxytryptamine↗

PubMed1990

Influence of urapidil and 8-OH-DPAT on brain 5-HT turnover and blood pressure in rats.

The effects of urapidil, of the selective 5-HT1A receptor agonist (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), and of the alpha 2-adrenoceptor agonist clonidine on the in vivo rate of synthesis of 5-hydroxytryptamine (5-HT) were determined in rat brain cortex and hypothalamus. Urapidil (10 mg/kg), 8-OH-DPAT (0.3 mg/kg) or clonidine (0.3 mg/kg; all drugs i.p.) caused significant reductions in 5-HT synthesis rate. Pretreatment with the selective 5-HT1A receptor antagonist spiroxatrine (SPX; 1 mg/kg s.c.) or the nonselective 5-HT1 receptor antagonist metitepine (1 mg/kg i.p.) abolished the effects of urapidil and 8-OH-DPAT, but not of clonidine. The effects of urapidil and 8-OH-DPAT on mean arterial blood pressure (MAP) and heart rate (HR) of pentobarbital-anesthetized, normotensive rats were measured following stereotaxic microinjection into the B1/B3 cell region of the ventral medulla. The mean percentage decreases induced by urapidil (3 micrograms) and 8-OH-DPAT (0.2 micrograms) amounted to (MAP/HR) -13%/-6% and -19%/-25%, respectively. The following pretreatments markedly attenuated or prevented the effects of intramedullary injections of urapidil or 8-OH-DPAT: (a) SPX (1 mg/kg s.c., 60 min): (b) intracisternal injection of the serotonergic neurotoxin 5,7-dihydroxytryptamine (5,7-DHT; 0.2 mg; 7-10 days); (c) bilateral injection of 5,7-DHT at the cervical level of the spinal cord (each side 5 micrograms; 7-10 days). The present results are compatible with an action of urapidil as agonist at central 5-HT1A receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

5,7-Dihydroxytryptamine↗