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PubMed1990

Interaction between norepinephrine and serotonin in the neuroendocrine control of growth hormone release in the rat.

Both alpha 2-adrenergic (alpha 2) and serotonergic (5HT) neurons are associated with stimulation of GH secretion via GRH release. The object of this study was to determine whether the 5HT system is involved in the stimulation of GH secretion by alpha 2-receptor agonists. There are two parts of this study. In the first, the relationship between alpha 2-5HT systems were analyzed by determining if alpha 2-stimulated GH release is mediated by 5HT. In this model, systemically administered alpha 2-agonists [clonidine (CLON) or UK14,304] were tested against 5HT antagonists (meterogoline or cyproheptadine) or 5HT synthesis inhibitors (p-chlorophenylalanine methylester hydrochloride). In the second, sites of 5HT-GRH interaction were determined by testing the response to CLON after 5HT neurotoxin [5,7-dihydroxytryptamine (5,7-DHT)] microinjection at specific hypothalamic nuclei. In both experiments sequential blood samples were withdrawn from silastic jugular cannulas in unanesthetized, freely moving animals. Metergoline (0.045 and 0.135 mg/kg, iv) and cyproheptadine (0.969 micrograms/kg, iv) suppressed, in a dose-dependent manner, the CLON (33 or 66 micrograms/kg, iv)-induced GH surge that was detected 15-30 min after injection in control animals. Both cyproheptadine (0.969 micrograms/kg, iv) and p-chlorophenylalanine (300 mg/kg, ip) effectively suppressed the UK14,304 (220 micrograms/kg, iv)-induced GH surge that occurred 15-30 min after injection in control animals. These data suggest that an intact 5HT system is required for alpha 2-stimulated GH release. 5,7-DHT neurotoxin microinjected into the midline arcuate nucleus (6 micrograms/mg,iv) or bilaterally into the ventromedial nucleus or perifornical area (4 micrograms/0.2 microliter) 5 days previously suppressed the CLON (30 micrograms/kg)-induced GH surge only in animals with arcurate nucleus lesions. To determine if the suppression was mediated by inhibition of GH-releasing hormone (GRH) or stimulation of somatostatin (SRIF), an additional experiment was conducted including 5,7-DHT arcuate nucleus-lesioned animals injected with anti-SRIF. Inasmuch as anti-SRIF failed to reverse the 5,7-DHT suppression of GH secretion, the results of this experiment suggest that GRH mediates NE-5HT-induced GH secretion. In conclusion, these data suggest that alpha 2 activation of GH secretion requires intact serotonergic terminals in the arcuate nucleus and most likely involves GRH rather than SRIF, release.

5,7-Dihydroxytryptamine↗

PubMed2001

Effect of chronic and acute administration of fluoxetine and its additive effect with morphine on the behavioural response in the formalin test in rats.

Serotonergic systems are involved in the central regulation of nociceptive sensitivity. Fluoxetine, a selective inhibitor of the reuptake of serotonin (5-hydroxytryptamine, 5-HT), was administered orally (0.16, 0.32, 0.8 mg kg(-1) daily for 7 days), intraperitoneally (0.04, 0.08, 0.16 mg kg(-1) day(-1) for 7 days and a single dose of 0.32 mg kg(-1)) and intracerebroventricularly (10 microg/rat) to rats and nociceptive sensitivity was evaluated using the formalin test (50 microL of 2.5% formalin injected subcutaneously). The effect of fluoxetine was also studied in the presence of 5,7-dihydroxytryptamine creatinine sulfate (5,7-DHT) and after co-administration with morphine. Oral (0.8 mg kg(-1)), intraperitoneal (0.16 and 0.32 mg kg(-1)) and intracerebroventricular (10 microg/rat) fluoxetine induced antinociception in the late phase of the formalin test. Furthermore, intrathecal administration of 5-HT (100 microg/rat) induced an analgesic effect. The analgesic effect of fluoxetine (0.16 and 0.32 mg kg(-1), i.p.) and 5-HT (100 microg/rat, i.t.) was abolished by pre-treatment with 5,7-DHT (100 microg/rat, i.t.). In addition, the analgesic effect of 5-HT (100 microg/rat, i.t.) was decreased by pre-treatment with naloxone (2 mg kg(-1), i.p.). Morphine (5 mg kg(-1), i.p.) induced analgesia that was increased by fluoxetine (0.32 mg kg(-1), i.p.). These results suggest that fluoxetine has an antinociceptive effect in tonic inflammatory pain through functional alteration of the serotonergic system and also potentiates the analgesic effect of morphine.

5,7-Dihydroxytryptamine↗

PubMed1988

Spinal cord TRH deficiency is associated with incomplete recovery of denervated muscle in the rat.

The raphe-spinal pathway, which contains co-localized serotonin (5-HT), thyrotropin-releasing hormone (TRH), and several TRH-prohormone-derived non-TRH peptides, projects to the ventral horn of the spinal cord. Pharmacologic ablation of this pathway with the 5-HT neurotoxin, 5,7-dihydroxytryptamine, in neonatal rats resulted in deficient recovery of plantar foot muscles, functionally denervated with botulinum toxin type A. Failure of reinnervation was suggested by slower and incomplete recovery of the plantar foot compound muscle action potential amplitude and by a reduced mean diameter of plantar foot muscle fibers in ablated rats. These findings indicate that deprivation of alpha motor neurons from descending raphe-spinal input interferes with their ability to respond to muscle-derived signals for reinnervation.

5,7-Dihydroxytryptamine↗

PubMed1999

Possible involvement of descending serotonergic systems in antinociception by centrally administered elcatonin in mice.

To elucidate the mechanisms of analgesic action of elcatonin, a synthetic analog of eel calcitonin, the effect of centrally injected elcatonin on acetic acid-induced writhing behavior was examined in mice. Intracisternal or intracerebroventricular injection of elcatonin significantly inhibited acetic acid-induced writhing behavior, while the intrathecal injection of elcatonin did not inhibit it. The inhibitory effect of intracisternal elcatonin was significantly attenuated by subcutaneous pretreatment with methysergide and (+/-)-propranolol or by intrathecal pretreatment with methysergide, (+/-)-propranolol, 1-(2-methoxyphenyl)-4-[4-(2-phthalimido) butyl]-piperazine hydrobromide (NAN-190) and granisetron, but not with (+/-)-atenolol or butoxamine. Further, the depletion of spinal 5-hydroxytryptamine (5-HT, serotonin) by pretreatment with 5,7-dihydroxytryptamine (5,7-DHT) significantly attenuated the inhibitory effect of intracisternally injected elcatonin on acetic acid-induced writhing behavior. These results suggest that the inhibitory descending serotonergic systems may be involved, through 5-HT1A and 5-HT3 receptors, in the production of an antinociceptive effect by centrally injected elcatonin.

5,7-Dihydroxytryptamine↗

PubMed1989

Enhancement of spinal monosynaptic reflexes with phenylethylamine and related drugs through descending noradrenergic neurons.

The effects of phenylethylamine (PEA) and related drugs, such as methamphetamine, phenelzine, methylphenidate, nomifensine and mazindol on the spinal monosynaptic reflex (MSR) were investigated in rats treated with 6-hydroxydopamine (6-OHDA) or 5,6-dihydroxytryptamine (5,6-DHT). PEA (1 x 10(-5) mol/kg, i.v.) increased the amplitude of MSR in control rats, but decreased the amplitude in rats treated with 6-OHDA. Although PEA-related drugs increased the amplitude of MSR, they did not change the MSR amplitude in 6-OHDA-treated rats. In 5,6-DHT-treated rats, PEA-related drugs increased the amplitude of MSR, whereas PEA produced a decrease. These results support our previous suggestion that the enhancement of MSR by these drugs might be mediated through release of noradrenaline or inhibition of noradrenaline uptake at the noradrenergic synapses.

5,6-Dihydroxytryptamine↗

PubMed1978

Interaction between noradrenergic and serotonergic mechanisms on the central regulation of blood pressure in the rat: a study using experimental central hypertension produced by chemical lesions of the locus coeruleus.

The interaction between noradrenergic and serotonergic mechanisms on the central regulation of blood pressure in the rat was studied, using central experimental hypertension produced by chemical lesions of the locus coeruleus (LC) with 6-hydroxydopamine (6-OHDA). The hypertension (LC-hypertension) was blocked by pretreatment with 6-OHDA intraventricularlly administered and also with desipramine. An increase of serotonin (5-HT) turnover in the cortex and especially in the spinal cord was revealed in the hypertension. Intraperitoneally administered para-chlorophenylalanine elevated blood pressure and reduced 5-HT and 5-hydroxyindole acetic acid content in the cortex and especially in the spinal cord, indicating a decrease 5-HT turnover. Intraventricularlly administered 5, 6-dihydroxytryptamine (5, 6-DHT) resulted in only bradycardia but not an elevation in blood pressure and did not block the development of LC hypertension, and lowered 5-HT content in the cortex and especially in the spinal cord. Intraspinally administrated 5, 6-DHT evoked mild but significant elevation in blood pressure but not in heart rate, and lowered 5-HT content only in the spinal cord. Furthermore, the disappearance of the LC was histologically observed in the rats with LC hypertension. The results of these experiments demonstrate that (1) LC hypertension is probably due to a specific lesion of the LC with 6-OHDA, (2) LC hypertension is accompanied by an increase of 5-HT turnover in the cortex and especially in the spinal cord, which may participate in a depressor function in LC hypertension, (3) ablation of bulbospinal serotonergic neurons produce mild elevation in blood pressure. (4) the balance between the activity of central noradrenerfic and serotonergic neurons may play a role in maintaining normotension, and their unbalance may induce hypertension.

5,6-Dihydroxytryptamine↗

PubMed1988

Effect of ketanserin on adrenal sympathetic nerve activity in rats.

The present study was undertaken to clarify the site for the sympathoinhibitory action of ketanserin in anesthetized rats. Intravenous (i.v.) administration of ketanserin (0.5 and 5 mg/kg) produced a decrease in preganglionic adrenal sympathetic nerve activity (ANA) that is accompanied with hypotension and bradycardia. Intracerebroventricular (i.c.v.) administration of ketanserin (200 micrograms/rat) also decreased ANA, blood pressure (BP) and heart rate (HR). Intrathecal (i.t.) administration of ketanserin (200 micrograms/rat), on the other hand, affected neither ANA, BP nor HR. These results indicate that the site of the sympathoinhibitory action of ketanserin is the supraspinal structures, and not at the spinal cord level. In addition, the decrease in ANA after i.v. administration of ketanserin (0.5 and 5 mg/kg) was attenuated significantly with pretreatment of 5,7-dihydroxytryptamine (200 micrograms/rat, i.c.v.) or 6-hydroxydopamine (200 micrograms/rat, i.c.v.). These findings suggest that the adrenal sympathoinhibitory action of ketanserin may be centrally mediated via both serotonergic and noradrenergic pathways in rats.

5,7-Dihydroxytryptamine↗

PubMed1991

Veratramine-induced behavior associated with serotonergic hyperfunction in mice.

The administration of veratramine produced generalized tremor, myoclonus, hindlimb abduction, backward gait and Straub tail, similar to the "5-hydroxytryptamine (5-HT) syndrome", in mice. Pretreatment with metergoline, methysergide, mainserin or cyproheptadine ameliorated veratramine-induced myoclonus and tremor. For suppression of other symptoms, mianserin and cyproheptadine were effective. Metergoline improved hindlimb abduction and Straub tail, but did not inhibit backward gait. Methysergide was ineffective for the remaining symptoms. 5-Methoxy-N,N-dimethyltryptamine (5-MeODMT) enhanced all these symptoms except for Straub tail. 8-Hydroxy-2-[di-n-propylamino] tetralin hydrobromide (8-OH-DPAT) augmented tremor, hindlimb abduction and backward gait, but did not influence myoclonus and Straub tail. 5-Methoxy-3[1,2,3,6-tetrahydropyridin-4-yl] 1H-indole (RU 24969) did not modify the symptoms. Destruction of 5-HT neurons using 5,6-dihydroxytryptamine (5,6-DHT) resulted in suppression of the syndrome. The denervation supersensitivity caused by 5,6-DHT did not increase the response to veratramine. These findings indicate that part of the site of action of veratramine may be the presynaptic 5-HT neurons.

5,6-Dihydroxytryptamine↗

PubMed1992

Pharmacological studies on lappaconitine: possible interaction with endogenous noradrenergic and serotonergic pathways to induce antinociception.

Systemic and intracerebroventricular (i.c.v.) injections of lappaconitine (LA) produced a dose-dependent inhibition of the response to thermal stimulation in sham-operated mice as assayed by the tail-immersion test. After spinal transection, the antinociceptive potencies of s.c.- or i.c.v.-administered LA were markedly reduced. Antinociception induced by systemically administered LA was clearly reduced by pretreatment with 6-hydroxydopamine or 5,7-dihydroxytryptamine through the i.c.v. and intrathecal (i.t.) routes. When LA was administered by i.c.v.-injection, the LA-induced antinociception was reduced by pretreatment with timolol, a beta-adrenergic antagonist, and ketanserin, a 5-HT2 antagonist. Administration of LA by the i.t. route resulted in a significant antinociceptive activity, which was also reduced by pretreatment with phenoxybenzamine, an alpha-adrenergic antagonist, and mianserin, a 5-HT1 antagonist. The results of these studies suggest that the central noradrenergic and serotonergic systems may be involved in the antinociception of systemically administered LA, and these pathways are mediated by beta-adrenoceptors and 5-HT2 receptors in the brain and alpha-adrenoceptors and 5-HT1 receptors in the spinal cord.

5,7-Dihydroxytryptamine↗

PubMed1992

Serotonergic mechanisms in anxiolytic effect of tandospirone in the Vogel conflict test.

To clarify which 5-HT1A receptors, autoreceptors located in the raphe nuclei or post-synaptic receptors in the forebrain areas receiving a 5-HT input, mediate the anticonflict action of tandospirone (a 5-HT1A receptor-related anxiolytics), the behavioral effects of tandospirone were studied in 5,7-dihydroxytryptamine (5,7-DHT) treated rats. By measuring both monoamines and their metabolite levels and densities of [3H]8-OH-DPAT binding in 5,7-DHT-treated rat brain, we confirmed that pretreatment with 5,7-DHT destroyed 5-HT neurons selectively without affecting postsynaptic 5-HT1A receptors located on the postsynaptic neurons. This selective destruction produced no significant changes in the drinking behavior of rats in either punished or unpunished sessions of the Vogel conflict test. Furthermore, this destruction altered neither the effect of tandospirone on punished responding in this procedure nor the potency of tandospirone to induce a flat body posture in rats, which is known as the "serotonin behavioral syndrome". These results suggested that the anticonflict action of tandospirone may be produced, at least in part, by binding to postsynaptic 5-HT1A receptors and activating them as agonists, and not to 5-HT1A autoreceptors located on the cell bodies of 5-HT neurons.

5,7-Dihydroxytryptamine↗

PubMed2005

Involvement of supraspinal imidazoline receptors and descending monoaminergic pathways in tizanidine-induced inhibition of rat spinal reflexes.

The neuronal pathways involved in the muscle relaxant effect of tizanidine were examined by measurement of spinal reflexes in rats. Tizanidine (i.v. and intra-4th ventricular injection) decreased the mono- and disynaptic (the fastest polysynaptic) reflexes (MSR and DSR, respectively) in non-spinalized rats. Depletion of central noradrenaline by 6-hydroxydopamine abolished the depressant effect of tizanidine on the MSR almost completely and attenuated the effect on the DSR. Co-depletion of serotonin by 5,6-dihydroxytryptamine and noradrenaline resulted in more prominent attenuation of tizanidine-induced inhibition of the DSR. Supraspinal receptors were then studied using yohimbine- and some imidazoline-receptor ligands containing an imidazoline moiety. Idazoxan (I1, I2, I3, and alpha2), efaroxan (I1, I3, and alpha2), and RX821002 (I3 and alpha2), but not yohimbine, an alpha2-adrenergic receptor antagonist with no affinity for I receptors, antagonized the inhibitory effects of tizanidine. Thus, supraspinal I receptors (most likely I3) and descending monoaminergic influences are necessary for tizanidine-induced inhibition of spinal segmental reflexes.

5,6-Dihydroxytryptamine↗

PubMed2001

Determination of NADH in frozen rat brain sections by laser-induced fluorescence.

Methods to assess metabolism are important analytical tools in neuroscience. The fluorophore nicotinamide adenine dinucleotide (NADH) is a parameter of cellular metabolism. NADH fluorescence was measured using a laser-based fluorescence detector with spectral and temporal filters. Distribution and intensity of NADH fluorescence were investigated in frozen brain sections. In sections containing hippocampus the intensity of NADH fluorescence was correlated to brain structures. In order to investigate the consequences of neurotoxic lesions, 5,7-dihydroxytryptamine was injected into the dorsal raphe nucleus 4 to 240 days prior to the measurement. NADH fluorescence decreased in the affected region by 50%, indicating that no recovery in metabolic activity had occurred.

5,7-Dihydroxytryptamine↗

PubMed2004

Constitutive activity of the serotonin2C receptor inhibits in vivo dopamine release in the rat striatum and nucleus accumbens.

Numerous research has pointed out that serotonin2c (5-HT2C) receptor, a subtype of 5-HT receptors belonging to the G-protein-coupled receptor superfamily, modulates the activity of mesencephalic dopamine (DA) neurons, the dysfunction of which is involved in devastating diseases such as schizophrenia, Parkinson's disease, and drug addiction. In the present study, using in vivo intracerebral microdialysis and Chinese hamster ovary (CHO) cells expressing 5-HT2C receptors to identify appropriate 5-HT2C receptor ligands, we sought to determine whether the property of 5-HT2C receptors to spontaneously activate intracellular signaling pathways in vitro (constitutive activity) participates in the tonic inhibitory control that they exert on DA release in the rat striatum and nucleus accumbens in vivo. In CHO cells, the purported antagonist 5-methyl-1-(3-pyridylcarbamoyl)-1,2,3,5-tetrahydropyrrolo[2,3-f] indole hydrochloride (SB 206553), but not 6-chloro-5-methyl-1-[6-(2-methylpiridin-3-yloxy)pyridin-3-yl carbamoyl] indoline (SB 242084), decreased basal inositol phosphate accumulation, thus behaving as a 5-HT2C inverse agonist. Its effect was prevented by SB 242084. In vivo, SB 206553 (1-10 mg/kg) elicited a dose-dependent and clear-cut increase in accumbal and striatal DA release compared with SB 242084 (1-10 mg/kg), and the 5-HT2C agonist S-2-(6-chloro-5-fluoroindol-1-yl)-1-methylethylamine hydrochloride (Ro-60-0175) (0.3-3 mg/kg) inhibited DA release. Pretreatment by SB 242084 reversed the change in DA release elicited by Ro-60-0175 and SB 206553. Furthermore, SB 206553-stimulated DA release was insensitive to reduction of 5-HT neuronal function induced by the 5-HT1A agonist (+/-)-8-hydroxy-2-dipropylaminotetralin or intra-raphe injections of 5,7-dihydroxytryptamine neurotoxin. The obtained results provide the first in vivo evidence that constitutive activity of the 5-HT2C receptor tonically inhibits mesencephalic DA neurons and underscore the need for a better understanding of the pathophysiological role of constitutive receptor activity.

5,7-Dihydroxytryptamine↗

PubMed2005

Prefrontal serotonin depletion affects reversal learning but not attentional set shifting.

Recently, we have shown that serotonin (5-HT) depletion from the prefrontal cortex (PFC) of the marmoset monkey impairs performance on a serial discrimination reversal (SDR) task, resulting in perseverative responding to the previously correct stimulus (Clarke et al., 2004). This pattern of impairment is just one example of inflexible responding seen after damage to the PFC, with performance on the SDR task being dependent on the integrity of the orbitofrontal cortex. However, the contribution of 5-HT to other forms of flexible responding, such as attentional set shifting, an ability dependent on lateral PFC (Dias et al., 1996a), is unknown. The present study addresses this issue by examining the effects of 5,7-dihydroxytryptamine-induced PFC 5-HT depletions on the ability to shift attention between two perceptual dimensions of a compound visual stimulus (extradimensional shift). Monkeys with selective PFC 5-HT lesions, despite being impaired in their ability to reverse a stimulus-reward association, were unimpaired in their ability to make an extradimensional shift when compared with sham-operated controls. These findings suggest that 5-HT is critical for flexible responding at the level of changing stimulus-reward contingencies but is not essential for the higher-order shifting of attentional set. Thus, psychological functions dependent on different loci within the PFC are differentially sensitive to serotonergic modulation, a finding of relevance to our understanding of cognitive inflexibility apparent in disorders such as obsessive-compulsive disorder and schizophrenia.

5,7-Dihydroxytryptamine↗

PubMed1985

Ablation of serotonergic nerves in the rat pancreas. Lack of effects on hormone secretion and intrinsic blood flow.

The aim of the present study was to evaluate the physiological role of intrapancreatic serotonergic nerves for endocrine pancreatic function. The specific uptake of [3H]5-hydroxytryptamine (5-HT) into pancreatic slices from the rat was completely abolished after an intrapancreatic injection of 5,7-dihydroxytryptamine (5,7-DHT). Since also high-affinity uptake of [3H]5-HT was absent it was concluded that intrapancreatic serotonergic nerves were destroyed. The effects of this selective denervation on glucose-stimulated insulin and somatostatin secretion were investigated with the aid of perfused rat pancreatic glands removed 3, 7 or 14 days after the injection of 5,7-DHT. Neither the basal release of these hormones nor their response to a glucose challenge was significantly altered by the ablation of the intrapancreatic serotonergic nerves. The microsphere technique was used to investigate the blood flow through the pancreatic islets in rats injected intrapencreatically with 5,7-DHT 4 days previously. No significant changes in either the whole pancreatic blood flow or the islet blood flow could be demonstrated. These result show that in normal physiological conditions the intrapancreatic serotonergic nerves do not affect the hormonal release from or the blood flow through the endocrine pancreas.

5,7-Dihydroxytryptamine↗

PubMed1979

Serotonin involvement in the control of phasic luteinizing hormone release in the rat: evidence for a critical period.

A marked surge of luteinizing hormone (LH) occurs daily at 18.00 h in oestrogen-treated ovariectomized rats maintained under regular lighting from 06.00 to 20.00 h. The administration of p-chlorophenylalanine (PCPA),p-chloramphetamine or 5,6-dihydroxytryptamine in treatments designed to cause a severe depletion of brain serotonin abolished this daily surge. Synthesis of serotonin may be temporarily restored in PCPA-treated animals by the administration of the serotonin precursor, 5-hydroxytryptophan. The effectiveness with which restoration of synthesis resulted in restoration of the LH surge varied according to the time at which the precursor was administered, the optimal time being 10.00 h. The results suggest that there is an essential, permissive function performed by serotonin in the production of the LH surge and that this function occurs during a critical period.

5,6-Dihydroxytryptamine↗

PubMed1987

Serotoninergic regulation of corticosterone secretion in domestic fowl.

The effects of serotoninergic drugs on adrenocortical function in domestic fowl were examined. Administration of the serotonin receptor agonist 2-(1-piperazinyl)quinoline maleate (quipazine), an inhibitor of serotonin metabolism, N-methyl-N-2-propynylbenzylamine HCl (pargyline), as well as serotonin itself, all increased plasma concentrations of corticosterone. The maximum responses to serotonin and quipazine occurred 1 h after treatment. The quipazine-stimulated response was partly prevented by the serotonin antagonist cyproheptadine. Cockerels pretreated with dexamethasone, a synthetic steroid known to inhibit pituitary ACTH release, showed attenuated responses to subsequent quipazine, pargyline or serotonin injection. Serotonin, quipazine and cyproheptadine did not affect corticosterone release directly from the adrenal gland incubated in vitro, nor did they affect adrenal responsiveness to ACTH stimulation. The neurotoxin 5,6-dihydroxytryptamine injected into day-old chicks decreased plasma concentrations of corticosterone for up to 7 days after treatment, with corresponding decreases in the hypothalamic concentration of serotonin, but not dopamine or noradrenaline concentrations. These results show that adrenal corticosterone secretion is regulated by a central serotoninergic system, probably acting on the hypothalamo-pituitary-adrenal axis.

5,6-Dihydroxytryptamine↗

PubMed1978

The effect of quipazine, a serotonin receptor agonist, on serum corticosterone concentration in rats.

Quipazine, a serotonin receptor agonist, increased serum corticosterone within 30 min after its i.p. injection (at 10 mg/kg) into rats; the effect persisted at 1 and 2 hrs, but not at 4 hrs. Elevation of serum corticosterone did not occur with a 1.25 mg/kg dose of quipazine but was dose-related over a 2.5-20 mg/kg dose range. The effect of quipazine was completely prevented by methergoline, a serotonin receptor antagonist. The effect of quipazine was present in rats pretreated with 5,7-dihydroxytryptamine to destroy serotonin nerves and was not enhanced (as was the effect of L-5-hydroxytryptophan) by fluoxetine pretreatment. These data are compatible with the idea that quipazine increases serum corticosterone as a consequence of direct stimulation of serotonin receptors in brain.

5,7-Dihydroxytryptamine↗