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PubMed1996

Role of endogenous 5-hydroxytryptamine in the regulation of gastric contractions by motilin in dogs.

It has been suggested that 5-hydroxytryptamine3 (5-HT3) receptors are involved in the control of phase III contractions in the stomach. We examined the effect of depletion of endogenous 5-HT by p-chlorophenylalanine (pCPA) on spontaneously and motilin-induced phase III contractions in conscious dogs, and the effect of 5,6-dihydroxytryptamine (5,6-DHT) in an isolated perfused dog stomach. Three-day treatment with pCPA significantly reduced plasma 5-HT concentration and 5-HT content in the stomach, and strongly suppressed the spontaneous and motilin-induced phase III contractions in the stomach. When spontaneous phase III contractions recovered in the stomach after a 3-day treatment, exogenous motilin induced typical phase III-like contractions, and the 5-HT content in the muscle layer was recovered to the normal pretreatment level. In the perfused stomach, 5,6-DHT decreased 5-HT content in the muscle layer alone and abolished motilin-induced contractions. In conclusion, endogenous 5-HT, probably in 5-HT neurons, plays an important role in the control of interdigestive phase III activity by motilin in the stomach.

5,6-Dihydroxytryptamine↗

PubMed1980

Effects of brain monoamine depletions on thermoregulation in rabbits.

Biochemical analyses revealed that 5,7-dihydroxytryptamine- (5,7-DHT) treated and 6-hydroxydopamine- (6-OHDA) treated rabbits, respectively, had a significant reduction in diencephalic 5-hydroxytryptamine (5-HT) and norepinephrine (NE) with minimal alterations in the other monoamines. Both 5,7-DHT-treated and 6-OHDA-treated animals, although showing the maintenance of normal body temperatures, did exhibit specific alterations in the thermoeffector outputs. The 5-HT-depleted animals displayed an increase in ear skin blood flow, respiratory heat loss, and metabolism at both ambient temperatures (Ta) of 22 and 2 degrees C. The NE-depleted animals displayed a decrease in metabolism at all levels of Ta tested. Also, the peripheral temperature threshold for the onset of heat loss responses were displaced to higher values than in control animals. In addition, the prostaglandin E1-induced fever was attenuated after the pretreatment of rabbits with either 5,7-DHT or 6-OHDA. The data indicate that brain levels of 5-HT and NE alter, in an apparently reciprocal fashion, the thermoregulatory responses of rabbits. Also, the integrity of 5-HT and NE pathways in brain is vital for the full functioning of a prostaglandin in producing a fever.

5,7-Dihydroxytryptamine↗

PubMed1981

Pituitary beta-endorphin, naloxone, and feeding in several experimental obesities.

The role of beta-endorphin in the development of several obesity syndromes was examined. Adult female hooded rats received ventromedial hypothalamic lesions, dorsolateral tegmental lesions, parasagittal hypothalamic knife cuts, intraventricular 5,7-dihydroxytryptamine, ovariectomy, control surgery, or were deprived to 75% of normal body weight. Dose-dependent suppression of food intake by the opiate antagonist naloxone (0.5, 1.8, 6.8, or 25.0 mg/kg, ip) was measured during once-daily 4-h food access periods. No difference was found among the groups at any dose. Pituitary beta-endorphinlike immunoreactivity (BELI) was substantially decreased in knife-cut rats, but was unaltered by other treatments. Obesity had no effect on BELI. In another experiment, rats made obese by prolonged maintenance on palatable foods had elevated pituitary BELI levels. Feeding mechanisms involving opioid peptides do not appear to be of etiological significance in the syndromes examined.

5,7-Dihydroxytryptamine↗

PubMed1987

Serotonin and feeding responses of rats to amino acid imbalance: initial phase.

The role of serotonin in the anorexic response of rats to an amino acid-imbalanced diet was investigated. After chronic depletion of serotonin with parachlorophenylalanine (PCPA, 300 mg/kg) or 5,7-dihydroxytryptamine (DHT, 200 micrograms/rat, intracisternally), initial intake of a mild isoleucine-imbalanced diet was reduced by 60% vs. a 17% reduction after saline injection. After acute treatment with the agonist, quipazine (quip, 5 mg/kg ip) or the precursor, tryptophan (TRP, 1% added to the diet), imbalanced diet intake was also exacerbated. PCPA and DHT may have caused receptor supersensitivity, such that the food intake depression after serotonin depletion was similar to that seen with the quip and TRP treatments. Injection of the autoreceptor agonist, 8-hydroxy-2(di-n-propylamino)tetralin (8-OH-DPAT, 500 micrograms/kg sc), to reduce transmission in the serotonergic systems resulted in an attenuation of the usual food intake depression of the amino acid-imbalanced diet (only a 7%, nonsignificant reduction). Also measurements made in the absence of pharmacological treatment showed that the ratio 5-hydroxyindole acetic acid-to-serotonin, a putative index of serotonin turnover, was increased 155% in the raphe nuclei and 140% in the hippocampus 3.5 h after ingestion of the mild isoleucine-imbalanced diet. Therefore increased serotonergic activity in some brain areas may be associated with the initial depression of food intake in rats fed an imbalanced amino acid diet.

5,7-Dihydroxytryptamine↗

PubMed1990

Pressor and sympathetic responses to dorsal raphe nucleus infusions of TRH in rats.

Pressor, tachycardic, and sympathoexcitatory responses to intracerebroventricularly (icv) infused thyrotropin-releasing hormone (TRH) were recorded in urethan-anesthetized rats to identify where centrally administered TRH acts in the brain. None of these responses was altered either by electrolytic lesions in the medial preoptic, posterior, or paraventricular hypothalamus or by chemical lesions produced by destroying catecholaminergic neurons with icv infused 6-hydroxydopamine. By contrast, when serotonergic neurons were similarly destroyed with 5,7-dihydroxytryptamine, TRH-induced tachycardia was inhibited. Attendant pressor responses were also inhibited by electrolytic lesions of the dorsal, but not of the median, raphe nucleus. Pressor and sympathoexcitatory responses elicited by infusing TRH directly into the dorsal raphe nucleus resembled those produced by icv infusion, and their magnitude diminished after pentolinium-induced ganglioplegia. These results are compatible with the interpretation that icv infused TRH may produce its cardiovascular and sympathetic effects by acting, at least in part, on serotonergic mechanisms located in the dorsal raphe nucleus.

5,7-Dihydroxytryptamine↗

PubMed1994

Role of serotonin and catecholamines in sympathetic responses evoked by stimulation of rostral medulla.

In halothane-anesthetized, paralyzed rats, single-pulse stimulation of nucleus raphe pallidus/obscurus (NR) evoked an inhibition followed by a single wave of excitation in 1) the mass discharge of lumbar and splanchnic sympathetic nerves (modal onset latencies: LSND 210 +/- 14 ms, SSND 161 +/- 5 ms) and 2) the unit activity of lumbar sympathetic vasoconstrictor neurons (LSVNs). Stimulation of the rostral ventrolateral medulla (RVL) produced two excitatory responses in LSND, SSND, and LSVN units (modal onset latencies: RVL peak I 98 +/- 8 ms for LSND and 62 +/- 2 ms for SSND; RVL peak II 210 +/- 15 ms for LSND and 160 +/- 6 ms for SSND). Most LSVNs received excitatory inputs from both raphe and RVL. NR peak was selectively attenuated (76%) by 5,7-dihydroxytryptamine [intracisternally (ic), 2-wk] and acute intrathecal (it) methiothepine (10 micrograms, 69%) or methysergide (40 micrograms, 72%). 6-Hydroxydopamine (2-wk ic) produced no effect. Phentolamine (20 micrograms it) or prazosin (20 micrograms it) reduced RVL peak II by > 94% and attenuated NR peak (phentolamine 67%, prazosin 46%). Intrathecal kynurenic acid produced proportionately larger reduction of RVL peak I than raphe peak or RVL peak II. Our interpretations are 1) LSVNs receive convergent excitatory inputs from midline raphe, parphyramidal area, and RVL, 2) bulbospinal serotonergic neurons mediate most of the sympathoexcitation evoked from NR and a portion of RVL peak II, 3) a catecholamine probably released by C1 cells mediates most of RVL peak II and a portion of the NR response, and 4) RVL peak I is predominantly mediated by an excitatory amino acid.

5,7-Dihydroxytryptamine↗

PubMed1997

Serotonergic afferents mediate activity-dependent entrainment of the mouse circadian clock.

The circadian pacemaker located in the suprachiasmatic nuclei (SCN) of the hypothalamus receives serotonergic afferents from the midbrain raphe nuclei, but the functional role of this projection is unclear. In rodents, locomotor activity increases serotonin content in the SCN, and serotonergic agonists phase shift the circadian clock in a manner closely similar to voluntary bouts of vigorous exercise, suggesting that serotonergic afferents could be part of the activity-dependent entrainment mechanism. We investigated this possibility by selectively lesioning serotonin terminals within and adjacent to the SCN by local microinjection of 5,7-dihydroxytryptamine in mice pretreated with desipramine. This treatment decreased serotonin content 96 +/- 1% and 5-hydroxyindole-3-acetic acid content below levels of detection (nearly 100%) but did not decrease norepinephrine content or neuropeptide Y immunoreactivity in the SCN. These lesions did not alter subsequent running activity levels, yet rendered mice unable to synchronize to a regularly scheduled 2-h wheel running paradigm that entrained sham-lesioned controls. Serotonin afferents are thus necessary for activity-dependent entrainment in the mouse.

5,7-Dihydroxytryptamine↗

PubMed2000

Dexfenfluramine and norfenfluramine: comparison of mechanism of action in feeding and brain Fos-ir studies.

Dexfenfluramine (dF) and dexnorfenfluramine (dNF), its metabolite, are anorectic agents that release serotonin (5-HT) and may have a direct postsynaptic action. The effects on the anorectic effects of dF and dNF of either acute (p-chlorophenylalanine, PCPA) or chronic (5,7-dihydroxytryptamine, 5,7-DHT) brain 5-HT depletions were studied in rats and compared with the actions of a 5-HT uptake inhibitor (fluoxetine) and 5-HT(1B/2C) receptor agonists [1-(3-trifluoromethyl-phenyl)-piperazine and 1-(3-chlorophenyl) piperazine]. The anorexia caused by these agonists was enhanced in rats with 5,7-DHT lesions, possibly a result of receptor supersensitivity. In contrast, fluoxetine anorexia was somewhat reduced in one study and was unchanged in a second. Both dF and dNF anorexias were enhanced in rats with 5,7-DHT lesions. In contrast, the anorectic effects of either dF or dNF were unchanged in PCPA-treated rats relative to controls. Compared with controls, 5, 7-DHT-lesion rats showed greatly increased dF- and dNF-induced Fos-like immunoreactivity (ir) in the paraventricular (PVN) and supraoptic (SON) hypothalamic nuclei, and in the median preoptic area (MnPO), but were similar to controls in most other areas. PCPA pretreatment increased dF- and dNF-induced Fos-ir in the PVN, SON, and MnPO. In controls, equianorectic doses of dF and dNF induced Fos-ir in similar brain regions, but dNF produced relatively larger effects than dF in SON, PVN, and MnPO. The data are discussed in terms of multiple pathways in the anorectic actions of dF and dNF.

5,7-Dihydroxytryptamine↗

PubMed1981

Pharmacologic study of respiratory afterdischarge.

Respiratory afterdischarge, an increased but slowly declining respiratory output lasting some minutes after cessation of a stimulus, is generated by a bulbopontine mechanism whose precise anatomic locus and neurophysiological mechanism are unknown. To determine if the mechanism responsible for the afterdischarge was due to one of the major long-acting central neurotransmitters, we studied a control group of animals and groups of animals that were pretreated with the antiserotonin agents, methysergide, parachlorophenylalanine, and 5,7-dihydroxytryptamine, the dopamine-norepinephrine antagonists alpha-methytyrosine and haloperidol, and the endorphin antagonist, naloxone. Anesthetized, paralyzed, vagotomized, and glomectomized cats were used. We measured phrenic activity before, during, and after carotid sinus nerve and calf muscle stimulation. None of the antagonists had an effect on the response to stimulation, on the magnitude of the afterdischarge, or on its time course during recovery. We conclude that these central neurotransmitters do not participate in the genesis of the respiratory afterdischarge.

5,7-Dihydroxytryptamine↗

PubMed2004

Serotonergic modulation in aplysia. I. Distributed serotonergic network persistently activated by sensitizing stimuli.

A common feature of arousing stimuli used as reinforcement in animal models of learning is that they promote memory formation through widespread effects in the CNS. In the marine mollusk Aplysia, sensitization is typically induced by tail-shock, an aversive reinforcer that triggers a state of defensive arousal characterized by escape locomotion and increased heart rate. Serotonin (5-HT) contributes importantly to sensitization of defensive reflexes as well as to the regulation of locomotion and heart rate. Although specific serotonergic neurons increase their firing after tail-shock, it remains unclear whether this effect is restricted to these neurons or whether tail-shock recruits a more global serotonergic system. In this study, we recorded from serotonergic neurons throughout the CNS, which were prelabeled with 5,7-dihydroxytryptamine, during an in vitro analog of sensitization training, tail-nerve shock. We found that most of the serotonergic neurons that we recorded from (80%) increased their firing rate for several minutes after nerve shock. Most serotonergic neurons in the pedal and abdominal ganglion were also excited by 5-HT and by intracellular activation of the two serotonergic neurons CB1/CC3. This interconnectivity between serotonergic neurons might contribute to spread excitation within a large proportion of the serotonergic system during sensitization training. It is also possible that serotonergic neurons could be activated by 5-HT present in the hemolymph via a neuro-humoral positive feedback mechanism. Overall, these data indicate that sensitization training activates a large proportion of Aplysia serotonergic neurons and that this form of learning occurs in a context of increased serotonergic tone.

5,7-Dihydroxytryptamine↗

PubMed1991

Neural control of swimming in Aplysia brasiliana. III. Serotonergic modulatory neurons.

1. We describe a group of serotonergic neurons in the pedal ganglia of Aplysia brasiliana and characterize their modulatory effects on the motoneuron input to swimming muscles of the parapodia. Each pedal ganglion contains one cluster of large neurons near its dorsomedial surface that fires in phase with opening (downstroke) of the parapodia; these have been designated parapodial opener-phase (POP) cells. 2. POP cells are large, number 15-20 per ganglion, have peripheral axons in parapodial nerves, have distinctively shaped action potentials, and fire in bursts phasically with motoneurons during the opening, or downstroke portion, of parapodial movement during fictive swimming. Firing individual POP cells with intracellular current indicates that they have no direct detectable effect on muscle, causing neither junction potentials nor contractions. 3. 5,7-Dihydroxytryptamine (5,7-DHT) staining, immunocytochemistry using serotonin (5-HT) antibodies, and direct biochemical measurements revealed that POP cells are serotonergic. Serotonergic nerve endings were also seen in parapodial muscle. 4. Simultaneous intracellular recordings and use of altered divalent concentrations revealed that no detectable direct synaptic interactions exist between POP cells and motor neurons. 5. When POP cells and motoneurons were simultaneously recorded while measuring muscle contractions, it was found that POP cell activity enhances motoneuron-induced tension by 120-900%, averaging around 300%. Variability in the efficacy of individual POP cells suggests that they may influence specific regions or groups of muscle fibers. 6. POP cell activity also significantly increased the rate of relaxation of parapodial muscle contractions, averaging about a 40% reduction in the time required to relax to one-half peak tension. Increased relaxation rate implies a postsynaptic change in muscle behavior. 7. The effectiveness of POP cells to increase contraction tension and relaxation rate was positively correlated with POP cell spike frequency. These effects were slow (seconds) in onset and could persist for a minute or more after cessation of POP firing. Concurrent motoneuron activity is not required for modulation by POP cells. 8. Simultaneous intracellular recording from a POP cell, motoneuron, and muscle fiber revealed that POP cell activity enhanced the amplitude of motoneuron-induced excitatory junction potentials (EJPs). Activity of POP cells did not alter muscle fiber membrane potential, but the experiments left open the possibility that EJP enhancement is presynaptic, postsynaptic, or a combination.(ABSTRACT TRUNCATED AT 400 WORDS)

5,7-Dihydroxytryptamine↗

PubMed1992

Neuronal modulation of foot and body-wall contractions in Aplysia californica.

1. Large neurons in the pedal ganglia of Aplysia californica were examined for their potential to modulate motoneuron-evoked contractions in foot and body-wall muscle. These neurons lie near the medial border of each pedal ganglion and have peripheral axons but no detectable motor effect. 2. Neurons in this region fire in rhythmic bursts during fictive escape crawling, and their action potentials resemble those recorded from parapodial opener-phase (POP) neurons in the swimming species, A. brasiliana. 3. Firing these neurons in conjunction with pedal motoneurons potentiates the force of contractions and increases their relaxation rate. Similar effects are produced by the serotonin (5-HT) analogue, bufotenine. 4. The modulatory neurons can be stained in vivo by 5,7-dihydroxytryptamine (5,7-DHT), suggesting they are serotonergic. 5-HT immunoreactivity is present in axons associated with foot and body-wall muscle. 5. Bath-applied 5-HT causes rhythmic bursting in the modulatory neurons. It appears likely that they are homologous to the POP cells of A. brasiliana.

5,7-Dihydroxytryptamine↗

PubMed2000

Neonatal 5,7-DHT lesions cause sex-specific changes in mouse cortical morphogenesis.

Both monoaminergic and cholinergic afferent projections to the neocortex putatively modulate cortical morphogenesis and plasticity. Previously we showed that neonatal electrolytic lesions of the cholinergic nucleus basalis magnocellularis (nBM) projections to the neocortex result in significant decreases of cortical layer width that correlate with cognitive alterations. Such electrolytic lesions, performed for lack of a selective neurotoxin in mice, may affect mono-aminergic fibers of passage. Here, we investigate the effects of neonatal 5,7 dihydroxytryptamine (5,7-DHT) focal injections into the nBM region on cortical laminar morphology in adult male and female mice. 5,7-DHT lesions on the first postnatal day resulted in significant cortical depletion of both serotonin and norepinephrine that attenuated with age. Generally, cortical layer widths increased in response to the lesion; the effects were layer, region, and sex specific. Previous reports from our laboratories described long-term behavioral alterations after comparable focal, neonatal 5,7-DHT lesions. The studies described here provide an anatomical basis for such behavioral alterations. Our data suggest that monoaminergic and cholinergic projections to the cortex may have opposite effects on the developing cortical neuropil. Jointly, our morphological and behavioral findings may have important implications for a variety of developmental disorders in humans and provide some insights into sex differences in the penetrance of these disorders.

5,7-Dihydroxytryptamine↗

PubMed2000

An endogenous serotonergic rhythm acting on 5-HT(2A) receptors may be involved in the diurnal changes in tuberoinfundibular dopaminergic neuronal activity and prolactin secretion in female rats.

The central serotonergic system has long been known to have a stimulatory role on the secretion of prolactin (PRL). The integrity of serotonergic neurotransmission is essential for the expression of the estrogen-induced afternoon PRL surge. Whether its effect on PRL involves change in the activity of tuberoinfundibular dopaminergic (TIDA) neurons has not been ascertained. In adult ovariectomized rats treated with estrogen, depletion of central serotonin (5-HT) by 5,7-dihydroxytryptamine (5,7-DHT, 200 microg/rat, i.c.v.) effectively prevented the afternoon fall in TIDA neuronal activity (using the levels of 3,4-dihydroxyphenylalanine and 3, 4-dihydroxyphenylacetic acid (DOPAC), and the ratio of DOPAC/dopamine in the median eminence as indices), and blunted the afternoon PRL surge. A single injection of a 5-HT(2A) receptor antagonist, ketanserin (5 mg/kg, i.p. at 12.00 h), also had the same effects on the diurnal changes in TIDA neuronal activity and PRL secretion as the treatment with 5,7-DHT did. Intracerebroventricular injection of a 5-HT(2) receptor agonist 2, 5-dimethoxy-4-iodoamphetamine (DOI) in the morning inhibited the TIDA neuronal activity and stimulated PRL secretion in a dose-dependent manner; while injection of a 5-HT(1) agonist, 8-hydroxy-dipropylaminotetralin, was without effect. Injection of DOI in 5,7-DHT-pretreated rats at 14.30 h also lowered the TIDA neuronal activity and reinstated the PRL surge. In all, endogenous 5-HT, acting through the 5-HT(2A) receptor, appears to exhibit an inhibitory effect on TIDA neuronal activity during the afternoon, which is essential for the PRL surge.

3,4-Dihydroxyphenylacetic Acid↗

PubMedDate not supplied

Effects of 5-HT denervation of the suprachiasmatic nuclei or lesions of the median raphe nucleus on daily torpor in the Djungarian hamster, Phodopus sungorus.

In the Djungarian hamster (Phodopus sungorus), using 5,7-dihydroxytryptamine (a specific neurotoxin), depletion of the serotonin (5-HT) fibers innervating the suprachiasmatic nuclei (SCN) was performed in animals displaying torpor bouts. The characteristics of postoperative torpor bouts in lesioned hamsters were similar to those observed before the denervation. 5-HT innervation of the SCN thus seems unnecessary for the expression and temporal organization of daily torpor. After chemical or thermic lesions of the 5-HT neurons of the anterior median raphe nucleus (MR) in hamsters displaying torpor bouts, the phenomenon of torpor was not prevented. In addition, hamsters lesioned on the day of transfer to short photoperiod (SP) displayed their first torpor bouts after the same duration of SP exposure as intact hamsters. These results suggest that, contrary to what is observed in hibernation, 5-HT neurons of the anterior part of the MR are not involved in the mechanisms governing the occurrence and seasonal timing of daily torpor.

5,7-Dihydroxytryptamine↗

PubMed1997

Alterations in the postnatal development of striatal preprotachykinin but not preproenkephalin mRNA expression in the serotonin-depleted rat.

We examined the effects of diminished serotonin (5-hydroxytryptamine, 5-HT) levels on the postnatal development of striatal tachykinin and enkephalin neuropeptide systems. Neonatal rats received intracisternal injection of vehicle or the 5-HT neurotoxin 5,7-dihydroxytryptamine (5,7-DHT; 100 micrograms) on postnatal day 2 followed by sacrifice 1-29 days later. Monoamine analysis by high-performance liquid chromatography with electrochemical detection revealed a drastic reduction of midbrain 5-HT levels, but not norepinephrine or dopamine, as early as 1 day and extending to 29 days following 5,7-DHT injection. Striatal preprotachykinin (PPT) mRNA levels were significantly increased 8 days following injection. However, PPT mRNA amounts failed to remain up-regulated, falling back to or below control levels during the second and third weeks following injection. By day 29, striatal PPT mRNA had normalized to control levels even though 5-HT amounts were still markedly reduced. Throughout the entire time course, striatal preproenkephalin mRNA levels did not significantly differ from control levels. These results suggest that striatal tachykinin, but not enkephalin, neurons may be transiently sensitive to lowered 5-HT neurotransmission during postnatal development.

5,7-Dihydroxytryptamine↗

PubMed1982

A serotonin agonist-antagonist reversible effect on Na+-K+-ATPase activity in the developing rat brain.

In brain of adult and developing rats the Na+-K+-adenosine triphosphatase (Na+-K+-ATPase) system seems to react to serotonin (5-HT) changes induced pharmacologically. A 5-HT agonist (quipazine) elicits a response of the enzyme activity in the cerebral cortex in vivo, which is neutralized with a 5-HT antagonist (methysergide). This effect was observed from day 21 to adulthood. Also in a state of 5-HT receptor hypersensitivity (rats treated early with 5,6-dihydroxytryptamine), the response of Na+-K+-ATPase to the 5-HT agonist was higher than without neurotoxic lesion of 5-HT paths. These data suggest an involvement of the Na+-K+-ATPase system in 5-HT receptor sensitivity in the rat brain.

5,6-Dihydroxytryptamine↗

PubMed1981

Lack of correlation between hypothalamic serotonin and the ether-induced ACTH secretion in adrenalectomized rats.

The central serotonergic system was manipulated using a serotonin receptor antagonist (cyproheptadine), electrolytic lesioning of the raphe nuclei and neurochemical destruction of the serotonergic terminals in the hypothalamus. The effects of these interventions on ether-induced ACTH secretion were studied in adrenalectomized rats. Serotonin, norepinephrine and dopamine concentrations were measured in the medial basal hypothalamus (MBH) or in individual nuclei of the hypothalamus and of certain midbrain regions. Cyproheptadine pretreatment inhibited ether-induced ACTH hypersecretion in adrenalectomized animals. Neither the electrolytic lesions of the midbrain raphe nuclei, nor the neurotoxic destruction of the hypothalamic serotonergic terminals (by intraventricular administration of 5,6-dihydroxytryptamine) caused any alteration of stimulated ACTH secretion after ether inhalation and/or long-term corticoid deficiency. These results suggest a lack of correlation between the activity of the central serotonergic system and the ACTH releasing effect of ether-stress in adrenalectomized rats.

5,6-Dihydroxytryptamine↗