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PubMed1989

Sleep state-specific neuronal activity in rat dorsal lateral geniculate nucleus is not altered by local serotonin and norepinephrine depletion.

The relay cells in dorsal lateral geniculate nucleus (dLGN) represent one among many populations of neurons throughout the neuraxis that display systematic alteration of spontaneous rate and pattern of discharge concurrent with change in state of arousal. Both noradrenergic (NE) and serotonergic (5-HT) systems innervate dLGN and are implicated in sleep-wake control mechanisms. Our study was designed to test the influence of these systems upon sleep state-related multiple unit activity in the dLGN. Two monoamine neurotoxins, 5,7-dihydroxytryptamine and 6-hydroxydopamine, were injected locally into dLGN to destroy NE and 5HT afferents individually and in combination. In three separate treatment groups, mean monoamine concentrations in dLGN were reduced in relation to the contralateral, vehicle-injected, control dLGN to: 1) NE-17%, 5HT-14%; 2) NE-46%, 5HT-28%, and 3) NE-6%, 5HT-77%. In no case was chronic sleep state-related cell activity in dLGN significantly altered. We conclude that afferent monoaminergic inputs are not critically related to the mechanisms underlying normative shifts in sleep state-related neuronal activity in dLGN.

5,7-Dihydroxytryptamine↗

PubMed1988

Reinnervation of dopamine neurons by regenerating serotonin axons in the rat medial zona incerta. A combined radioautographic and immunocytochemical ultrastructural study.

Cellular relationships between serotonin (5-HT) axons and tyrosine hydroxylase (TH)-containing neurons were examined by combined (3H)5-HT uptake radioautography and TH immunocytochemistry in the medial zona incerta (ZI) of adult rats, 7 and 50 days after an intracerebral injection of 5,7-Dihydroxytryptamine (5,7-DHT). Seven days post-lesion, only rare, scattered (3H)5-HT-labeled axon terminals were apparent in the zone of the medial ZI accessible to intraventricularly injected (3H)5-HT. In contrast, in sham-injected animals (3H)5-HT-labeled varicosities were numerous and often observed adjacent to TH-immunoreactive perikarya and dendrites. Fifty days post 5,7-DHT injection, the density of (3H)5-HT-labeled terminals approximated that seen in sham-treated animals. At the ultrastructural level, these regenerated 5-HT axons were similar in size, shape and content to those observed in sham-operated rats. Also, as in sham, some of the (3H)5-HT-labeled axons were directly apposed to TH-immunopositive labeled profiles. The latter included large dendritic shafts and dendritic spines, but only rare perikarya. In both sham- and 5,7-DHT-treated animals a few of the contacts between (3H)5-HT-labeled and TH-immunoreactive profiles exhibited an asymmetric synaptic differentiation. These results indicate that 5-HT fibers in the medial ZI, following regeneration, can reestablish normal relationships and even synapses with a given population of chemically identified cells.

5,7-Dihydroxytryptamine↗

PubMed1990

Stimulation of a bulbospinal 5-HT pathway in the rat brain produces hyperglycaemia.

The glucoregulatory role of spinally projecting serotonin (5-HT) neurones near the ventrolateral surface of the medulla oblongata was investigated by stimulating these nerve cells in normal rats and in rats with selective chemical ablation of 5-HT nerves in the spinal cord. Electrical stimulation of the lateral medulla produced hyperglycaemia in normal rats; the increase in blood glucose was proportional to the intensity and frequency of stimulation. Furthermore, microinjection of kainic acid or L-glutamate at the same sites also produced hyperglycaemia. This stimulation-induced hyperglycaemia was significantly reduced by spinal transection or adrenalectomy. Selective destruction of spinal 5-HT nerves produced by intraspinal injection of 5,7-dihydroxytryptamine also reduced the magnitude of the hyperglycaemia response to electrical stimulation of the lateral medulla. This indicates that stimulation of 5-HT nerve cells adjacent to the ventrolateral surface of the medulla oblongata and projecting to the spinal cord increases the adrenal-sympathetic efferent activity and leads to hyperglycaemia in rats.

5,7-Dihydroxytryptamine↗

PubMed1981

An evidence for adrenergic involvement in the choroidal circulation.

The ciliary nerve endings of adult albino rats were observed by transmission electron microscopy after the injection of 5,6-dihydroxytryptamine. The content of both large and small granular vesicles in these endings markedly increase in density by administration of the drug. The result suggests that the endings derive from the adrenergic nerve fiber.

5,6-Dihydroxytryptamine↗

PubMed1979

Absence of indoleamine-accumulating neurons in the retina of humans and cynomolgus monkeys.

Indoleamine-accumulating neurons have previously been detected in cats, rabbits, goldfish, chicken, pigeons, and Cebus monkeys, and were therefore also looked for in humans and in Old World monkey. Cynomolgus irus. The monkey eyes were injected intravitreally with 50 microgram 5,6-dihydroxytryptamine, 5 microgram alpha-methylnoradrenaline, or both drugs simultaneously. The human retinas were incubated in either drug. Previous observations on the distribution of dopaminergic neurons were confirmed in the two species, but no indoleamine-accumulating neurons were detected. The result emphasizes the similarity between human and Old World monkey retinas and contrasts them with the retina of the New World monkeys.

5,6-Dihydroxytryptamine↗

PubMed1981

Lesion of serotonergic neurons antagonizes clonidine induced suppression of avoidance behavior and locomotor activity in rats.

The effects of clonidine on avoidance acquisition and locomotor activity were studied in male Wistar rats with 5,6-dihydroxytryptamine (5,6-DHT) lesions of the median raphe nucleus. Lesioned animals showed marked depletion in forebrain serotonin and 5-hydroxyindole acetic acid concentrations. clonidine (0.2 mg/kg IP in a single daily dose for 6 consecutive days) inhibited avoidance acquisition and reduced locomotor activity in unlesioned rats. In 5,6-DHT rats clonidine failed to produce depressive effect. The resistance of raphe-lesioned rats to clonidine is discussed on the basis of possible interaction between noradrenergic and serotonergic brain systems.

5,6-Dihydroxytryptamine↗

PubMed1981

Evidence against the involvement of serotonergic mechanisms in wet dog shake behavior induced by carbachol chloride in rats.

The intracerebroventricular administration of carbachol chloride induced a characteristic wet dog shake response in rats. Neither 5,6-dihydroxytryptamine, a serotonergic depletor, nor DL-p-chlorophenylalanine, an inhibitor of 5-HT synthesis, affected wet dog shakes induced by carbachol. Putative antiserotonergic drugs such as cyproheptadine, danitracen and pizotifen antagonized carbachol-induced wet dog shakes, but the 5-HT-receptor antagonist methergoline did not significantly affect the response. These results indicated that carbachol-induced wet dog shakes in rats are probably not related to increased activity of central serotonergic mechanisms. Additionally, the present experiments showed that the anticholinergic properties of the potent serotonergic blockers cyproheptadine, danitracen and pizotifen must be taken into account, and these drugs should be used with care as relatively selective pharmacological tools.

5,6-Dihydroxytryptamine↗

PubMed1979

Mediation of central prostaglandin effects by serotoninergic neurons.

Ten days after administration of 5,6-dihydroxytryptamine, which causes degeneration of central serotoninergic neurons, the depressive behavioral effects of PGF2 alpha and PGE2 were evidently inhibited. Central chemical serotoninectomy abolished the hyperthermic and hypertensive effects of PGF2 alpha, but only slightly affected those of PGE2. It is concluded that serotoninergic neurons mediate the depressive behavioral action of both PGF2 alpha and PGE2. They also mediate the hyperthermic and hypertensive action of PGF2 alpha but not of PGE2. This suggests that these prostaglandins have different central modes of action.

5,6-Dihydroxytryptamine↗

PubMed1980

Head-twitch response induced by tyramine.

The intracerebroventricular (IC) administration of tyramine (TyA) induced a characteristic head-twitch response in mice pretreated with safrazine, a monoamine oxidase inhibitor. Safrazine-pretreated mice exhibited similar head-twitches following the IC treatment of serotonin (5-HT). The maximum dose of 5-HT which did not elicit head-twitches significantly potentiated TyA-induced head-twitches. Antiserotonergic drugs such as morphine and dimethothiazine antagonized TyA-induced head-twitches. A serotonergic denervator, 5,6-dihydroxytryptamine, potentiated head-twitch induced by TyA or 5-HT. Both TyA-induced and 5-HT-induced head-twitches were inhibited by dopamine and noradrenaline, while catecholaminergic denervators such as reserpine and 6-hydroxydopamine, and diethyldithiocarbamic acid, a dopamine-beta-hydroxylase inhibitor, increased the TyA response. These results indicate that head-twitches induced by TyA may be mediated via the serotonergic system and may inhibit the catecholaminergic system.

5,6-Dihydroxytryptamine↗

PubMed1980

Importance of the Locus coeruleus and involvement of alpha-adrenergic receptors in the post-decapitation reflex in the rat.

The latency, duration, hindlimb kick frequency, and total activity components of the post-decapitation reflex (PDR) were measured in the rat using a movement-sensitive transducer. Reduction of brain and spinal cord norepinephrine (NE) caused by neonatal administration of 6-hydroxydopamine (6-OHDA) or 5,7-dihydroxytryptamine, which also reduced brain serotonin, decreased all components of the PDR. Depletion of serotonin or dopamine alone reduced the vigor of the reflex, suggesting that these pathways can influence the PDR but are not essential for the response. Lesions of neurons in the Locus coeruleus, made electrolytically or with 6-OHDA, decreased the intensity of the PDR, with the 6-OHDA-induced lesion being more effective. Depletion of forebrain NE terminals with 6-OHDA did not alter the PDR, consistent with a critical involvement of spinal noradrenergic fibers. The PDR was also decreased by phentolamine and prazosin, but not by propanolol, suggesting an involvement of alpha-adrenergic receptors in the response. This hypothesis was further supported by the finding that the efficacy of a variety of drugs (such as tricyclic antidepressants, phenothiazines, and anti-hypertensive compounds) for blocking the reflex was apparently related to their affinity for alpha-adrenergic receptors. Thus, the PDR is dependent on noradrenergic fibers in the spinal cord and may provide a simple screen for drugs with suspected alpha-adrenergic blocking properties or for agents that disrupt the function of central noradrenergic fibers.

5,7-Dihydroxytryptamine↗

PubMed1982

Involvement of a central dopaminergic system in 5-methoxy-N,N-dimethyltryptamine-induced turning behaviour in rats with lesions of the dorsal raphé nuclei.

The turning behaviour induced by 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) has been investigated in rats with lesions of the dorsal raphé nucleus (DRN). 5-MeODMT caused a dose-related contralateral turning in rats with 5,7-dihydroxytryptamine (5,7-DHT) lesions of the substantia nigra and a similar effect was observed in DRN-lesioned rats. In contrast, a dose-related ipsilateral turning was observed when 5-MeODMT was injected into rats with 5,7-DHT lesions of the striatum. These results suggest that the effects of 5-MeODMT in DRN-Lesioned rats are mediated via the substantia nigra. The contralateral turning induced by 5-MeODMT in rats with a 5,7-DHT lesion of the DRN was significantly reduced when a second 5-hydroxydopamine lesion was placed in the striatum, but not when it was placed in the nucleus accumbens. Thus the nigrostriatal dopaminergic system seems to be involved in 5-MeODMT-induced turning. The release of tritium from slices of substantia nigra previously labelled with [3H]-dopamine was inhibited by 5-MeODMT (10(-7) to 10(-5) M) and this effect was blocked by methysergide in a concentration-related manner. Tetrodotoxin (10(-7) M) failed to antagonise 5-MeODMT. These results suggest that 5-MeODMT can inhibit dopamine release from nigral dendrites, which could in turn enhance nigrostriatal activity by reducing the auto-inhibitory actions of dopamine, thereby causing contralateral turning in DRN-lesioned rats.

5,7-Dihydroxytryptamine↗

PubMed1981

Immobilization stress in rats: effect on rectal temperature and possible role of brain monoamines in hypothermia.

Immobilization of albino rats for 2 h showed ambient temperature-dependent changes in rectal temperature, hypothermia at temperatures below 30 degrees C, and hyperthermia at 35 degrees C and above. Adrenalectomized (Adre) rats showed more hypothermia compared to sham operated controls at 25 +/- 2 degrees C. The increased hypothermia in adrenalectomized rats was reversed by 10 mg/kg IP or 100 microgram/rat ICV of hydrocortisone. Groups of rats pretreated with desmethylimipramine (DMI, 25 mg/kg IP) and 6-hydroxydopamine (6-HD, 100 microgram/rat ICV) or methyl ester of parachlorophenylalanine (ME-PCPA, 100 microgram/rat ICV for 3 days) or 5,6-dihydroxytryptamine (DHT, 75 microgram/rat ICV) showed significantly less hypothermia at the end of 2 h of immobilization. Applying analysis of variance test, the hypothermia in Adre, ME-PCPA and DHT groups, was found to be not significantly different from their respective control groups between 0 and 45 min of immobilization but was significantly different between 45 to 120 min of immobilization. DMI-6-HD group however, showed significant difference between 0--45 min only and not between 45--120 min of immobilization. The results suggest that the early phase of immobilization induced hypothermia between 0--45 min is dopamine and the late phase of hypothermia between 45--120 min is 5-hydroxytryptamine mediated.

5,6-Dihydroxytryptamine↗

PubMed1979

The antinociceptive effect of intracerebroventricularly administered prostaglandin E1 in the rat.

It is generally accepted that prostaglandins (PGs) are nociceptive substances. However, earlier studies from this laboratory indicated that morphine analgesia, in the rat, was not only serotonin mediated, but involved PGs as well. Several PG synthesis inhibitors were shown to inhibit morphine analgesia and PGE1 was shown to potentiate the antinociceptive effect of morphine. Intraperitoneal administration of PGE1, but not PGE2 and PGF2alpha, elicited antinociceptive effect per se, by the radiant heat method. The present study was undertaken to confirm the antinociceptive action of PGE1, after intracerebroventricular administration, against nociceptive impulses induced by radiant heat, pressure, and high frequency electric current. PGE1 produced a dose-dependent antinociceptive effect by the radiant heat and pressure methods. It potentiated the antinociceptive action of morphine by the electrical stimulation method. The antinociceptive action of PGE1 was not evident in 5,6-dihydroxytryptamine-pretreated rats, suggesting that this effect is serotonin mediated. The present study thus confirms the antinociceptive action of PGE1 and suggests that, unlike its peripheral action, the central action of PGE1 results in suppression of nociceptive responses which may be serotonin mediated.

5,6-Dihydroxytryptamine↗

PubMed1981

Effect of modification of brain serotonin (5-HT), norepinephrine (NE) and dopamine (DA) on ethanol tolerance.

Rats were permanently depleted of brain dopamine (DA), serotonin (5-HT), 5-HT + norepinephrine (NE), or NE + DA by intraventricular injection of either 5,7-dihydroxytryptamine (5,7-DHT) or 6-hydroxydopamine (6-OHDA) with or without pretreatment with desmethylimipramine (DMI). Following 1 week of recovery from surgery, daily treatment with ethanol (5 g/kg, PO) or isocaloric sucrose was carried out for a period of 20-25 days. Testing at 5-day intervals showed that chronic ethanol treatment produced tolerance to the hypothermic and motor impairing effects of ethanol. Depletion of 5-HT alone retarded tolerance, while depletion of NE or DA alone produced no effect. Combined depletion of both NE and 5-HT, however, completely inhibited tolerance development. The inhibition of tolerance development by combined depletion of both NE and 5-HT is discussed in terms of a reciprocal relationship between these two systems.

5,7-Dihydroxytryptamine↗

PubMed1980

A fluorescence histochemical study of the monoamine-containing cell in the developing frog taste organ.

Sequential changes in the monoamine-containing cell (MC cell) of the developing frog tongue has been studied by fluorescence histochemistry using uptake of 5,6-dihydroxytryptamine. At st. 16, a few yellow fluorescent cells, here called MC cells, appeared in random order at the uppermost layer of the dorsal epithelium. They were round or elliptical in shape. At st. 18 the MC cells, greatly transformed, were found at the periphery of the sensory disc primordium which first appears during this stage. The MC cell was made up of three parts: perikaryon, process and terminal portion. The perikaryon was located at the upper half of the epithelium and from it a single process stretched vertically toward the basal lamina, above which the dilated terminal portion was found. Thereafter the perikaryon gradually moved toward the basal layer while remaining at the periphery of the disc primordium. Meanwhile the terminal portion moved over the basal lamina toward the center of the disc primordium. At st. 22, the whole of the MC cell lay flat above the basal lamina. The perikaryon was localized at the periphery of the sensory disc and from there the process stretched toward the center. Thus, the morphology of MC cells resembled the adult state, except for smaller size. MC cells were never observed in the subepithelial connective tissue in the present study. This seems to suggest that the MC cell of the frog fungiform papilla is of epithelial origin.

5,6-Dihydroxytryptamine↗

PubMed1980

Enhanced behavioural, electrocortical and hyperthermic effects of serotonin-like agents after impairment of serotonin transmission in fowl brain.

In adult fowls and in young chicks (Gallus domesticus) the effects were studied on body temperature, behaviour and electrocortical activity of 5-HT and other direct or indirect serotonin agonists given into the III cerebral ventricle in conditions of prolonged impairment of serotoninergic transmission. In chicks pretreated with 5,6-dihydroxytryptamine the subsequent intraventricular injection of 5-HT produced more intense and longer-lasting hyperthermic response and behavioural and electrocortical sleep. On the other hand fenfluramine given intraventricularly in fowls pretreated with 5,6-DHT did not produce significant body temperature and behavioural changes. After 14 and 21 day treatment with methysergide the subsequent administration of 5-HT, fenfluramine and quipazine produced in fowls an hyperthermic response and behavioural sleep more marked and longer-lasting than in control animals. The present experiments show that in conditions of chronic impairment of 5-HT function there is an enhanced behavioural and body temperature response to 5-HT and drugs acting by releasing endogenous 5-HT or 5-HT agonists.

5,6-Dihydroxytryptamine↗

PubMed1981

Effects of intracerebroventricular injection of clonidine on metabolic, respiratory, vasomotor and temperature responses in the rabbit.

1. The thermoregulatory outputs (including metabolic, respiratory and vasomotor activities) produced by an injection of clonidine or 5-hydroxytryptamine (5-HT) into the third cerebral ventricle of conscious rabbits were assessed at three different ambient temperatures (Ta) of 2, 22 and 32 degrees C. 2. When injected into the third cerebral ventricle, both clonidine and 5-HT produced a dose-dependent hypothermia in rabbits at both 2 and 22 degrees C Ta. The hypothermia was due to a decrease in metabolic heat production (M) at 2 degrees C Ta, while at 22 degrees C Ta the hypothermia was due to cutaneous vasodilatation. There were no changes in respiratory evaporative heat loss. 3. Furthermore, the clonidine-induced hypothermia was greatly reduced by pretreatment of the animals with either 5,6-dihydroxytryptamine (impairment of central 5-HT pathways) or yohimbine (alpha-adrenergic blocking agent), but not by 6-hydroxydopamine (impairment of central catecholamine pathways). 4. The results indicate that clonidine may act on the alpha-adrenergic receptors located on central 5-HT pathways to produce a hypothermic action by promoting a decrease in heat production or an increase in heat loss in the rabbit.

5,6-Dihydroxytryptamine↗

PubMed1979

Evidence for a receptor supersensitivity following impairment of central serotoninergic activity in the rabbit.

In order to investigate whether a chronic impairment of neuronal serotoninergic transmission in the CNS could result in a receptor supersensitivity, rabbits were pretreated either with 5,6-dihydroxytryptamine (5,6-DHT) or p-chlorophenylalanine (PCPA) and then tested for their hyperthermic response to serotoninergic agonists. A previous (10 days before) intracerebroventricular injection of 5,6-DHT (75 microgram into each cerebral ventricle) significantly potentiated the increase in body temperature induced either by quipazine (1 mg/kg i.v.) or by 5-hydroxytryptophan (5-HTP 2 mg/kg i.v.) in combination with a MAO inhibitor (phenylethylhydrazine 10 mg/kg i.v. 16 h before). Pretreatment with PCPA (100 mg/kg s.c. four times on alternate days, the last dose 48 h before the experiment) also enhanced the hyperthermic effect of quipazine, whereas it inhibited the hyperthermic response to 5-HTP plus MAO inhibitor. These results suggest the existence of a receptor supersensitivity following prolonged blockade of serotoninergic neuronal transmission in the CNS.

5,6-Dihydroxytryptamine↗