PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Dihydroxytryptamines”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 703 records · Page 39Linked to original sources
PubMed1987

Supersensitive beta-adrenergic receptors are down-regulated in rat brain by mianserin administration.

Experiments were undertaken to determine whether alterations in rat brain monoaminergic tone influence the manner in which mianserin administration modifies beta-adrenergic receptor function. Whereas the chronic administration of mianserin had little effect on isoproterenol-stimulated cAMP accumulation in control cerebral cortical slices, treatment with this antidepressant prevented or reversed beta-adrenergic receptor super-sensitivity resulting from reserpine or 6-hydroxydopamine administration. In contrast, 5,7 dihydroxytryptamine treatment had no effect on beta-adrenergic receptor activity, or on the ability of mianserin to modify isoproterenol-stimulated cAMP accumulation. The results indicate that antidepressant-induced alterations in beta-adrenergic receptor activity may, in some cases, be a function of receptor sensitivity at the time of drug administration.

5,7-Dihydroxytryptamine↗
PubMed1981

Depletion in amygdaloid 5-hydroxytryptamine concentration and changes in social and aggressive behaviour.

5,7-Dihydroxytryptamine (10 and 20 microgram) was microinjected bilaterally into the amygdaloid complex of rats and resulted in 55% and 80% depletion in 5-hydroxytryptamine concentration, respectively. The lesioned animals exhibited fewer dominance behaviours and submitted more often to an intruder into their home-cages than did the vehicle-injected controls. The lesioned rats were also more submissive than were the controls when they were intruding into another rat's territory. Only the higher dose of toxin altered social investigatory behaviour when this was measured in an arena in which neither rat had established territory. The lesioned rats displayed less social interaction and had reduced levels of motor activity. The results are compared with those of other studies in which there has been regional or general depletion of brain 5-hydroxytryptamine concentration.

5,7-Dihydroxytryptamine↗
PubMed1981

Radioautographic evidence for an innervation of the subcommissural organ by GABA-containing nerve fibres.

Light-and electron-microscopic radioautographic studies were carried out in rats after intraventricular injection of [3H]GABAergic elements in the subcommissural organ (SCO). This amino acid is specifically accumulated in SCO ependymocytes and numerous nerve terminals and fibres. Some labelled terminals contain clear round vesicles and large granular vesicles and sometimes display synaptic contacts on the SCO ependymocytes. They disappear after 5,7-dihydroxytryptamine (5,7-DHT) treatment or lesions of mesencephalic raphé nuclei. They are morphologically and pharmacologically similar to the serotonin-containing terminals of the basal SCO. The other labelled terminals contain exclusively clear round vesicles, are dispersed throughout the SCO and survive after the 5,7-DHT treatment or raphé nuclei lesions; some of them are in synaptic contact with neuronal elements of the basal SCO. In both SCO ependymocytes and fibres or terminals, [3H]GABA is accumulated according to the pharmacological criteria of a GABA neuronal uptake. Under the same experimental conditions [3H[glutamine and beta[3H]alanine fail to label the SCO: [3H] glutamate produces a very light labelling and [3H] serotonin is accumulated only in nerve profiles of the basal SCO. These results, and the presence of a glutamate decarboxylase activity in the SCO, suggest the existence of GABA-synthesizing elements in the SCO and could indicate the possible involvement of GABA in the secretory activity of the SCO.

5,7-Dihydroxytryptamine↗
PubMed1987

Ultrastructural organization of regenerated serotonin axons in the dorsomedial hypothalamus of the adult rat.

The ultrastructural organization of regenerated serotonin (5-HT) axons was examined in the dorsomedial hypothalamus (DMH) of the adult rat using high-resolution radioautography after intraventricular infusion of [3H]5-HT. An analysis of the microenvironment of the [3H]5-HT-labelled terminals in the DMH was made 30 and 50 days after unilateral injection of 5,7-dihydroxytryptamine (5,7-DHT) or vehicle solution into the dorsolateral hypothalamus. In sham-treated animals [3H]5-HT-labelled axons were small, contained many small clear vesicles, one or more large granular vesicles, and showed only rare synaptic specializations. In 5,7-DHT-treated animals the internal organization of [3H]5-HT-labelled profiles resembled that of sham-treated animals. A tendency toward increased synaptic frequency was found for [3H]5-HT-labelled terminals in the 5,7-DHT-treated group 50 days post-lesion, and an increase in the number of [3H]5-HT-labelled terminals abutting unlabelled perikarya was found in both 30- and 50-day post-lesion groups as compared to sham-treated groups. No other differences in ultrastructural environment were found between sham- and 5,7-DHT-treated animals at either 30 or 50 days post-lesion. These results suggest that 5-HT fibres in the hypothalamus regenerate with a great deal of cellular specificity.

5,7-Dihydroxytryptamine↗
PubMed1978

Correlation between acidic phospholipids and serotonin and between lysolecithin and dopamine in ganglia of the marine mussel, Mytilus edulis.

These studies have demonstrated a positive correlation between the acidic phospholipids and the serotonin content and between the lysolecithin and the dopamine content in the cerebral, pedal and visceral ganglia of Mytilus edulis. These relationships were further supported by experiments utilizing 6-hydroxydopamine and 5,6-dihydroxytryptamine.

5,6-Dihydroxytryptamine↗
PubMed1995

Serotonin and alcohol-related brain damage.

Preliminary results from the immunohistochemical examination of the brainstems of chronic alcoholics, suggest that alcohol may have a role in damage to the principal serotonergic (5HT) nuclei. This view is reinforced by evidence from previous animal experiments which demonstrated a reduction in 5HT neurons in the brains of alcohol-preferring rats and selective neurotoxicity to 5HT neurons following 5,6-dihydroxytryptamine-induced increased ethanol intake. It is speculated that, like other neurotoxins, alcohol or its metabolites cause degeneration of 5HT axons and axon terminals. It is possible that if axonal damage is sufficiently severe and chronic, the eventual consequence is cell death. This could be due to insufficient opportunity for repair and regrowth under repeated and sustained insults of high alcohol consumption.

5,6-Dihydroxytryptamine↗
PubMed1990

Effect of serotonergic lesion on "anxious" behaviour measured in the elevated plus-maze test in the rat.

5,7-Dihydroxytryptamine (250 micrograms) was administered intracerebroventricularly to rats to lesion central serotonergic neurones. Fourteen days later the rats were tested in the elevated plus-maze "anxiety" model in comparison to sham lesioned animals. Twenty-four hours later, the rats were killed and serotonin levels and [3H]paroxetine binding measured in cortical and hippocampal membranes. The lesion destroyed 81% of the serotonergic innervation in the cortex and 99% in the hippocampus as determined by endogenous serotonin levels. Lesioned rats had an increased ratio of open/total arm entries in the elevated plus-maze, reflecting a decreased level of "anxiety". These results are compatible with the implication of serotonin in the control of anxiety and suggest that an anxiolytic effect may be induced by lowering the level of serotonergic activation.

5,7-Dihydroxytryptamine↗
PubMed1991

Effect of chronic treatment with 8-OH-DPAT in the forced swimming test requires the integrity of presynaptic serotonergic mechanisms.

The effect of chronic treatment with 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) on rats' behaviour in the forced swimming test was studied in animals injected intracerebroventricularly with 150 micrograms 5,7-dihydroxytryptamine (5,7-DHT) or given three oral doses of parachlorophenylalanine (PCPA). A single dose of 0.25 mg/kg 8-OH-DPAT significantly reduced rats' immobility in 5,7-DHT-sham-operated animals 24 h after a 14-day schedule of 0.25 mg/kg 8-OH-DPAT or saline subcutaneously twice daily. The effects of acute 8-OH-DPAT in both chronically 8-OH-DPAT- and saline-treated animals were prevented by 5,7-DHT which caused a marked depletion of brain serotonin (5-HT). Since animals treated with both 8-OH-DPAT and 5,7-DHT were more active in an open field than those receiving the substances separately, the forced swimming behaviour was analyzed in more detail in subsequent experiments. PCPA treatment completely prevented the increase in struggling caused by acute and chronic 8-OH-DPAT, administered as in the previous experiment, but did not modify the reduction of floating caused by 8-OH-DPAT. PCPA and 8-OH-DPAT, alone or in combination, did not modify rats' activity in an open field. Finally, 0.5 and 1.0 micrograms 8-OH-DPAT in the nucleus raphe dorsalis significantly increased struggling and reduced floating to the same extent in animals which had received 0.25 mg/kg 8-OH-DPAT or saline subcutaneously twice daily for 14 days. It thus appears that the antidepressant-like effects of chronic treatment with 8-OH-DPAT in the forced swimming test require the integrity of presynaptic serotonergic mechanisms.

5,7-Dihydroxytryptamine↗
PubMed1994

Depletion of brain serotonin by 5,7-DHT: effects on the 8-OH-DPAT-induced changes of sleep and waking in the rat.

The effect of 5-HT1A receptor agonist 8-OH-DPAT on sleep and wakefulness was studied in rats with selective serotonin depletion after ICV administration of the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT). Injection of 8-OH-DPAT to vehicle-treated animals induced biphasic effects, such that low doses (0.010 mg/kg) which act perferentially on the somatodendritic autoreceptor decreased wakefulness (W) and increased slow wave sleep (SWS), while higher doses (0.375 mg/kg) which stimulate postsynaptic receptors caused opposite effects. REM sleep was suppressed irrespective of the dosage given. Injection of the 0.010 mg/kg dose in the 5,7-DHT-treated rats did not result in significant changes in sleep or W. On the other hand, the 0.375 mg/kg dose produced changes in sleep variables which were similar to those described in the vehicle-treated animals. Our findings tend to indicate that increased SWS after low doses of 8-OH-DPAT depends upon the activation of inhibitory somatodendritic 5-HT1A receptors, while increased W after higher doses of the compound is related to stimulation of postsynaptic receptors.

5,7-Dihydroxytryptamine↗
PubMed1992

Actions and some interactions of 5-HT1A ligands in the elevated X-maze and effects of dorsal raphe lesions.

Effects of 5-HT1A agonists and partial agonists on open/total arm entry ratio (OTR) have been examined in the elevated X-maze anxiety model. 8-OH-DPAT (0.05-0.2 mg/kg), RU 24969 (0.5-2.0 mg/kg) and BAY R 1521 (0.1-1.2 mg/kg) produced dose-dependent reductions in OTR, signifying anxiogenic effects. Buspirone reduced OTR only at doses (0.25-5.0 mg/kg) decreasing total entries; gepirone (0.1-5.0 mg/kg) was inactive. Ipsapirone (0.25-5.0 mg/kg) increased OTR and at 1.0 mg/kg antagonised the anxiogenic action of 8-OH-D-PAT, RU 24969 and BAY R 1531. Gepirone (2.5 mg/kg) failed to antagonise 8-OH-DPAT, but the dose was limited by its effect on total entries. The anxiogenic effect of a low dose of 8-OH-DPAT was also prevented by p-chlorophenylalanine (p-CPA) pretreatment and reversed to anxiolytic by 5,7-dihydroxytryptamine lesions of dorsal raphe, which spared median raphe. These lesions also abolished the anxiolytic effect of ipsapirone without affecting the anxiogenic response to yohimbine. This study provides preliminary evidence that 8-OH-DPAT may be capable of acting as an agonist and ipsapirone as an antagonist at a presynaptic site related to dorsal raphe which is separate from the site of action of yohimbine. 5-HT1A agonists and partial agonists may have multiple sites and/or mechanisms of action in the elevated X-maze.

5,7-Dihydroxytryptamine↗
PubMed1993

Serotonin and genetic differences in sensitivity and tolerance to ethanol hypothermia.

Mice have been selectively bred for genetic sensitivity (COLD) or insensitivity (HOT) to acute ethanol-induced hypothermia. COLD mice readily develop tolerance to the hypothermic effects of ethanol (EtOH) when it is chronically administered, while HOT mice do not. A number of studies have implicated serotonergic systems in both sensitivity and the development of tolerance to the hypothermic and ataxic effects of EtOH. In the experiments reported here, we administered the serotonin (5HT) neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) to HOT and COLD mice before the acute and chronic administration of equipotent doses of EtOH. 5,7-DHT lesions significantly reduced (by about 65%) whole brain levels of 5HT in both selected lines. This treatment reduced sensitivity to acute EtOH hypothermia in COLD, but not in HOT mice, and blocked the development of tolerance only in COLD mice. Metabolites of 5HT, norepinephrine, and dopamine were generally increased in hypothalamic and brain stem tissue after acute EtOH injection, but HOT and COLD mice were not differentially susceptible to these effects. These results suggest that genes affecting 5HT systems may mediate some of the differences in response to the hypothermic effects of EtOH characterizing HOT and COLD mice.

5,7-Dihydroxytryptamine↗
PubMed1992

Impaired acquisition of temporal differentiation performance following lesions of the ascending 5-hydroxytryptaminergic pathways.

Nineteen rats received injections of 5,7-dihydroxytryptamine into the dorsal and median raphe nuclei; 16 rats received sham injections. The rats underwent 50 daily training sessions under an interresponse-time-greater-than-15-seconds (IRT greater than 15 s) schedule of sucrose reinforcement. The lesioned group showed impaired acquisition of temporal differentiation, in that their response rates remained significantly higher and their obtained reinforcement frequencies significantly lower than those of the control (sham-lesioned) group. Comparison of the IRT frequency distributions obtained from the two groups during the last 5 days of training showed that the lesioned group produced a significantly higher proportion of very short IRTs (less than 3 s) than the control group; when these short IRTs were disregarded, the lesioned group displayed a significantly lower mean IRT and a significantly higher coefficient of variation than the control group. The levels of 5-hydroxytryptamine (5HT) and 5-hydroxyindoleacetic acid in the parietal cortex, hippocampus, amygdala, nucleus accumbens and hypothalamus were markedly reduced in the lesioned group, but the levels of noradrenaline and dopamine were not significantly affected by the lesion. The results suggest that destruction of the ascending 5HTergic pathways may reduce animals' capacity to inhibit positively reinforced operant behaviour, and may impair temporal discrimination.

5,7-Dihydroxytryptamine↗
PubMed1994

Facilitated acquisition of a temporal discrimination following destruction of the ascending 5-hydroxytryptaminergic pathways.

This experiment examined the effect of destroying the 5-hydroxytryptaminergic (5HTergic) pathways on the acquisition and performance of discrimination between two brief time intervals. Rats that had received injections of 5,7-dihydroxytryptamine into the dorsal and median raphe nuclei, and sham-lesioned control rats were trained in a series of discrete trials to press lever A following a 200-ms presentation of a light stimulus and lever B following an 800-ms presentation of the same stimulus. Both groups gradually acquired accurate performance, attaining 80%-85% accuracy by the end of 40 sessions. The lesioned group learnt the task significantly faster than the control group. When stable performance had been attained, "probe" trials were introduced in which the light was presented for intermediate durations. Both groups showed sigmoid functions relating percent choice of lever B to log stimulus duration. The bisection point (duration corresponding to 50% choice of lever B) did not differ significantly between the two groups; however, the Weber fraction was significantly smaller in the lesioned group than in the control group. The levels of 5HT and 5-hydroxy-indole-acetic acid were markedly reduced in the brains of the lesioned rats, but the levels of noradrenaline and dopamine were not altered. The results indicate that destruction of the 5HTergic pathways facilitates acquisition of a temporal discrimination. The lack of an effect of the lesion on the bisection point contrasts with our previous finding using longer stimulus durations; it is suggested that different behavioural processes may underlie millisecond-range and second-range temporal discrimination, and that these may be differently affected by 5HT depletion.

5,7-Dihydroxytryptamine↗
PubMed1993

Effect of lesions of the ascending 5-hydroxytryptaminergic pathways on choice between delayed reinforcers.

The possible involvement of the ascending 5-hydroxytryptaminergic (5HTergic) pathways in determining the effectiveness of delayed positive reinforcers was investigated using Mazur's (1984) adjusting-delay paradigm. Fourteen rats received injections of 5,7-dihydroxytryptamine into the dorsal and median raphe nuclei; 12 rats received sham lesions. The rats made repeated choices in a two-lever operant conditioning chamber between a smaller reinforcer delivered after a 2-s delay and a larger reinforcer delivered after a variable delay, the length of which was determined by the subject's previous choices. When the two reinforcers consisted of one and two food pellets, the "indifference point" (the delay to the larger reinforcer that rendered the two reinforcers equally effective) was shorter in the lesioned group than in the control group. Increasing the sizes of the reinforcers to three and six pellets reduced the indifference point in both groups and abolished the between-group difference. The levels of 5HT and 5-hydroxyindoleacetic acid (5HIAA) in the parietal cortex, hippocampus, amygdala, nucleus accumbens and hypothalamus were greatly reduced in the lesioned group, but the levels of noradrenaline and dopamine were not significantly affected. The results are consistent with the suggestion that the 5HTergic pathways play a role in maintaining the effectiveness of delayed reinforcers.

5,7-Dihydroxytryptamine↗
PubMed1995

The role of the ascending 5-hydroxytryptaminergic pathways in timing behaviour: further observations with the interval bisection task.

This experiment examined the effect of destroying the 5-hydroxytryptaminergic (5HTergic) pathways on rats' ability to discriminate between two durations. Rats received injections of 5,7-dihydroxytryptamine into the median and dorsal raphe nuclei or sham lesions. They were trained to press lever A following a 2-s presentation of a light and lever B following an 8-s presentation of the light. For some rats, the levers were inserted into the chamber immediately after stimulus presentation ("no-poke-requirement"); for others, the levers were not inserted until a flap covering the food tray positioned midway between the levers had been depressed ("poke-requirement"). When stable performance was attained, "probe" trials were introduced in which the light was presented for intermediate durations. Logistic functions were derived relating percent choice of lever B to log stimulus duration. Under the "no-poke-requirement" condition, the bisection point (duration yielding 50% choice of lever B) was shorter in the lesioned rats than in the control rats. Under the "poke-requirement" condition, this effect of the lesion was attenuated. There was no effect of the lesion on the Weber fraction under either condition. The levels of 5HT and 5-hydroxyindoleacetic acid were reduced in the brains of the lesioned rats, but the levels of noradrenaline and dopamine were not altered. It is proposed that rats may attain accurate timing under the interval bisection task by moving from one lever to the other during stimulus presentation; this movement may be facilitated by destruction of the 5HTergic pathways.(ABSTRACT TRUNCATED AT 250 WORDS)

5,7-Dihydroxytryptamine↗
PubMed1993

Effect of lesions of the ascending 5-hydroxytryptaminergic pathways on timing behaviour investigated with an interval bisection task.

Seventeen rats received injections of 5,7-dihydroxytryptamine into the dorsal and median raphe nuclei: 12 rats received sham injections. The rats were trained in a series of discrete trials to press lever A following a 2-s presentation of a light stimulus and to press lever B following an 8-s presentation of the same stimulus. Both groups learnt the task rapidly and maintained > 90% accuracy throughout the experiment. When stable performance had been attained, "probe" trials were introduced in which the light was presented for intermediate durations. Both groups showed sigmoid functions relating percent choice of lever B to log stimulus duration. The bisection point (duration corresponding to 50% choice of lever B) was significantly shorter in the lesioned group than in the control group. There was no significant difference between the slopes of the psychophysical functions or the Weber fractions derived for the two groups. The levels of 5-hydroxytryptamine (5HT) and 5-hydroxyindoleacetic acid in the parietal cortex, hippocampus, amygdala, nucleus accumbens and hypothalamus were markedly reduced in the lesioned group, but the levels of noradrenaline and dopamine were not significantly affected by the lesion. The results confirm the involvement of 5HTergic function in timing behaviour, but suggest that destruction of these pathways does not disrupt the capacity for temporal discrimination.

5,7-Dihydroxytryptamine↗
PubMed1994

Effect of lesions of the ascending 5-hydroxytryptaminergic pathways on timing behaviour investigated with the fixed-interval peak procedure.

Twelve rats received injections of 5,7-dihydroxytryptamine into the dorsal and median raphe nuclei; 12 rats received sham lesions. The rats were then trained for 60 sessions under a discrete-trials fixed-interval schedule (peak procedure). In half the trials, a reinforcer became available 40 s after trial onset, and the trial was terminated upon reinforcer delivery; the remaining trials were 120 s in duration, and reinforcement did not occur in these trials. Performance during the 120-s trials was characterized by increasing response rate during the first 40 s of the trial, declining response rate between 40 s and 80 s, and a secondary increase in response rate during the final 40 s of the trial. The lesioned group showed a broader "spread" of the response rate function than the control group (time between attainment of 70% of the peak response rate and subsequent decline of response rate below this level); however, the peak response rate and the time from trial onset until attainment of the peak response rate did not differ significantly between the groups; the spread/peak-time ratio was significantly greater in the lesioned group than in the control group. The levels of 5-hydroxytryptamine (5HT) and 5-hydroxyindoleacetic acid in the parietal cortex, hippocampus, amygdala, nucleus accumbens and hypothalamus were markedly reduced in the lesioned group, but the levels of noradrenaline and dopamine were not significantly affected by the lesion. The results confirm the involvement of 5HTergic function in timing behaviour.

5,7-Dihydroxytryptamine↗