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PubMed1982

The effects of intracerebroventricular administration of 5,6-dihydroxytryptamine to neonatal rats.

5,6-Dihydroxytryptamine was administered intracerebroventricularly to neonatal rats on days 3 and 6 (25, 50, 75 or 100 micrograms) or on day 12 (50, 75 or 100 micrograms) after birth. Administration on days 3 and 6 increased serotonin (5-HT) in the diencephalon, decreased it in the telencephalon and produced variable results in the brainstem. The dose of 100 micrograms eliminated the peak in locomotor activity that normally occurs at day 15. Administration on day 12 produced increased 5-HT levels in the diencephalon and the brainstem. The dose of 100 micrograms delayed the decrease in activity after the peak. Administration on days 3 and 6 or on day 12 produced non-specific damage throughout the brain, although dopamine levels were normal. The behavioral effects did not correspond with the neurochemical effects and probably were due to the pronounced non-specific effects of the treatment.

5,6-Dihydroxytryptamine↗
PubMed1983

Role of descending monoaminergic neurons in the control of sexual behavior: effects of intrathecal infusions of 6-hydroxydopamine and 5,7-dihydroxytryptamine.

The present study concerns the possible participation of descending monoamine pathways in the control of sexual behavior. Male and female rats received micro-injections of the neurotoxins, 6-hydroxydopamine (6-OHDA) or 5,7-dihydroxytryptamine (5,7-DHT), in the spinal subarachnoid space, which were found to deplete spinal synaptosomal uptake of radiolabeled noradrenaline and serotonin to 46.7% and 34.5%, respectively. Whereas intrathecal 5,7-DHT did not affect sexual behavior appreciably, female 6-OHDA-treated rats showed less sexual receptivity and proceptivity when exposed to constant estradiol; similarly treated males had prolonged post-ejaculatory refractory periods and were more sensitive than controls to androgen deprivation.

5,7-Dihydroxytryptamine↗
PubMed1983

Role of ventral mesencephalic reticular formation and related noradrenergic and serotonergic bundles in turning behaviour as investigated by means of kainate, 6-hydroxydopamine and 5,7-dihydroxytryptamine lesions.

A unilateral kainate (KA) infusion (2 x 0.15 micrograms, 2 x 0.25 micrograms) in the ventral mesencephalic reticular formation (MRF) resulted in spontaneous contraversive turning lasting only a few days. Upon challenge with apomorphine (0.5 mg/kg s.c.) or amphetamine (5 mg/kg i.p.) the contraversive turning could be reinstated. The incidence, as well as the intensity, of the drug-induced response decreased over the 45 days of observation. KA infused in the ventral MRF induced typical lesions after doses of 2 x 0.15 micrograms but resulted in demyelination after 2 x 0.25 micrograms. These lesions failed to reduce noradrenaline (NA), serotonin (5 HT) or dopamine (DA) in various forebrain areas. Unilateral lesion of ascending NA projections by 6-OHDA infusion (4 micrograms) within the NA bundles coursing in the mesencephalon or near the locus coeruleus, failed to induce motor asymmetries. Unilateral selective lesion of the ventral NA bundle by local 6-OHDA (2 micrograms) infusion also failed to induce motor asymmetries, either spontaneously or in response to dopaminergic drugs. Unilateral lesion of ascending 5-HT projections by the tegmental infusion of 5,7-dihydroxytryptamine (10 micrograms) also failed to induce motor asymmetries in response to dopaminergic drugs but resulted in contraversive circling in response to 5-hydroxytryptophan. These data indicate that intrinsic neurones of the ventral MRF play a role in turning behaviour and exclude, in contrast with previous studies, a role of NA or 5-HT projections in the contraversive turning responses to DA receptor agonists obtained after lesions of the ventral MRF.

5,7-Dihydroxytryptamine↗
PubMed1984

The effects of putative 5-hydroxytryptamine receptor active agents on D-amphetamine self-administration in controls and rats with 5,7-dihydroxytryptamine median forebrain bundle lesions.

Animals in which 5,7-dihydroxytryptamine (5,7-DHT) was bilaterally injected into the median forebrain bundle (MFB) and sham lesioned animals were allowed access to an apparatus which delivered, upon lever pressing, intravenous D-amphetamine injections. MFB lesioned rats achieved stable self-injections patterns and self-administered more drug per test session than controls. A number of agents known to either directly or indirectly affect 5-hydroxytryptamine (5-HT) receptor function were administered prior to D-amphetamine access. The responses to these pretreatments in lesioned vs non-lesioned rats were markedly different. Pretreatment with L-tryptophan reduced the number of D-amphetamine self-injections in sham lesioned rats but had no effect in MFB lesioned animals. Fluoxetine pretreatment, likewise, reduced responding in non-lesioned rats and had no observable effect in lesioned animals. Quipazine markedly reduced self-injection in control rats but was not evaluated in the lesioned group. The putative 5-HT antagonists utilized, cyproheptadine and methysergide, unpredictably reduced self-injection frequency of non-lesioned animals in a dose related manner. When MFB lesioned animals were pretreated with cyproheptadine, rapid bursts of lever pressing were observed and 3 of 6 animals thus treated died as a result (presumably amphetamine overdose). In the remaining animals, methysergide produced a similar marked increase in self-injection rate. While these data may suggest that, in some instances, non-serotonergic mechanisms are involved, for the most part it would appear that 5-HT containing neurons are of major import in some aspect of D-amphetamine self-administration.

5,7-Dihydroxytryptamine↗
PubMed1986

Circadian corticosterone rhythm did not develop in rats seven weeks after destruction with 5,7-dihydroxytryptamine of the serotoninergic nerve terminals in the suprachiasmatic nucleus at the age of 16 days.

In order to study the role of the serotoninergic innervation of the hypothalamic suprachiasmatic nucleus (SCN) in the development of the circadian rhythm of corticosterone 5,7-dihydroxytryptamine (5,7-DHT) selectively destroying the serotoninergic structures was injected into the cell group of 16-day-old male rats prior to the appearance of the corticosterone rhythm. Rats treated with 5,7-DHT did not show circadian fluctuations in plasma corticosterone concentrations 3, 5 and 7 weeks after the injection of the neurotoxin. Their hypothalamo-pituitary-adrenal system responded to ether stress. Immunocytochemistry revealed that only a very few serotonin immunoreactive elements were visible in the SCN of the 5,7-DHT-treated rats. The results indicate that serotoninergic innervation of the SCN is essential for the development of the corticosterone rhythm.

5,7-Dihydroxytryptamine↗
PubMed1987

5,6-Dihydroxytryptamine, a serotonergic neurotoxin, is formed endogenously in the rat brain.

Methamphetamine (MA) in high doses produces long-term toxic effects on the serotonergic system in the rat brain, including depletions of 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid and reductions in 5-HT reuptake and tryptophan hydroxylase activity. In this study, the formation of 5,6-dihydroxytryptamine (5,6-DHT), a serotonergic neurotoxin, was observed in the rat hippocampus after a single 100 mg/kg injection of MA. The 5,6-DHT was detected by reverse-phase high-performance liquid chromatography with electrochemical detection in tissue samples taken 0.5-4 h after MA administration; the highest levels of 5,6-DHT (0.032 ng/mg wet tissue) were detected at 1 h. Following administration of MA, 5-HT was also depleted in the neocortex, but 5,6-DHT was not detected as frequently in this brain region as in the hippocampus. Comparisons were made between the long-term hippocampal 5-HT depletions seen either after an injection of MA or after intraventricular 5,6-DHT infusions and the levels of 5,6-DHT measured in the hippocampus shortly after each treatment. The amount of 5,6-DHT produced after MA administration appears to be adequate to cause the observed long-term 5-HT depletions. We suggest that 5,6-DHT formed from 5-HT may mediate the neurotoxic effects of MA on serotonergic nerve terminals.

5,6-Dihydroxytryptamine↗
PubMed1987

Endogenously produced 5,6-dihydroxytryptamine may mediate the neurotoxic effects of para-chloroamphetamine.

Para-chloroamphetamine (PCA) has been used to deplete brain serotonin (5-HT) in numerous studies of serotonergic involvement in various behaviors and physiological functions. PCA is believed to cause long-lasting depletions of 5-HT by causing the selective degeneration of serotonergic nerve terminals, but the mechanism by which it exerts this neurotoxic effect is not understood. In this experiment, 5,6-dihydroxytryptamine (5,6-DHT), a serotonergic neurotoxin, was detected by high performance liquid chromatography in the rat hippocampus 0.5-4 h after a single 15 mg/kg i.p. injection of PCA. 5,6-DHT was also detected in the somatosensory cortex following PCA administration, but much less frequently than in the hippocampus. Degenerating nerve terminals were observed in the striatum and somatosensory cortex in silver-stained brain sections from rats injected with PCA 1 or 2 days prior to sacrifice. Laminae III and IV of the somatosensory cortex also contained degenerating neuronal perikarya. The neurochemical and histological effects of PCA are very similar to those produced by a large dose of methylamphetamine (MA) in that both drugs are toxic to serotonergic nerve terminals and neuronal perikarya in the somatosensory cortex. We hypothesize that the formation of 5,6-DHT, perhaps from endogenous 5-HT, may mediate the toxic effects of PCA, MA and other amphetamine-related drugs on serotonergic neurons and on a subpopulation of cortical neurons.

5,6-Dihydroxytryptamine↗
PubMed1988

Micturition in the unanesthetized rat: effects of intrathecal capsaicin, N-vanillylnonanamide, 6-hydroxydopamine and 5,6-dihydroxytryptamine.

Unanesthetized rats chronically implanted with vesical and intrathecal catheters were injected intrathecally (i.t.) with either capsaicin (CAP), N-vanillylnonanamide (VN), 6-hydroxydopamine (6-OHDA), or 5,6-dihydroxytryptamine (5,6-DHT). The volume-evoked micturition reflex was assessed by cystometrography before, and 2 h, 1 day and 7 days after injection. In control and vehicle-injected rats, the infusion of saline into the bladder resulted in a periodic contraction of the bladder with synergic sphincter relaxation. One day after i.t. CAP and VN (70 micrograms each), 50% and 30% of the animals displayed a blockade of the micturition reflex, respectively. In these animals, the infusion of saline resulted in a gradual rise in bladder pressure up to a plateau (overflow pressure) equivalent to the predrug bladder opening pressure. When the plateau was reached, continuous dribbling of urine with no bladder contractions was observed. Most of the affected rats displayed some micturition responses by day 7. Following i.t. injection of 5,6-DHT (20 micrograms) or 6-OHDA (20 micrograms), the micturition reflex displayed small but significant increases in bladder volume with no changes in pressure profile. Small primary afferents, sensitive to the neurotoxic effects of CAP and VN appear to play a major tonic role in the regulation of the micturition reflex in unanesthetized rats. Serotonergic and adrenergic descending pathways might play a role in the maintenance of resting bladder tone.

5,6-Dihydroxytryptamine↗
PubMed1989

Monosynaptic connections between serotonin-containing neurones labelled by 5,6-dihydroxytryptamine-induced pigmentation in the snail Helix pomatia L.

Microelectrophysiological experiments were carried out on in vivo 5,6-dihydroxytryptamine-induced pigment-labelled serotonin-containing neurones of Helix pomatia. Excitatory chemical monosynaptic connections were found between the giant pedal LP3 neurone and several follower cells in the visceral and right parietal ganglia. These neurones have previously been described to be involved in regulation of visceral functions. Monitoring changes in identified monosynaptic connections between pairs of serotonin-containing neurones aids the cellular analysis of behavioural plasticity.

5,6-Dihydroxytryptamine↗
PubMed1990

Serotonin reinnervation of the rat organum vasculosum laminae terminalis (OVLT) after 5,7-dihydroxytryptamine deafferentation.

The time course and pattern of serotonin (5-HT) reinnervation in the rat organum vasculosum laminae terminalis (OVLT) following intracerebroventricular administration of 5,7-dihydroxytryptamine were examined by means of [3H]5-HT uptake radioautography. 5-HT axonal varicosities reappeared in the OVLT within 3 months post-lesion. Six months later, they were found to have preferentially reinvested the neurohemal contact area (juxtavascular zone) of the organ. Regenerated terminals further increased in number. At the end of a 16-month survival time, they displayed normal-looking distributional patterns, similar to those of age-matched control animals, and formed new synaptic junctions in the juxtaventricular zone. The cellular mechanisms possibly responsible for 5-HT recovery in the OVLT are discussed.

5,7-Dihydroxytryptamine↗
PubMed1991

Cardiovascular effects of the local injection of 5,7-dihydroxytryptamine into the nodose ganglia and nucleus tractus solitarius in awake freely moving rats.

The role of the nucleus tractus solitarius (NTS) serotonergic afferents in cardiovascular (CV) regulation is yet to be established. However, several findings suggest that in this nucleus the serotonergic endings coming from the nodose ganglia (NG) are involved in the control of blood pressure (BP). The purpose of the present study was to identify the CV effects of the destruction of this NG-NTS serotonergic pathway. For that, the BP, BP variability (BPV) and heart rate (HR) effects of the local microinjection of 5,7-dihydroxytryptamine (5,7-DHT), into the NG and NTS were investigated in awake freely moving rats. The local degeneration of serotonergic elements was associated with a significant decrease in the 5-HT and 5-hydroxyindole acetic acid levels within the NG and NTS in 5,7-DHT treated rats. In addition, the microinjection of the neurotoxin in both structures produced a transient and significant increase in BP. This effect was of greater amplitude and associated with an increase in BPV in NG lesioned rats. These results may indicate that the NG-NTS serotonergic pathway participates in the transfer of the messages arising from the aortic baroreceptors. However, the vagal component of the baroreflex assessed with the phenylephrine test was not significantly modified in NG lesioned animals as compared to controls. Consequently, if the present data suggest that the NG-NTS serotonergic pathway plays a depressor role in BP regulation, its involvement in the reflex CV responses triggered by the stimulation of the aortic baroreceptors has yet to be established.

5,7-Dihydroxytryptamine↗
PubMed1991

5,7-Dihydroxytryptamine injections increase glial fibrillary acidic protein in the hypothalamus of adult rats.

The distribution and levels of glial fibrillary acidic protein (GFAP) were determined in the adult rat hypothalamus following axotomy of serotonin (5-HT) neurons. Seven days after unilateral intrahypothalamic injection of the 5-HT neurotoxin, 5,7-dihydroxytryptamine, there was a marked increase in the number of GFAP-labelled astrocytes in the ipsilateral hypothalamus of 5,7-DHT-treated as compared to sham-treated rats. In addition, levels of GFAP were significantly increased 7 days after 5,7-DHT injection.

5,7-Dihydroxytryptamine↗
PubMed1991

Effect of 6-hydroxydopamine and 5,7-dihydroxytryptamine on tissue uptake and cell nuclear retention of corticosterone in the rat hypothalamus.

Previous studies have shown that norepinephrine and serotonin can modulate the glucocorticoid (GC) binding capacity in the hippocampus. The aim of the present study was to evaluate the role of these neurotransmitters in regulating GC receptors in the hypothalamus. Injection of the neurotoxin 6-hydroxydopamine (6-OHDA) into the ventral noradrenergic bundle (VNAB) and 5,7-dihydroxytryptamine (5,7-DHT) into the raphe nuclei caused a marked depletion in norepinephrine and serotonin, respectively, in the paraventricular nucleus (PVN) and mediobasal hypothalamus (MBH). The injection of these neurotoxins did not change the basal levels of ACTH and corticosterone. Injection of 6-OHDA into the VNAB caused a significant reduction in the cell nuclear binding of corticosterone in the PVN but not in the MBH. Conversely, injection of 5,7-DHT into the raphe nuclei caused a significant reduction in cell nuclear binding of corticosterone in the MBH but did not affect binding in the PVN. These results demonstrate that at least part of the nuclear corticosteroid receptors in the PVN and MBH are differentially regulated by the noradrenergic and serotonergic systems.

5,7-Dihydroxytryptamine↗
PubMed1992

Ultrastructural, biochemical and electrophysiological changes induced by 5,6-dihydroxytryptamine in the CNS of the snail Helix pomatia L.

The serotonin neurotoxin, 5,6-dihydroxytryptamine (5,6-DHT), was injected into the body cavity of snails. Changes induced in the central nervous system (CNS) by the neurotoxin were studied by morphological, electrophysiological and biochemical techniques for up to 90 days following injection. The neurotoxin induced a variety of ultrastructural alterations during the early phase (1st to 6th days) following treatment. On day 6 after treatment, membranous structures first appeared in the synaptic-like areas and apparently migrated to cell bodies where they were detected by day 14. Their number increased with time. Neurotoxin-induced structural alterations were found in neuronal processes and cell bodies of the serotonergic metacerebral giant cells injected intracellularly with horseradish peroxidase and in serotonin immunoreactive axons. These findings suggest that the toxin-induced alterations are rather selective for the serotonin-containing neuronal elements. The neurotoxin decreased the concentration of 5-HT in and [3H]5-HT uptake into cerebral and pedal ganglia, with a maximum effect between the 3rd and 5th day following drug administration. 5-HT levels and 5-HT uptake returned to normal by 19-21 days after treatment. The concentration of dopamine and of [3H]DA uptake capacity were reduced between 3-5 days after injection of 5,6-DHT by 6-7 days following treatment. The transmission from identified serotonergic synapses to targets was reduced beyond day 5 after 5,6-DHT administration. By 15 days after treatment, synaptic transmission between the metacerebral giant cell (MGC) and buccal followers was blocked. Transmission recovered by day 21 after 5,6-DHT. Comparison of the time-course of functional and structural recovery indicates that while functional recovery takes place within 21 days after treatment, certain structural alterations, e.g. the membranous structures and dense particles, remain in the nerve fibres and cell bodies. These may serve as specific intracellular markers of the serotonin-containing neuronal elements long after functional recovery from the effect of 5,6-DHT.

5,6-Dihydroxytryptamine↗
PubMed1992

Early post-natal administration of 5,7-dihydroxytryptamine destroys 5-HT neurons but does not affect spatial memory.

The neurotransmitter serotonin (5-hydroxytryptamine, 5-HT) may play an important role in learning and memory. It has also been suggested that 5-HT abnormalities may mediate some aspects of the cognitive disorders associated with Korsakoff syndrome and Alzheimer's Disease. The effect of intracisternally applied 5-HT neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT) on learning and memory in rodents was evaluated. Three-day-old rat pups were treated with pargyline (40 mg/kg, i.p.) followed by 5,7-DHT (50 micrograms/pup) and returned to the dam for a month. At 75 days of age, rats were tested on a learning set problem in the Morris water maze for 5 days followed by 30 days of testing in a 12-arm radial maze with 8 of the 12 arms baited. In the Morris water maze, the latency to locate the hidden platform did not differ significantly for 5,7-DHT treated and control rats (F less than 1.0). Similarly, 5,7-DHT treated rats performed comparably to controls on the 12-arm radial maze (F less than 1.0). At 106 days of age the assay of tryptophan hydroxylase activity in the dorsal raphe nuclei and hippocampus showed marked reduction (86%, 78%, respectively) in 5,7-DHT treated animals compared to vehicle injected controls. Immunocytochemical analysis was consistent with the biochemical results. In 5,7-DHT treated animals there was severe loss of neurons that bind 5-HT antibody in the dorsal and medial raphe nuclei.(ABSTRACT TRUNCATED AT 250 WORDS)

5,7-Dihydroxytryptamine↗
PubMed1993

Changes in activity and mRNA for rat tryptophan hydroxylase and aromatic L-amino acid decarboxylase of brain serotonergic cell bodies and terminals following neonatal 5,7-dihydroxytryptamine.

In the present study, we examined time-dependent changes in activity, mRNA and immunoreactivity of the serotonin biosynthetic enzymes, tryptophan hydroxylase (TPH) and aromatic L-amino acid decarboxylase (AADC) in dorsal raphe nucleus (DRN), caudal brainstem and hypothalamus, following intracisternal injection of 5,7-dihydroxytryptamine (5,7-DHT) in neonatal rats. TPH activity in central serotonergic cell bodies and terminals was reduced to 20-30% of control levels at 1-8 weeks after neonatal, low-dose 5,7-DHT injection (24 micrograms free base). In contrast, AADC activity was either not changed or decreased to 40% of control levels, depending on the region. In situ hybridization and immunocytochemical staining indicated that 5,7-DHT caused a marked reduction in TPH and AADC message levels as well as the number of 5-HT and AADC-immunoreactive cells within the DRN as early as 1 week after 5,7-DHT. Even 15 weeks after drug administration recovery did not occur. This apparent neuronal loss was region-specific suggesting that some serotonergic neurons are more resistant to neonatal 5,7-DHT treatment than others. Taken together, these studies indicate that neonatal treatment with 5,7-DHT produces a marked and permanent (up to 15 weeks) reduction in the number of central serotonergic neurons.

5,7-Dihydroxytryptamine↗
PubMed1993

Serotonin depletors, 5,7-dihydroxytryptamine and p-chlorophenylalanine, cause sprouting in the CNS of the adult snail.

The effects of 5,7-dihydroxytryptamine (5,7-DHT) and p-chlorophenylalanine (PCPA) on neuronal morphology were investigated in Achatina fulica by backfilling the cerebrobuccal connective with nickel-lysine. Backfilling 21 days following injections of either 5,7-DHT or PCPA revealed supernumerary staining of fibers in different pathways of the cerebral and buccal ganglia and novel staining of somata in the cerebral ganglia. HPLC measurements confirm that drug treatments led to a 30-46% depletion of serotonin (5-HT) in the buccal ganglia. These results support the role suggested for 5-HT as a neuritogenic modulator and additionally advise caution in the use of pharmacological depletors in studies examining serotonergic function.

5,7-Dihydroxytryptamine↗
PubMed1993

Increase of central 5-HT1B binding sites following 5,7-dihydroxytryptamine axotomy in the adult rat.

The effects of selective axotomy of serotoninergic neurons produced by an intracerebroventricular injection of 5,7-dihydroxytryptamine (200 micrograms free base) on 5-HT1B binding sites labeled with S-CM-G-[125I]TNH2 were investigated by quantitative autoradiography in the rat brain. Results show, 21 days after surgery, an upregulation of 5-HT1B receptors in the entorhinal cortex and the dorsomedial and suprachiasmatic nuclei of the hypothalamus. The cellular localization of those 5-HT1B receptors exhibiting post-lesion plastic properties is discussed.

5,7-Dihydroxytryptamine↗