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At least 325 records · Page 18Linked to original sources
PubMed1986

Early postnatal administration of 5,7-dihydroxytryptamine: effects on substance P and thyrotropin-releasing hormone neurons and terminals in rat brain.

Substance P, thyrotropin-releasing hormone (TRH) and serotonin are putative neurotransmitters which have been proposed to co-exist in some brain neurons. Our previous immunocytochemical and biochemical studies have demonstrated that 85-100% of all serotonin neurons are destroyed following neonatal 5,7-dihydroxtryptamine (5,7-DHT) treatment. In this study, we have determined the effect of neonatal 5,7-DHT and desipramine (DMI) treatment on the biochemical content and immunocytochemical localization of substance P and TRH throughout the brain. Interestingly, we have observed that virtually all substance P- and TRH-immunoreactive cells in the ventral pons-medulla are destroyed by the neurotoxin. However, peptide-containing neurons in other regions were not affected. Additionally, we measured the peptide content and found that TRH is significantly decreased in the spinal cord (-50%) and pons-medulla (-20%), but not in other brain regions. Substance P content was not significantly altered in any region, even after a greater than 90% reduction of serotonin. These data indicate that the co-localized substance P and TRH forms a small proportion of the total peptide in brain.

5,7-Dihydroxytryptamine↗
PubMed1986

Effect of 5,7-dihydroxytryptamine on the concentration of individual proteins in different areas of the rat brain.

Proteins which are apparently regulated in concentration in two different areas of the rat brain by the indole neurotransmitter serotonin were identified using two-dimensional gel electrophoresis combined with computerized scanning densitometry. Reduction in central serotonin levels produced a decrease in the concentration of 3 different proteins (2 in the parietal cortex, 1 in the hippocampus). Two proteins, both in the hippocampus, were elevated in concentration following serotonin depletion. These results demonstrate that there exist in the brain a limited number of proteins whose concentration is influenced by serotonin.

5,7-Dihydroxytryptamine↗
PubMed1980

Unilateral 5,7-dihydroxytryptamine lesions of the dorsal raphe nucleus (DRN) and rat rotational behaviour.

A unilateral lesion in the dorsal raphe nucleus (DRN) resulted in a decreased concentration of 5-hydroxytryptamine (5-HT) in the ipsilateral striatum (CS), anterior cortex and substantia nigra (SN), a loss of [3H]5-HT uptake sites in the cortex and striatum and a selective reduction in 5-HT turnover in the substantia nigra. The directly acting 5-HT agonist 5-methoxy-N,N-dimethyltryptamine induced contralateral turning behaviour in the lesioned animals, whilst the 5-HT releasing agent, p-chloroamphetamine, induced ipsilateral rotation. All rotational behaviour was blocked by haloperidol and the turning behaviour in response to 5-MeODMT was blocked by methysergide. The data presented suggest that the DRN innervates the SN and CS differentially and that nigral 5-HT receptors become supersensitive after denervation of the DRN-SN pathway.

5,7-Dihydroxytryptamine↗
PubMed1983

6-Hydroxydopamine and 5,7-dihydroxytryptamine selectively reduce dopamine and 5-hydroxytryptamine metabolites in cerebroventricular perfusates of rats.

The efflux into the lateral cerebral ventricles of metabolites of dopamine (DA) and 5-hydroxytryptamine (5HT) was determined in unanesthetized rats bearing chronically implanted push-pull cannulae. Pretreatment with 6-hydroxydopamine (6-OHDA) reduced the basal efflux of 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), but not of 5-hydroxyindoleacetic acid (5HIAA). The haloperidol-induced increase in the efflux of DOPAC and HVA was markedly attenuated in the 6-OHDA-pretreated rats. In rats treated with 5,7-hydroxytryptamine (5,7-DHT) the basal efflux of DOPAC and HVA was unaffected, while that of 5HIAA was markedly reduced; in these animals the ability of L-tryptophan to increase the perfusate content of 5HIAA was abolished. These results indicate that metabolites of DA and 5HT appearing in cerebroventricular perfusates of rats originate from DA and 5HT neuronal terminals in the brain.

5,7-Dihydroxytryptamine↗
PubMed1986

The behavioral effects of depletions of brain serotonin induced by 5,7-dihydroxytryptamine vary with time after administration.

Ether-anesthetized Sprague-Dawley rats were depleted of brain serotonin (5HT) by intraventricular injections of 50 micrograms 5,7-dihydroxtryptamine (57DHT). Oral pretreatment with 25 mg/kg desmethylimipramine was used to protect brain noradrenergic neurons from 57DHT. Liquid chromatographic assays revealed that this treatment did not significantly alter catecholamine levels but depleted hippocampal 5HT by 92% and striatal 5HT by 45%. Three or eleven days after lesioning, locomotor and exploratory behavior was characterized in separate groups of animals with a behavioral pattern monitor (BPM). On Days 4 and 12, the animals were retested following saline or 1.0 mg/kg amphetamine. Three days after depletion, lesioned rats exhibited a decrease rate of habituation of locomotor activity relative to controls. When challenged with amphetamine (1.0 mg/kg), 5HT-depleted rats exhibited increased corner and decreased center activity, as well as stereotyped patterns of locomotion. Eleven days following lesion, 5HT-depleted rats exhibited habituation rates greater than controls; amphetamine challenge yielded patterns of activity similar to those of control animals. These results show that central serotonergic pathways play an important role in modulating both spontaneous and amphetamine-elicited activity in rats, and that compensatory mechanisms operate over time to alter the behavioral effects of 57DHT-induced depletions of brain 5HT.

5,7-Dihydroxytryptamine↗
PubMed1978

Developmental plasticity of central serotonin neurons after 5,7-dihydroxytryptamine treatment.

Systemic administration of 5,7-HT to newborn rats produces an altered development of the 5-HT neurons in the central nervous system, with marked regional differences. 5,7-Hydroxytryptamine can enter the brain and elicit its neurotoxic actions after systemic administration in the neonatal stage due to an incompletely developed blood-brain barrier, which for 5,7-HT is elaborated between postnatal Days 5 and 7. Treatment with 5,7-HT at birth produces marked and permanent 5-HT denervation in the cerebral cortex and spinal cord, whereas hyperinnervation occurs in the 5-HT cell body-near regions (mesencephalon-pons-medulla). The latter effect is seen within the first week postnatally. Treatment with 5,7-HT also affects NA neurons in a similar manner, although the action is exerted preferentially on 5-HT neurons. A selective effect on 5-HT neurons can be achieved by DMI pretreatment, after which both NA and DA neurons develop normally. No signs of any interaction among growing 5-HT, NA, and DA neurons can be observed. Studies of the postsynaptic 5-HT receptor in vitro with [3H]-5-HT and [3H]LSD binding indicate that this receptor develops independently of presynaptic 5-HT nerve terminals. Neither 5-HT denervation nor 5-HT hyperinnervation was accompanied by any change in receptor-binding characteristics or receptor density. The results available are compatible with the view that the consequences for 5-HT neurons that occur after neonatal 5,7-HT administration are mainly due to a "pruning effect." The developing 5-HT neurons seem to be programmed to produce a certain quantity of nerve terminal arborizations, which they try to conserve after 5-HT-induced injury, leading to the observed rearrangement of 5-HT nerve terminals.

5,7-Dihydroxytryptamine↗