Disease relevance of 5,7-DIHYDROXYTRYPTAMINE

• Juvenile male rats given intracerebroventricular injections of 5,7-dihydroxytryptamine, following treatment with desmethylimipramine, maintained body weight gains of 5 to 6 grams per day into adulthood and grew much larger than control rats [1].
• Hyperphagia and increased growth in rats after intraventricular injection of 5,7-dihydroxytryptamine [1].
• A myoclonic syndrome consisting of tremor, myoclonus, and seizures was produced following the systemic administration of 5-hydroxytryptophan to adult rats previously given intracisternal injections of 5,7-dihydroxytryptamine and systemic desmethylimipramine, but not in their controls [2].
• Compared to vehicle-injected animals with injection of vehicle alone, microinjection of a serotoninergic neurotoxin 5,7-dihydroxytryptamine into the NRM significantly increased thermal hyperalgesia and Fos protein expression in lumbar spinal cord after hindpaw inflammation [3].
• Injections of 5,7-dihydroxytryptamine (5,7-DHT) in the dorsal and medial raphe nuclei, producing a partial loss of 5-HT neurons, induced rapid and transient increases in glial fibrillary acidic protein immunoreactivity indicative of a reactive gliosis, but no changes in the S100beta or tenascin-C normally secreted by astroglial cells [4].

Psychiatry related information on 5,7-DIHYDROXYTRYPTAMINE

• 5,7-Dihydroxytryptamine lesions of crayfish serotonin-containing neurons: effect on the lateral giant escape reaction [5].
• Effects of neonatal administration of 5,7-dihydroxytryptamine on locomotor activity [6].
• The effects of 5,7-dihydroxytryptamine lesions of the median and of the dorsal raphe nuclei on social interaction in the rat [proceedings] [7].
• 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) [8].
• Leeches were injected with the cytotoxic analog of serotonin, 5,7-dihydroxytryptamine (5,7-DHT) producing selective lesions of the peripherally projecting serotonin-containing neurons, and which in turn abolished their feeding behavior [9].

High impact information on 5,7-DIHYDROXYTRYPTAMINE

• Selective lesions of the forebrain serotonergic system were made by injecting 5,7-dihydroxytryptamine into the midbrain raphe nuclei [10].
• Fetal raphe cells transplanted into the hypothalamus reversed facilitation of feminine sexual behavior in rats with brain lesions induced by 5,7-dihydroxytryptamine [11].
• The disappearance of the hybridization signal for GAP-43 mRNA after intracerebroventricular injections of the neurotoxins 5,7-dihydroxytryptamine (5,7-DHT) or 6-hydroxydopamine (6-OHDA) indicated that high levels of GAP-43 are synthesized in the serotonergic neurons of the raphe nuclei and in the catecholaminergic neurons of the SNc, VTA, and LC [12].
• Control, partial septal-lesioned (SL), 5,7-dihydroxytryptamine (5,7-DHT)-injected (DHT), double-lesioned (5,7-DHT and SL; DL), and DL rats that were transplanted with embryonic raphe grafts into the hippocampus (RG) were tested in a spatial task in a water maze and in an active avoidance shuttle-box task [13].
• Embryonic Retzius cells were identified in dissociated cultures by their violet-blue fluorescence acquired by preincubation of intact ganglia or embryos in culture medium containing the autofluorescent 5-HT analog 5,7-dihydroxytryptamine [14].

Chemical compound and disease context of 5,7-DIHYDROXYTRYPTAMINE

• A monoamine-accumulating ganglion cell type has been identified in an in vitro preparation of the cat's retina by a catecholamine-like fluorescence that appears following intravitreal injections of dopamine and the indoleaminergic transmitter analog, 5,7-dihydroxytryptamine (5,7-DHT) [15].
• 4. Lesioning of central 5-hydroxytryptaminergic neurones with 5,7-dihydroxytryptamine (75 micrograms, i.c.v.) had no influence on the reduction in clonidine mydriasis produced by repeated administration of either desipramine or ECS [16].
• The effects of 5,7-dihydroxytryptamine and L-tryptophan treatment on ethanol tolerance in the rat, as measured by the moving-belt test of motor impairment and by hypothermia, were examined in separate studies [17].
• Effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and 5,7-dihydroxytryptamine on the locomotor activity and striatal amines in C57BL/6 mice [18].
• Groups of rats were given either an electrolytic MR lesion or were injected locally with the serotonin neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) or the excitotoxin ibotenic acid, and their subsequent locomotor activities were compared in the open field and in photocell cages [19].

Biological context of 5,7-DIHYDROXYTRYPTAMINE

• Recent reports have indicated that the down-regulation in the number of beta-adrenergic receptors following DMI treatment does not occur if the serotonin system has been impaired following parachlorophenylalanine (PCPA) or 5,7-dihydroxytryptamine injection [20].
• Thus, not only the total numbers of binding sites for these two ligands in control rats but also their respective increases following intracerebral 5,7-dihydroxytryptamine treatment were very similar [21].
• The role of hypothalamic and midbrain serotonergic systems in the control of ovulation in the rat has been investigated using 5,7-dihydroxytryptamine (5,7-DHT) lesioning in conjunction with desmethylimipramine pretreatment [22].
• Neurotoxin lesions were placed stereotaxically in lactating rats on day 1 of lactation by 5,7-dihydroxytryptamine microinjection into the dorsal raphe (DR), median raphe (MR), or superior colliculus (SC), an area devoid of serotonergic perikarya [23].
• The animals were pretreated 7 days earlier with intracisternally administered 5,7-dihydroxytryptamine (5,7-DHT 200 microgram/kg plus desipramine 5 mg/kg i.v.). 2 5,7-DHT (plus desipramine) failed to decrease both basic blood pressure and heart rate measured before sino-aortic denervation [24].

Anatomical context of 5,7-DIHYDROXYTRYPTAMINE

• Reninlike concentration was increased in the medulla oblongata (p less than 0.005) and the brainstem (p less than 0.02) after 5,7-dihydroxytryptamine treatment [25].
• Distribution of calcitonin gene-related peptide in rat and rabbit spinal cords: effect of intrathecal 5,7-dihydroxytryptamine [26].
• In an additional experiment, intracerebroventricular administration of the selective serotonergic toxin 5,7-dihydroxytryptamine, which decreased forebrain 5-HT levels by 85-90%, did not block 8-OH-DPAT's ability to increase impulsive choice [27].
• To examine this hypothesis, the neurotoxin 5,7-dihydroxytryptamine was administered locally in rat amygdala [28].
• Lesions of the anterior hypothalamus, amygdala, and the hippocampal commissure as well as lesions with 6-hydroxydopamine and 5,7-dihydroxytryptamine failed to decrease striatal somatostatin levels [29].

Associations of 5,7-DIHYDROXYTRYPTAMINE with other chemical compounds

• Potentiated 5-hydroxytryptophan response suppression following 5,7-dihydroxytryptamine raphe lesions in an animal model of depression [30].
• Experiments with 5,7-dihydroxytryptamine- and kainic acid-induced lesions indicated that this specific binding site was localized post-synaptically with respect to serotoninergic neurons [21].
• Intraventricular 5,7-dihydroxytryptamine increases thyrotropin-releasing hormone content in regions of rat brain [31].
• Lesioning brain 5-HT neurones using 5,7-dihydroxytryptamine (5,7-DHT; 50 micrograms i.c.v.) produced a 210% (p less than 0.01) increase in the number of 5-HT2-mediated head-twitches induced by 5-methoxy-N,N-dimethyltryptamine (2 mg/kg) [32].
• Pentobarbital-anesthetized (60 mg/kg, i.p.) male Sprague-Dawley rats were stereotaxically microinjected with 1 microl of a 5 microg/microl solution of the serotonergic neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) into either the dorsal or median raphe nucleus [33].

Gene context of 5,7-DIHYDROXYTRYPTAMINE

• Opioid receptor-like 1 (NOP) receptors in the rat dorsal raphe nucleus: evidence for localization on serotoninergic neurons and functional adaptation after 5,7-dihydroxytryptamine lesion [34].
• The ability of cells to specifically take up the serotonin analog 5,7-dihydroxytryptamine was also up-regulated by brain-derived neurotrophic factor in both rostral and caudal raphe cultures [35].
• Adult male rats were pretreated with the 5-HT depleting agent p-chlorophenylalanine, the 5-HT neurotoxin 5,7-dihydroxytryptamine, the partial 5-HT1A agonist 8-(2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl)-8- azaspirol[4,5]-decane-7,9-dione (BMY 7378) or the 5-HT1C/2 antagonist ritanserin [36].
• We showed that the serotonin (5-HT) neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) reduces brain tissue 5-HT, decreases expression of 5-HT transporter (SERT) protein, and increases expression of glial fibrillary acidic protein (GFAP) [37].
• In cultures from the caudal E14 raphe saturating concentrations (5 ng/ml) of TGF-beta2 and -beta3 augmented numbers of tryptophan hydroxylase (TpOH) -immunoreactive neurons and cells specifically taking up 5,7-dihydroxytryptamine (5,7-DHT) by about 1.7-fold over a period of 4 days [38].

Analytical, diagnostic and therapeutic context of 5,7-DIHYDROXYTRYPTAMINE

• Quantitative autoradiography of multiple 5-HT1 receptor subtypes in the brain of control or 5,7-dihydroxytryptamine-treated rats [39].
• Intracerebral microinjection of 5,7-dihydroxytryptamine (5,7-DHT) into the MR nucleus produced dose-related decrements in litter growth after either 4 micrograms (sham, 1.35 +/- 0.05; MRL, 1.04 +/- 0.05 g/pup X day; P less than 0.001) or 8 micrograms 5,7-DHT (sham, 1.35 +/- 0.06; MRL, 0.87 +/- 0.11 g/pup X day; P less than 0.001) [40].
• By contrast, intraventricular injection of the neurotoxin 5,7-dihydroxytryptamine (75 microgram free base, for 10 days) caused a 77% depletion of brain serotonin and attenuated the rise in beta-END-LI levels in response to immobilization (3.28 +/- 0.20 vs. 1.83 +/- 0.25 ng/ml) [41].
• Alterations in 8-hydroxy-2-(dipropylamino)tetralin-induced neuroendocrine responses after 5,7-dihydroxytryptamine-induced denervation of serotonergic neurons [42].
• Serotonergic terminals in the neural sheath of the blowfly nervous system: electron microscopical immunocytochemistry and 5,7-dihydroxytryptamine labelling [43].

References