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PubMed1978

Effects of central 5,7-dihydroxytryptamine on the medical hypothalamic syndrome in rats.

The present study attempted to replicate and extend two recent studies that implicated aberrant brain 5-HT neurotransmission in the etiology of overeating and BW grain. Adult female rats received 25 mg/kg of desipramine hydrochloride 30--45 min prior to an intracisternal injection of 200 microgram (free base) of 5,7-DHT creatinine sulfate or its 1% ascorbic acid aqueous vehicle. After 7 weeks of measuring food intake, water intake, and BW change, rats from both groups received radiofrequency lesions of the MH or sham surgery. After 5 additional weeks of intake and BW measurements, all rats were tested for 24-hr acceptance of varying sucrose and quinine solutions and for 25-day acceptance of a high-fat replacement diet. While 5,7-DHT depleted brain 5-HT by 45%, it did not induce overeating and BW gain alone nor did it modify the overeating, obesity, or "finickiness" produced by hypothalamic injury. Several factors that relate to specificity, sufficiency, and compatibility with other 5-HT depletory techniques were discussed, as were factors of similarity and dissimilarity between this and the previous experiments that we attempted to replicate.

5,7-Dihydroxytryptamine↗
PubMed1981

[Effects of intraventricular injection of 5,7-dihydroxytryptamine on monoamines and sleep in the kitten (author's transl)].

Intraventricular injections of 5,7-DHT (.15 mg/g of brain weight) were performed in kittens aged 5 or 30 days. The neurotoxin induced a significant decrease of 5-HT and NA levels in the forebrain in both age groups, whereas a slight increase of each amine was observed respectively in the raphe and lateral brain stem of the younger group (Fig. 1). Pretreatment with desmethylimipramine (20 mg/kg I.P.) resulted in a protection of the noradrenergic system from the neurotoxin (Fig. 2). From the neurophysiological standpoint, 5,7-DHT induced a major paradoxical sleep (PS) insomnia in the one-month-old group, whereas no alteration of PS was observed in the younger group (Fig. 3). The DMI pre-treatment did not modify these results. The hypothesis of brain stem sprouting is discussed, and it is concluded that the serotoninergic system does not mediate the sleep regulation in the early post-natal period.

5,7-Dihydroxytryptamine↗
PubMed1994

Effects of the altered serotonergic signalling by neonatal treatment with 5,7-dihydroxytryptamine, ritanserin or clomipramine on the adrenocortical stress response and the glucocorticoid receptor binding in the hippocampus in adult rats.

The aim of the present study is to investigate the effect of neonatal alterations in 5-HT signalling on the regulation of endocrine stress response in adult rats. The neonatal blockade of 5-HT transmission by 5,7-DHT or ritanserin treatment did not alter the density of glucocorticoid receptor (GR) binding sites in the hippocampus, although a 5,7-DHT-induced lesion was clearly shown to decrease in 5-HT content by greater than 80% in the hippocampus. In addition, the animals pretreated with the blockade of 5-HT transmission during early life did not exhibit a hyperresponsiveness of the adrenocortical response to stress. On the other hand, the neonatal administration of the 5-HT uptake inhibitor, clomipramine, was shown to lower the stress responsiveness of the adrenocortical axis in adulthood.

5,7-Dihydroxytryptamine↗
PubMed1999

Selective destruction of brain serotonin neurons by 5,7-dihydroxytryptamine increases responding for a conditioned reward.

RATIONALE: Previously, we have shown that increasing 5-hydroxytryptamine (5-HT) activity attenuates responding for conditioned reward (CR), and the response potentiating effect of d-amphetamine on this behaviour. OBJECTIVES: The present experiments examined the effects of reducing 5-HT function on responding for CR. METHODS: In experiment 1, thirsty rats were trained to associate a CS+ with water delivery. The neurotoxin 5,7-DHT was then injected into the dorsal and median raphe nuclei. Subsequently, rats were treated with intraaccumbens d-amphetamine (1, 3, 10 micrograms) or saline and given access to two levers. One lever delivered the CS+ (now termed a CR), while the other was inactive. In experiment 2, the lesion was carried out prior to conditioning, and approach behaviour to the water magazine was measured during CS+ periods. Subsequently, rats were allowed to respond for the CS. In experiment 3, non-deprived rats learned to associate a CS+ with 10% sucrose; these animals also experienced a CS- which was not paired with sucrose. During a test phase responses on the two levers delivered either the CS+ or the CS-. RESULTS: 5,7-DHT substantially reduced 5-HT levels in striatum and hippocampus. In experiment 1, responding for the CR was enhanced by both d-amphetamine and 5-HT depletion in an additive fashion. In experiments 2 and 3, the discriminative control over behaviour exerted by the CS+ was not affected by 5-HT depletion. However, compared to control animals 5-HT-depleted rats showed higher levels of operant responding for the CR. CONCLUSIONS: Serotonin depletion selectively enhances responding for CR. Although 5-HT depletion did not potentiate the effects of d-amphetamine, it is suggested that CRs activate the mesolimbic dopamine system, and that removal of an inhibitory influence of 5-HT on the activity of this system results in increased responding for CR in 5,7-DHT-treated rats.

5,7-Dihydroxytryptamine↗