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PubMed1980

5,7-Dihydroxytryptamine lesions of the amygdala reduce amphetamine- and apomorphine-induced stereotyped behaviour in the rat.

5,7-Dihydroxytryptamine lesions directed towards the central nucleus of the amygdala produced an apparently selective and localised destruction of 5HT terminals within the amygdaloid complex, without damage to dopamine neurons. Such lesions attenuated the biting responses produced by both amphetamine and apomorphine, suggesting that 5HT within this area may play an important role in the mediation of these behavioural effects.

5,7-Dihydroxytryptamine↗
PubMed1979

The effects of 5,7-dihydroxytryptamine lesions of extrapyramidal and mesolimbic sites on spontaneous motor behaviour, and amphetamine-induced stereotypy.

5,7-Dihydroxytryptamine lesions of the nucleus accumbens septi, or substantia nigra, resulted in a twofold increase in spontaneous locomotor activity. Striatal 5HT depletion also raised basal activity levels, as well as increasing rearing behaviour in an open field. The sterotyped responses to all doses of amphetamine tested (2.5--10 mg/kg, i.p.) were enhanced by lesions of the nucleus accumbens or substantia nigra. Striatal lesions only affected the response to the lowest dose of amphetamine. Lesions of the tuberculum olfactorium were without effect on spontaneous or amphetamine induced responses. The results support the concept of a modulatory 5HT influence on nigro-striatal function, and suggest that 5HT in the nucleus accumbens has an antagonistic role with respect to dopamine function in this site.

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PubMed1983

Effect of 5,7-dihydroxytryptamine on Auerbach's plexus in the ileum of guinea-pig.

Action of 100 mg/kg of 5,7-dihydroxytryptamine on Auerbach's plexus in the ileum of the guinea-pig has been studied using Falck and Hillarp's formaldehyde condensation technique. The drug caused partial disappearance of the adrenergic nerve profiles initially but after 10 days of treatment all the lost fibers reappeared.

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PubMed1986

Increased tryptophan hydroxylase activity in serotonergic nerve terminals spared by 5,7-dihydroxytryptamine.

Adult rats received intraventricular injections of 5,7-dihydroxytryptamine (5,7-DHT) to destroy serotonin (5-HT)-containing nerve terminals throughout the brain. When the animals were killed 3 or 21 days later, we observed a marked decrease in 5-HT content in septum and hippocampus and a parallel decline in in vitro high affinity 5-HT uptake. 5-Hydroxyindoleacetic acid (5-HIAA) concentrations also were reduced but by a much smaller extent, resulting in significant increases in the ratio of 5-HIAA to 5-HT. These changes were accompanied by similar increases in the ratio of tryptophan hydroxylase (TPH) activity to 5-HT content. The relative increases in TPH activity resulted from two temporally distinct processes, the first of which appeared to be an activation that could be mimicked in vitro by Ca2+-dependent phosphorylation. We conclude that, after partial damage to 5-HT neurons, there is a compensatory increase in the synthesis and release of 5-HT from those terminals that remain.

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PubMed1978

Inhibition of 5,7-dihydroxytryptamine-induced supersensitivity to 5-hydroxytryptophan in mice by treatment with cycloheximide.

Intracisternal injection of 5,7-dihydroxytryptamine (5,7-DHT) following treatment with desmethylimipramine induced development of behavioral supersensitivity to the intraperitoneally administered serotonin precursor 5-hydroxytryptophan (5-HTP) in the mouse. This behavioral syndrome, characterized by tremor and muscle twitches (myoclonus), showed a clear dose-response relationship with 5,7-DHT as well as with 5-HTP. Mice lesioned with a low dose of 5,7-DHT (20 micrograms) or a placebo were treated repeatedly with a protein synthesis inhibitor, sycloheximide (45 mg/kg, s.c., every 12 h for up to 10 days). This treatment resulted in a reversible decrease of cerebral protein synthesis varying between 70 and 20% with time between treatments. The myoclonic response to 5-HTP in animals pretreated with 5,7-DHT and by cycloheximide showed a decrease in intensity within 24 h when evaluated quantitatively by an electronic activity monitor, the results of which were confirmed by direct observation. Cycloheximide also exerted a similar, though smaller, effect following full development of sensitivity to 5-HTP over 10 days. These effects may de mediated by inhibition of rapidly turning over serotonin receptor proteins, although their interpretation is somewhat obscured by possible toxic effects of cycloheximide.

5,7-Dihydroxytryptamine↗
PubMed1978

Effect of p-chloroamphetamine and 5,7-dihydroxytryptamine on rotation and dopamine turnover.

Injections of p-chloroamphetamine (PCA) or 5,7-dihydroxytryptamine (DHT) (after pretreatment with desmethylimipramine) into the median raphe nucleus (MRN) caused depletions of 5-HT and 5-HIAA in the cortex and striatum, and a decrease of cortical 5-HT uptake without affecting NE uptake. Unilateral injections of these neurotoxins into the MRN caused contralateral rotation, which was blocked by haloperidol. The size of the lesion correlated with the rate of rotation and the decrease in 5-HT turnover in the cortex. We also found a significant correlation between the rate of rotation and the decrease in cortical 5-HT turnover, and the increase in striatal DA turnover. Moreover, there was a significant correlation between the decrease in cortical 5-HT turnover and the increase in striatal DA turnover. It was found that injections of DHT into the SN produced similar behavioral and biochemical changes as did the MRN lesions. In this model, amphetamine and apomorphine produce turning in the same direction, whereas they have opposite effects after lesions of the nigrostriatal pathway where postsynaptic DA supersensitivity occurs. Presynaptic changes appear to determine turning in this model. An inhibitory role of the serotonergic MRN on the dopaminergic nigrostriatal pathway mediated via the substantia nigra (SN) is suggested.

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PubMed1978

Behavioral and prolactin responses to 5-hydroxytryptophan in rats treated during development with 5,7-dihydroxytryptamine.

The serotonin precursor, 5-hydroxytryptophan (5-HTP), can induce a behavioral syndrome characterized by rigidity, splayed feet, tremor, head weaving, salivation and forepaw treading. This response to 5-HTP was markedly potentiated in adult rats treated intracisternally with 5,7-dihydroxytryptamine (5,7-DHT) during development. Prevention of the 5,7-DHT-induced reduction of brain norepinephrine with pargyline or desipramine did not diminish the potentiation of 5-HTP, suggesting that noradrenergic fibers are not contributing to the altered 5-HTP response. It was also found that treatments with 5,7-DHT potentiated the release of prolactin and the disruption of responding in a fixed-ratio operant task induced by 5-HTP. Other experiments indicated that 5,7-DHT treatments potentiated 5-HTP without affecting the action of L-dihydroxyphenylalanine. In addition, administration of the decarboxylase inhibitor, R0-4-4602, at a dose that inhibits enzyme activity in brain, blocked the 5-HTP-induced behavioral syndrome in 5,7-DHT-treated rats, indicating that 5-HTP must be converted to serotonin for 5-HTP to alter behavior. Thus, the present studies indicate that destruction of serotonergic fibers during development can produce permanent changes in central serotonergic mechanisms.

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PubMed1979

Regeneration of normal terminal innervation patterns by central noradrenergic neurons after 5,7-dihydroxytryptamine-induced axotomy in the adult rat.

The regeneration of central adrenergic axons has been followed between 5 days and 18 months after 5,7-dihydroxytryptamine(5,7-DHT)-induced axotomy in the adult rat, using fluorescence histochemistry in combination with noradrenaline (NA) determinations and [3H]NA uptake measurements. The axonal and terminal degeneration caused by the 5,7-DHT treatment (150 micrograms intraventricularly) was, by 1--2 weeks after injection, accompanied by a 70% reduction of NA in the forebrain and 30% reduction in the brain stem, and by 43--85% reductions in the [3H]NA uptake capacity in various regions of the brain and spinal cord. Signs of sprouting of the drug-lesioned axons were evident along the terminal axon segments at 5 days after treatment. The sprouts increased rapidly in length and number during the subsequent weeks and by 2--6 months after injection new NA terminal systems of relatively normal density and distribution had been re-established in many initially denervated regions. In parallel there was a recovery of endogenous NA and [3H]NA uptake to the pre-injection levels in the brain, and to levels 50--75% of normal in the cervical and thoracic spinal cord. Four successive phases of the regeneration process are distinguished: (1) primary sprouting from the lesioned NA axon stumps, occurring within the first week after treatment; (2) seemingly random growth and proliferation of the newly formed sprouts during the second and third weeks; (3) directed, forward growth of some of the sprouts leading to a partial restoration of the original fibre paths, branching patterns and terminal networks within 3--6 months; (4) a concomitant removal of at least part of the abnormally directed sprouts. Although the original fibre architecture was quite accurately restored in many areas the regeneration was not always correct. Hyperinnervation patterns and abnormal terminal arrangements were often formed, and in the spinal cord the down-growth of the regenerating axons occurred predominantly along a route that is inconspicuous in the normal rat. It is concluded that at least certain types of central neurons regenerate very efficiently provided the conditions are favourable, and that under such conditions axonal regeneration in the mammalian CNS is subjected to regulatory mechanisms that can be very precise. The results provide evidence that the adult mammalian CNS possesses mechanisms for axonal guidance which allow the accurate regeneration of lesioned axonal tracts and branching patterns, as well as mechanisms of recognition making possible the re-establishment of the original terminal connections.

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PubMed1979

Effect of midbrain raphe lesion or 5,7-dihydroxytryptamine treatment on the prolactin-releasing action of quipazine and D-fenfluramine in rats.

The role of brain serotonin in regulating prolactin (PRL) secretion has been investigated by studying the effect of quipazine and D-fenfluramine, two serotonin-like drugs, on plasma PRL levels under various experimental conditions. Quipazine (5, 10 and 20 mg/kg i.p.) and D-fenfluramine (5, 7.5 and 10 mg/kg i.p.) induced dose-related increases in plasma PRL levels in male rats. Intraventricular injection of 5,7-dihydroxytryptamine (5,7-DHT) or electrolytic lesion of the nucleus raphe medianus (MR), which caused a marked and selective depletion of hypothalamic serotonin levels, significantly reduced the PRL-releasing effect of both quipazine and D-fenfluramine. These results suggest that the effect of these drugs on PRL release is mediated through a serotonergic mechanism in the brain.

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PubMed1980

Increased sensitivity to intracerebroventricular infusion of serotonin and deaminated indoles after lesioning rat with dihydroxytryptamine.

Rats were prepared with a chronic intracerebroventricular cannula, and treated with intracisternal 5,7-dihydroxytryptamine (DHT) after i.p. desmethylimipramine or control vehicle. After recovery, they were tested behaviorally by direct observation and electronic monitoring of motor activity. Intraventricular infusion of a placebo or 5-hydroxyindoleacetic acid (5-HIAA) had little effect, but serotonin (5-HT) decreased, and norepinephrine increased locomotor activity in intact rats. Following pretreatment with 5,7-DHT, a small increase in locomotor activity was noted which was not altered by intracranial infusion of vehicle. In contrast, infusions of 5-HT produced a striking dose-dependent (ED50 = 5 micrograms/min) pattern of hyperactivity, 'myoclonic' jerking movements, postural changes, and autonomic responses. Norepinephrine increased locomotor activity in the DHT-lesioned rats (but not significantly more than in controls), but failed to produce the myoclonic syndrome. The deaminated indoles, indoleacetaldehyde and 5-HIAA were more potent than 5-HT in producing the myoclonic response; tryptamine when infused at an equimolar dose had no effect. The putative serotonin antagonists, cyproheptadine and methiothepin (i.p.), were more effective in blocking responses to infused 5-HT than to equipotent doses of deaminated indoles. These behavioral responses may represent exaggerated ex"itatory effects mediated by serotonin in the brain stem and spinal cord, possibly modified by altered forebrain mechanisms. A neurophysiologic or neuropharmacologic role for deminated indoles should be reconsidered as they may not merely be inactive metabolites.

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PubMed1982

Function of serotonin in physiologic secretion of growth hormone and prolactin: action of 5,7-dihydroxytryptamine, fenfluramine and p-chlorophenylalanine.

Growth hormone (GH) and prolactin secretory patterns in male rats chronically implanted with venous cannulae were studied in response to treatments known to acutely or chronically deplete central serotonin (5-HT) or to permanently destroy a high proportion of 5-HT neural structures. Spontaneous prolactin secretion was little affected by chronic 5-HT depletion produced by 5,7-dihydroxytryptamine (5,7-DHT) or parachlorophenylalanine (PCPA). Acute 5-HT release induced by fenfluramine produced sustained prolactin secretion in intact and 5-HT-depleted rats. GH secretion was inhibited by PCPA, and for 3 days following 5,7-DHT, but was normal by 7 and 21 days. Acute 5-HT release stimulated by fenfluramine unexpectedly inhibited GH in intact and 5-HT-depleted rats. It is concluded that 5-HT is a potent facilitatory neurotransmitter for prolactin; and it appears to have both facilitatory and inhibitory effects on GH. Recovery of GH secretory patterns within 7 days of 5,7-DHT treatment indicates that mechanisms act rapidly to compensate for depletion of 5-HT, and that it is difficult to achieve functional depletion of 5-HT for more than a few days.

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PubMed1982

Enhancement of footshock-induced analgesia by spinal 5,7-dihydroxytryptamine lesions.

The analgesia induced by 30-s footshock (1 mA) is enhanced and attenuated by decreasing and increasing the extraneuronal availability of serotonin (5-HT), respectively. In the present work we have shown the effect to be mediated by spinal 5-HT systems as the response was increased by depletion of spinal but not brain 5-HT following injection of 5,7-dihydroxytryptamine into the spinal cord or raphe magnus. Injection of 5,7-DHT into the medial raphe which depleted brain but not spinal 5-HT was without effect.

5,7-Dihydroxytryptamine↗
PubMed1983

Intrahypothalamic 5,7-dihydroxytryptamine facilitates feminine sexual behavior and decreases [3H]imipramine binding and 5-HT uptake.

5,7-Dihydroxytryptamine (5,7-DHT) injected into the hypothalamus facilitated feminine sexual behavior in ovariectomized, estrogen-treated female rats beginning 9 days post-lesion. 5,7-DHT treatment was associated with decreased [3H]5-HT but not [3H]NE uptake in the whole hypothalamus and with decreased [3H]-imipramine binding in some hypothalamic nuclei. These data provide the first demonstration using chemical lesions that 5-HT neurons may exert tonic inhibition on hormone-mediated feminine sexual behavior.

5,7-Dihydroxytryptamine↗
PubMed1984

Tryptophan hydroxylase in hippocampus and midbrain following unilateral injection of 5,7-dihydroxytryptamine.

We have previously shown using anatomical methods that partial denervation of the rat hippocampus by removal of serotonergic (5-HT) fibers in the cingulum bundle induces sprouting of intact 5-HT fibers reaching the hippocampus in the fornix-fimbria. The biochemical properties of collateral sprouting fibers have remained largely uncharacterized. Thus, the rate-limiting enzyme in 5-HT synthesis, tryptophan hydroxylase (TPOH), was studied to determine whether new sprouts possess the ability to synthesize 5-HT. Unilateral stereotaxic injections of 5 micrograms 5,7-dihydroxytryptamine were made into the cingulum bundle of adult rats in order to produce partial and selective deafferentation of the hippocampus. Following injection, enzyme activity in the hippocampus declined gradually and bilaterally, reaching minimal levels by 7 days post-lesion. This decrease in enzyme activity was paralleled by a decrease in the Vmax and an increase in the Km of TPOH for tryptophan. Enzyme activity began to increase after 14 days post-lesion, reaching maximal levels by 60 days, but never returning to pre-lesion levels in the ipsilateral side. In midbrain, site of neuronal cell bodies of hippocampal 5-HT projections, enzyme activity gradually increased, reaching a maximum by 28 days after the lesion. These results indicate that 5-HT fibers remaining in the hippocampus following partial denervation are able to compensate biochemically for those removed by cingulum bundle lesions. Biochemical compensation may depend on increased synthesis of TPOH molecules in midbrain cell bodies with subsequent transport into sprouts of intact fibers in the hippocampus.

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PubMed1984

The effect of 5,7-dihydroxytryptamine on the serum corticosterone resistance to suppression by dexamethasone.

The effect of serotonin (5-HT) deficiency on hypothalamic-pituitary-adrenal (HPA) activity was investigated by using 5,7-dihydroxytryptamine (5,7-DHT) for the selective destruction of central 5-HT neurons, and corticosterone response to suppression by dexamethasone as the index of HPA activity. Dexamethasone was shown to significantly suppress serum corticosterone levels in sham-treated rats, but did not suppress corticosterone in the 5,7-DHT-lesioned animals. This finding supports the conclusion that 5-HT is involved in the negative feedback mechanism of HPA regulation.

5,7-Dihydroxytryptamine↗
PubMed1984

Regeneration of serotonergic fibers in the rat hypothalamus following unilateral 5,7-dihydroxytryptamine injection.

The time course of degeneration and regeneration of serotonin (5-HT) fibers in the rat hypothalamus was studied with 5-HT immunocytochemistry and [3H]5-HT uptake following unilateral injections of 5,7-dihydroxytryptamine (5,7-DHT) into the dorsolateral hypothalamus. Within 3 days of the lesion, 5-HT fibers in the ipsilateral hypothalamus were swollen and darkly stained for 5-HT. In the contralateral hypothalamus few swollen fibers were apparent and these were generally restricted to the area adjacent to the fornix. Swollen 5-HT fibers were evident in the ipsilateral hypothalamus 3-19 days post-lesion in the medial forebrain bundle (MFB) during which time there was a gradual decrease in their density. In the medial and periventricular areas of the ipsilateral hypothalamus there were essentially no 5-HT fibers 7-30 days post-lesion. Sprouting 5-HT fibers were observed 12-19 days post-lesion. Thirty days post-lesion the density of 5-HT fibers in the MFB appeared normal; however, medial and periventricular areas remained denervated. Fifty days post-lesion there was an apparent bilateral hyperinnervation in the lateral and dorsomedial hypothalamic areas of 5,7-DHT-injected animals as compared to sham-injected animals. The morphological data were paralleled by changes in [3H]5-HT uptake. Seven days post-lesion specific high affinity uptake was reduced to 27% of sham in the ipsilateral hypothalamus and to 53% of sham in the contralateral hypothalamus. By 50 days post-lesion, specific high affinity uptake of [3H]5-HT was 141% of sham in the ipsilateral hypothalamus and 96% of sham in the contralateral hypothalamus.

5,7-Dihydroxytryptamine↗
PubMed1984

Supersensitivity to the respiratory stimulatory effect of TRH in 5,7-dihydroxytryptamine-treated rats.

Rats treated neonatally with pargyline and 5,7-dihydroxytryptamine (5,7-DHT) have an elevated paCO2 and reduced minute ventilation when given 0.7% halothane in oxygen as adults. Serotonin content in the spinal cord of 5,7-DHT treated rats was undetectable and TRH content was reduced by 35%. The 5,7-DHT treated rats were supersensitive to the increase in minute ventilation and CO2 sensitivity produced by intraventricular TRH. It is possible that the supersensitivity to exogenous TRH after neonatal 5,7-DHT treatment may be secondary to decreased availability of TRH in the CNS.

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PubMed1985

Intrahypothalamic 5,7-dihydroxytryptamine: temporal analysis of effects on 5-hydroxytryptamine content in brain nuclei and on facilitated lordosis behavior.

The long-term relationship between serotonin (5-HT) levels in discrete hypothalamic nuclei and female rat sexual behavior, the lordosis response, was examined following intrahypothalamic injection of 5,7-dihydroxytryptamine (5,7-DHT). One week following 5,7-DHT injection, 5-HT levels in the ventromedial hypothalamic nucleus, dorsomedial nucleus, anterior hypothalamic nucleus and the medial preoptic nucleus were approximately 90% depleted as compared to sham animals. Other hypothalamic and preoptic areas including the arcuate-median eminence, vertical nucleus of diagonal band and lateral septal nucleus showed smaller reductions in 5-HT, from 40 to 70% of sham values. At this time estrogen-dependent lordosis behavior in the lesioned group was facilitated. Behavioral facilitation was greatest at 4 weeks post lesion when depletion of 5-HT in the VMN was maximal. 5-HT levels increased at 57 days after 5,7-DHT treatment in most areas, and by 71 days post lesion, no significant differences in 5-HT levels were found between sham and 5,7-DHT-treated groups. Concomitant with the increases in 5-HT, facilitated lordosis behavior gradually decreased. Loss of behavioral facilitation appeared to be most closely related to increases in content of 5-HT in the ventromedial nucleus. These results further support the hypothesis that 5-HT endings in the hypothalamus exert tonic inhibitory regulation over hormone-dependent lordosis in the female rat. They also indicate that regenerating 5-HT fibers in the hypothalamus can reinstate a normal pattern of hormone-dependent behavioral function.

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