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PubMed1985

Rostral hypothalamic microinfusions of 5,7 dihydroxytryptamine produce anatomically and neurochemically selective depletions of hippocampal serotonin and increase the influence of estrogen and food deprivation on locomotor activity.

Ovariectomized Long-Evans rats received bilateral rostral hypothalamic infusions of 5,7-dihydroxytryptamine (5,7-DHT). Neurochemical determination of catecholamines (CA) and indoleamines in the hippocampus, hypothalamus and mesencephalon revealed that 5,7-DHT infusions had no effect on CA content in these areas nor in mesencephalic serotonin or 5-hydroxyindoleacetic acid (5-HIAA). However, the neurotoxin produced significant decreases in hippocampal serotonin and 5-HIAA. Serotonin-depleted animals exhibited an increase in both spontaneous and estradiol-induced wheel running. In addition it was found that serotonin-depleted animals exhibit an enhanced activity response to starvation. Because estrogen is thought to decrease serotonergic transmission, the enhanced activity response to estrogen may be secondary to an estrogen-related exaggeration of the 5,7-DHT-induced serotonin depletion. The increased activity effect of starvation may indicate that serotonin-depleted animals do not effectively mobilize energy stored as lipid.

5,7-Dihydroxytryptamine↗
PubMed1985

Thyrotropin releasing hormone but not histidyl-proline diketopiperazine is depleted from rat spinal cord following 5,7-dihydroxytryptamine treatment.

Histidyl-proline diketopiperazine (His-Pro DKP) has been proposed as a metabolite of thyrotropin releasing hormone (TRH). Since spinal cord TRH arises from serotoninergic (5-HT) neurons in the brainstem, a 5-HT neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT), was injected into the lateral ventricle of 7 rats, and the levels of TRH and His-Pro DKP in the spinal cord were studied 5 weeks later. In comparison to the saline treated controls, 5,7-DHT treated animals showed marked depletion of TRH throughout the spinal cord, especially in the lumbosacral area where almost 90% disappeared, (0.28 +/- 0.02 vs. 2.46 +/- 0.01 ng/mg protein; P less than 0.0001). In contrast, His-Pro DKP showed no significant change in any region. Since 5,7-DHT lowers spinal cord TRH by destroying TRH perikarya in the medulla, we conclude that spinal cord His-Pro DKP is not derived from the same neurons as TRH.

5,7-Dihydroxytryptamine↗
PubMed1987

In vivo labeling of serotonin-containing neurons by 5,7-dihydroxytryptamine in Aplysia.

Intrahemocoelial administration of 5,7-dihydroxytryptamine (5,7-DHT) to Aplysia californica induces a transient (less than 4 h) behavioral alteration. About 5 weeks after 5,7-DHT treatment, 5-hydroxytryptamine (5-HT)-containing neurons develop dark brown pigmentation. These labeled 5-HT neurons have normal physiological and pharmacological properties when investigated electrophysiologically. This contrasts with the long-term neurotoxic effect of 5,7-DHT on vertebrate neurons. This technique will greatly facilitate visual identification of 5-HT-containing neurons and study of their physiology and actions.

5,7-Dihydroxytryptamine↗
PubMed1987

Temporal effects of intrahypothalamic 5,7-dihydroxytryptamine: relationship between serotonin levels and [3H]serotonin binding.

The relationship between serotonin (5-HT) levels and [3H]5-HT binding in discrete hypothalamic areas was examined in separate groups of animals at various times, following unilateral intrahypothalamic injection of 5,7-dihydroxytryptamine (5,7-DHT). Seven days post-5,7-DHT lesion, 5-HT levels were significantly decreased in both the ipsilateral and contralateral ventromedial and dorsomedial hypothalamic nuclei (VMN, DMN). In the lateral hypothalamic area (LHA), 5-HT levels were significantly decreased only ipsilaterally. Fifty days postlesion, 5-HT levels in the ipsilateral VMN remained significantly below sham, while the DMN and LHA returned to sham values. Seven days after 5,7-DHT there was a significant increase in [3H]5-HT labeling densities in the ipsilateral and contralateral ventromedial hypothalamic area as well as in the ipsilateral LHA. In contrast, in the dorsomedial hypothalamic area there was no increase in [3H]5-HT binding. Fifty days postlesion, no significant differences in [3H]5-HT binding between 5,7-DHT and sham were observed in any areas examined. This data provides further evidence for the regeneration of 5-HT fibers in the hypothalamus and demonstrates that the relationship between [3H]5-HT binding and 5-HT levels varies from one hypothalamic area to another.

5,7-Dihydroxytryptamine↗
PubMed1987

Effects of 5,7-dihydroxytryptamine on serotonin1 and serotonin2 receptors throughout the rat central nervous system using quantitative autoradiography.

The effects of the serotonin neurotoxin 5,7-dihydroxytryptamine (5,7-DHT), on serotonin1 (5-HT1) and 5-HT2 receptors were investigated using the high degree of resolution provided by quantitative autoradiography in an effort to determine the synaptic location of these receptors. 5,7-DHT treatment resulted in a decrease in 5-HT1 binding in the dentate gyrus and CA3c/4 of the anterior hippocampus and in the dorsal raphe nucleus, whereas no changes were observed in the posterior hippocampus nor in many other brain structures. 5-HT2 receptors exhibited no changes in any brain area examined in response to 5,7-DHT treatment, despite over 90% serotonin depletion in most of the forebrain nuclei examined. The results indicate that at least some of the 5-HT1 sites labelled by [3H]5-HT in the hippocampus and dorsal raphe nucleus are presynaptic, whereas 5-HT2 receptors are probably postsynaptic. In addition, the distribution profiles of 5-HT1 and 5-HT2 binding sites were compared in the rat central nervous system at various anatomical levels. 5-HT1 binding sites were identified using [3H]5-HT, while 5-HT2 binding sites were labelled with [3H]ketanserin. Both receptor subtypes displayed distinctly different localization patterns, which, in most cases was the inverse of the other pattern. In the brainstem it is significant that 5-HT2 receptors are concentrated in the facial nucleus and the motor nucleus of the trigeminal nerve, areas known to influence head and facial movement. The serotonin-mediated head-shake response occurs when 5-HT2 receptors are activated. In contrast, 5-HT1 receptors are distributed throughout the brainstem and in specific portions of the spinal cord. These areas are thought to control the serotonin behavioral syndrome and this behavior is 5-HT1A-mediated. All raphe nuclei were devoid of 5-HT2 receptors; only 5-HT1 receptor were found in these nuclei. Correlations with serotonin terminal distribution patterns are discussed. The pattern of 5-HT2 receptor distribution was also compared with the pattern of alpha 1 receptors, using [3H]prazosin in order to determine whether [3H]ketanserin significantly labels alpha 1 receptors. Although some similarities exist, overlap of binding did not occur in other nuclei, indicating that alpha 1 contamination of this system is probably negligible.

5,7-Dihydroxytryptamine↗
PubMed1987

Effect of 5,7-dihydroxytryptamine on the food-aversive conditioning in the snail Helix lucorum L.

The effects of 5,7-dihydroxytryptamine (5,7-DHT), a drug which selectively ablates serotonergic terminals, were examined on acquisition of food-aversive conditioned reflex in the snail Helix lucorum. The percent of feeding reactions decreased from 80 to 15% in the conditioned group of animals after 5-8 pairings of food and electric shock. The behavioral performance of 5,7-DHT-injected animals after the same training session coincided with the data received from the unpaired control group: the percent of feeding reactions remained the same as before the training. Conditioning was carried out on the semi-intact 'lip-CNS' preparations as well. Intracellular recordings from the neurons responding to the withdrawal reaction confirmed the results of the behavioral experiments. Elaboration of associative changes was effective on preparations made from normal snails, whereas no changes were noted in 5,7-DHT-treated and pseudoconditioned animals. In 5,7-DHT-treated animals some components of the feeding behavior and withdrawal reaction changed as well. The appetitive phase duration of feeding lengthened significantly, moreover the sensitization of the withdrawal reaction evoked by rhythmic tactile stimulation disappeared in preparations made from drug-treated snails.

5,7-Dihydroxytryptamine↗
PubMed1989

The amine-depleting effects of 5,7-dihydroxytryptamine (5,7-DHT) in C57BL/6 mice do not increase with age.

A recent approach to identifying the factors that predispose neurons to an early death in Parkinson's or Alzheimer's disease has been to study how the effect of specific neurotoxins are altered by increasing maturity. We determined the dose-related serotonin and norepinephrine-depleting effects of the selective neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT), in C57BL/6 mice of 2 different ages. Norepinephrine and serotonin in the hippocampus were assayed 1 week after the intracerebroventricular (i.c.v.) administration of 5,7-DHT. 5,7-DHT produced an equivalent, dose-related depletion of hippocampal norepinephrine in both age groups. Since the effects of 5,7-DHT on noradrenergic neurons may, at least in part, depend on the monoamine oxidase (MAO)-generated formation of hydrogen peroxide and associated oxy-radicals, this result suggests that noradrenergic neurons do not become more vulnerable to oxidative stress with aging. We also found that the noradrenergic-depleting effects of 5,7-DHT were blocked by the non-selective MAO inhibitor pargyline (50 mg/kg, i.p.), while the selective MAO B inhibitor deprenyl (10 mg/kg, i.p.) failed to prevent this depletion. These latter results suggest that it is the A form of MAO that plays an important role in the mechanism of 5,7-DHT-induced noradrenergic toxicity. Somewhat unexpectedly, older mice were found to be less susceptible to the serotonin-depleting effects of 5,7-DHT. Although the mechanism by which this compound damages serotonergic neurons is uncertain, our results show that the increased susceptibility of serotonergic neurons to 5,7-DHT in young animals extends well beyond the neonatal period.

5,7-Dihydroxytryptamine↗
PubMed1989

The role of serotonin in the control of cerebral activity: studies with intracerebral 5,7-dihydroxytryptamine.

Intact rats treated with centrally acting antimuscarinic (atropinic) drugs display large amplitude irregular slow waves in both the neocortex and hippocampus during behavioral immobility and some stereotyped automatic behaviors (Type 2 behavior). However, rhythmical slow activity in the hippocampus and low voltage fast activity in the neocortex occur in close correlation with spontaneous changes in posture, head movement, walking, rearing, swimming or struggling when held (Type 1 behavior). It has previously been proposed that these waveforms, jointly referred to as atropine-resistant cerebral activation (ARCA) are dependent on ascending serotonergic projections. As a further test of this hypothesis, we have studied rats in which forebrain levels of serotonin and 5-hydroxyindoleacetic acid were reduced to 3-10% of control levels as a result of multiple intrabrainstem injections of 5,7-dihydroxytryptamine. This treatment strongly reduced or abolished ARCA in most cases but did not reduce atropine-sensitive cerebral activation which appears to be dependent on ascending cholinergic projections from the basal forebrain to the cerebral cortex. Therefore, ARCA appears to be dependent on ascending serotonergic inputs to the forebrain.

5,7-Dihydroxytryptamine↗
PubMed1989

A general role for serotonin in the control of behavior: studies with intracerebral 5,7-dihydroxytryptamine.

Multiple injections of 5,7-dihydroxytryptamine (5,7-DHT) into the rat brainstem reduced forebrain levels of serotonin and 5-hydroxyindoleacetic acid to 3-10% of the levels observed in control rats that had received intrabrainstem injection of a Locke's solution vehicle. This treatment reduced or abolished atropine-resistant cerebral activation (ARCA) in most cases. In rats in which ARCA was impaired or lost, a number of behavioral abnormalities were observed. These included: high levels of locomotion in an open field test; a deficiency in swimming to, and climbing upon, a visible platform in a water-filled tank; deficient social behavior; and impaired performance in a simple test of active avoidance. These deficits were not due to low level motor impairment. The 5,7-DHT-treated rats displayed a circadian rhythm of activity in running wheels. It is proposed that ascending serotonergic projections are an important component in the cerebral control of the Type 1 behavior with which the occurrence of ARCA is closely linked. Since Type 1 behavior includes such motor patterns as walking and manipulation of objects with the limbs, which are essential components of a great variety of behavioral performances, it is to be expected that a loss of ascending serotonergic function will result in a generalized deficit in behavior.

5,7-Dihydroxytryptamine↗
PubMed1989

Intra-raphe neurokinin-induced hyperactivity: effects of 5,7-dihydroxytryptamine lesions.

Rats were implanted with cannulae in the median raphe nucleus (MR). 5,7-Dihydroxytryptamine (5,7-DHT) or vehicle was infused either directly through the MR cannula, or bilaterally into the medial forebrain bundle (MFB). The MR 5,7-DHT lesions completely blocked the hyperactivity elicited by injections into the MR of the neurokinin (NK) 3 agonists, DiMe-C7 and senktide, and the NK-2 agonist, neurokinin A. In contrast, the MFB 5,7-DHT lesions did not affect the locomotor hyperactivity produced by intra-MR administration of DiMe-C7 and senktide, but appeared to attenuate the effects of NKA. The data indicate that intra-raphe neurokinin-induced hyperactivity is mediated by 5-HT neurons, and that 5-HT projections to the forebrain may be involved in the behavioral activation induced by intra-raphe neurokinin A administration, but not that induced by intra-MR NK-3 agonists.

5,7-Dihydroxytryptamine↗
PubMed1990

Sequential course of uptake of intravitreal 5,7-dihydroxytryptamine by carp retinal cells.

The sequential course of uptake by retinal cells of intravitreally injected 5,7-dihydroxytryptamine (5,7-DHT) together with dopamine (DA) was investigated in juvenile carp retinas, which were removed at various intervals (1-24 h) after injection. The cells taken up 5,7-DHT were visualized immunohistochemically with anti-serotonin (5-HT) antibody and FITC-conjugated IgG. After a mixture of 5,7-DHT and DA (2.5, 10 or 20 micrograms each) was given, large-sized indoleamine (IA) amacrine cells first (1-4 h), and then small-sized indoleamine-accumulating amacrine amacrine (IAA) cells (4-12 h), bipolar cells (8-12 h) and in some cases photoreceptor cells (12-24 h) were sequentially observed, and finally the immunoreactive structures almost disappeared around 24 h after injection. When the mixture of 5,7-DHT and DA (10 micrograms each) was injected into the eyes of reserpinized fish, the same sequential uptake of 5,7-DHT was seen in a faster time course, but additionally various classes of retinal cells (horizontal, ganglion and Müller cells) became visible as irregular clusters. However, DA cells were never visualized at any stages of all the experiments, indicating that DA cells do not take up 5,7-DHT in the carp retina, which was further confirmed by double labeling of 5-HT- and tyrosine hydroxylase-like immunoreactive cells. Double labeling also revealed that 5,7-DHT-accumulating bipolar cells appear to represent a subclass different from that of protein kinase C-like immunoreactive bipolar cells.

5,7-Dihydroxytryptamine↗
PubMed1982

Neonatal intraspinal 6-hydroxydopamine, 5,7-dihydroxytryptamine or their combination: effects on nociception and morphine analgesia.

Newborn rats received two injections of intraspinal 6-hydroxydopamine (6-OHDA, 10 micrograms) or 5,7-dihydroxytryptamine (5,7-DHT, 8 micrograms preceded by s.c. desmethylimipramine) or a 'cocktail' of both neurotoxins. The two injections were separated by 24 h. When assayed in adulthood, the 6-OHDA rats showed a substantial (about 80%) depletion of spinal norepinephrine (NE) but an elevation of brainstem NE. Conversely, the 5,7-DHT rats showed a modest (about 60%) loss of spinal serotonin (5-HT) but an elevation of brainstem 5-HT. Rats receiving combined 6-OHDA plus 5,7-DHT showed rostro-caudal, decreasing gradients of spinal NE and 5-HT depletions, with the largest loss in the lumbar cord. These depletions were much less than those observed after the respective single neurotoxin treatments. Neither the single nor combined neurotoxin treatments altered the tail-flick analgesia induced by morphine (1.0, 3.0 or 7.5 mg/kg s.c.). Basal nociception, however, was altered by the neurotoxins but in a sexually dimorphic manner. The 6-OHDA lowered baseline tail-flick latencies in females while 5,7-DHT elevated latencies in males. Like the 6-OHDA-only rats, the combined 6-OHDA plus 5,7-DHT lowered latencies in females. We conclude that neither spinal NE nor 5-HT are essential to morphine analgesia but do participate in nociception, seemingly in a sexually dimorphic fashion.

5,7-Dihydroxytryptamine↗
PubMed1984

Increased behavioural response to 5-methoxy-N,N-dimethyltryptamine but not to RU-24969 after intraventricular 5,7-dihydroxytryptamine administration.

Chemical lesioning of the 5-hydroxytryptamine neurones in the brain with 5,7-dihydroxytryptamine (200 micrograms i.c.v., 14 or 21 days previously) resulted in an enhanced behavioral response following administration of the 5-hydroxytryptamine receptor agonist 5-methoxy-N,N-dimethyltryptamine (2.5 mg/kg). The increase in the behavioural response showed a positive correlation with the decrease in whole brain 5-hydroxytryptamine levels. In contrast, there was no increase in the hyperlocomotion produced by the 5HT1 receptor agonist RU-24969 (3.5 mg/kg). The results are discussed in relation to the proposed 5-hydroxytryptamine receptor subtypes.

5,7-Dihydroxytryptamine↗
PubMed1988

Supersensitivity of 5,7-dihydroxytryptamine-treated rats to the respiratory depressant and antitussive effects of dihydrocodeine.

The present study sought to determine whether rats, treated neonatally with 5,7-dihydroxytryptamine (5,7-DHT), have an increased sensitivity to the respiratory and cough-depressant effects induced by dihydrocodeine. The serotonin (5-HT) levels in the whole brain of 5,7-DHT-treated rats were reduced to 19% of the corresponding control values. The 5,7-DHT-treated rats were supersensitive to the depression in frequency of respiration and cough reflex produced by i.p. administration of dihydrocodeine. The increased sensitivity to dihydrocodeine in terms of the depression of frequency of respiration and the cough reflex in 5,7-DHT-treated rats could possibly have been due to changes in the sensitivity of serotonergic receptors.

5,7-Dihydroxytryptamine↗
PubMed1989

1-5-Hydroxytryptophan-induced flat body posture in the rat: antagonism by ritanserin and potentiation after 5,7-dihydroxytryptamine.

1-5-Hydroxytryptophan (1-5-HTP)-induced flat body posture (FBP) was antagonized by ritanserin in doses that were lower than those needed to antagonize head-twitches (HTW) and forepaw treading (FPT). 5,7-Dihydroxytryptamine (5,7-DHT) potentiated 1-5-HTP-induced FBP but not HTW or FPT. Ritanserin interacted with 5-HT2 and 5-HT1c receptors. 1-5-HTP-induced FBP could be mediated by postsynaptic 5-HT1c receptors and could serve as a behavioral model of postsynaptic 5-HT1c receptor stimulation in the CNS.

5,7-Dihydroxytryptamine↗
PubMed1986

3H-5-hydroxytryptamine accumulation by rat brain synaptic vesicles in a membrane-impermeant medium, and selective reduction by 5,7-dihydroxytryptamine.

In order to examine possible selectivity of amine uptake by synaptic vesicles, the ATP-stimulated accumulation of 3H-5-hydroxytryptamine (5HT) by synaptic vesicles from rat whole brain was examined in a medium comprised largely of membrane-impermeant anions (d-tartrate). Such media have previously been shown to stabilize vesicular accumulation of several neurotransmitters. Accumulation of 3H-5HT did not occur in tartrate medium alone, but was increased biphasically with increasing concentrations of both potassium phosphate and potassium bicarbonate. At optimal concentrations of each anion (10 mM), stable accumulation of 3H-5HT was observed at 37 degrees (26.1 +/- 1.2 pmol/mg protein; Km 6 X 10(-7) M), which was reduced by greater than 95% in the absence of K2ATP, at 4 degrees C, in the presence of 10(-6) M reserpine, or in the presence of the proton ionophore carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP). Uptake was significantly antagonized by millimolar concentrations of Na+, Mg++ or Cl-, but was unaffected by ouabain (10(-5) M). Pretreatment of animals with 5,7-dihydroxytryptamine (5,7-DHT) (200 micrograms, intraventricular) 10 days prior to sacrifice reduced endogenous 5HT levels by 70%, while levels of endogenous norepinephrine (NE) and dopamine (DA) were unaffected. Accumulation of 3H-5HT, examined in the presence of 10(-6) M NE to block 3H-5HT accumulation by vesicles from noradrenergic nerve endings, was reduced by 40% in vesicles from treated animals. Vesicular accumulation of 3H-(-)-NE and 3H-DA was unaffected by 5,7-DHT treatment. The data suggest the possibility of preferential accumulation of 3H-5HT by vesicles arising from serotonergic nerve endings.

5,7-Dihydroxytryptamine↗
PubMed1986

The effect of intracerebroventricular 5,7-dihydroxytryptamine on morphine analgesia is time-dependent.

The analgesic effect of morphine in the tail immersion test was studied in rats three and ten days after intracerebroventricular 5,7-dihydroxytryptamine (5,7-DHT) given to selectively destroy serotonergic neurons. Morphine analgesia was reduced three but not ten days after the neurotoxin. Ten days after 5,7-DHT, the inhibiting effect of metergoline, a serotonin antagonist, on morphine analgesia was still present, suggesting that functional recovery of the serotonergic system may partly explain the different results.

5,7-Dihydroxytryptamine↗
PubMed1984

The effects of 5,7-dihydroxytryptamine and p-chlorophenylalanine on thyrotrophin-releasing hormone in regions of the brain and spinal cord of the rat.

The distribution of thyrotrophin-releasing hormone (TRH) and 5-hydroxytryptamine (5-HT) were compared in ten regions of the rat brain and in lumbar spinal cord. After dissection, using a cutting box and tissue punches, TRH was measured by radioimmunoassay and 5-HT by HPLC with electrochemical detection. Within the brain the highest levels of TRH were found in the median eminence and the remaining hypothalamus. There were also relatively high levels in the suprachiasmatic nucleus, septal nuclei and nucleus accumbens. Highest levels of 5-HT were found in the raphe nuclei, hypothalamic nuclei, nucleus accumbens, stria terminalis, septal nuclei and hippocampus. 5,7-Dihydroxytryptamine (5,7-DHT; 200 micrograms, i.c.v.) markedly reduced levels of 5-HT in brain and spinal cord. In the ventral lumbar cord there was a comparable decrease of TRH and 5-HT (-80%) and a smaller but significant decrease in the nucleus accumbens (-55%) and septal nuclei (-38%). p-Chlorophenylalanine (PCPA; 250 mg/kg X 2) reduced levels of 5-HT (-80%), without significantly altering those of noradrenaline. p-Chlorophenylalanine also significantly reduced levels of TRH in the nucleus accumbens (-72%) but not in the other regions of brain or spinal cord taken. The results are discussed in relation to the previously described co-existence of TRH and 5-HT in the spinal cord and the possible alternative forms of interactions between amine and peptide in the nucleus accumbens.

5,7-Dihydroxytryptamine↗