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PubMed1987

Potentiation in phencyclidine-induced serotonin-mediated behaviors after intracerebroventricular administration of 5,7-dihydroxytryptamine in rats.

Phencyclidine (PCP)-induced behaviors were compared with 5-methoxy-N,N-dimethyltryptamine (5-MeODMT)- and p-chloroamphetamine-induced behaviors in rats pretreated with ritanserin or 5,7-dihydroxytryptamine (5,7-DHT) in order to investigate whether PCP interacts with 5-hydroxytryptamine2 (5-HT2) receptors. Head-twitch and wet-dog shake induced by p-chloroamphetamine, a 5-HT releaser, and head-twitch induced by PCP were blocked completely by pretreatment with ritanserin, a specific 5-HT2 receptor blocker, but other behaviors induced by p-chloroamphetamine, PCP and 5-MeODMT, a 5-HT agonist, were not. The intensity of head-weaving, turning, backpedalling and hind-limb abduction induced by 5-MeODMT and the intensity of head-weaving, turning and head-twitch induced by PCP were markedly greater in the rats 2 weeks after the 5,7-DHT, a 5-HT neurotoxin-injection. Contrarily, 5-HT-mediated behaviors induced by p-chloroamphetamine were attenuated in the 5,7-DHT-treated rats. 5,7-DHT-treatment increased the number of 5-HT1 ([3H]-5-HT), 5-HT2 ([3H]ketanserin) and PCP ([3H]PCP) binding sites in the synaptic membrane of rat brain, but decreased the brain level of 5-HT (41% of control). These results may indicate that PCP as a 5-HT2 agonist induces head-twitch via 5-HT2 receptors, and that PCP induces head-weaving and turning via 5-HT1 receptors and/or some other mechanisms in rats.

5,7-Dihydroxytryptamine↗
PubMed1986

Quantitative autoradiography of multiple 5-HT1 receptor subtypes in the brain of control or 5,7-dihydroxytryptamine-treated rats.

The distribution of the 2 main types (A and B) of 5-HT1 binding sites in the rat brain was studied by light-microscopic quantitative autoradiography. The 5-HT1A sites were identified using 3H-8-hydroxy-2-(N-dipropylamino)tetralin (3H-8-OH-DPAT) or 3H-5-HT as the ligand. In the latter case, it was shown that 3H-5-HT binding to 5-HT1A sites corresponded to that displaceable by 0.1 microM 8-OH-DPAT or 1 microM spiperone. The "non-5-HT1A" sites labeled by 3H-5-HT in the presence of 0.1 microM 8-OH-DPAT corresponded mainly to 5-HT1B sites. 5-HT1A binding was notably high in limbic regions (dentate gyrus, CA1 and CA3 hippocampal regions, lateral septum, frontal cortex), whereas 5-HT1B binding was particularly concentrated in extrapyramidal areas (caudate nucleus, globus pallidus, substantia nigra). Except in the latter regions, where only one class of 5-HT1 sites was found, both 5-HT1A and 5-HT1B sites existed in all areas examined. The selective degeneration of serotoninergic neurons produced by an intracerebral injection of 5,7-dihydroxytryptamine was associated only with a significant loss of 5-HT1A binding to the dorsal raphe nucleus (-60%) and of 5-HT1B binding to the substantia nigra (-37%). These results are discussed in relation to the possible identity of 5-HT1A and/or 5-HT1B sites with the presynaptic 5-HT autoreceptors controlling nerve impulse flow and neurotransmitter release in serotoninergic neurons.

5,7-Dihydroxytryptamine↗
PubMed1978

Biochemical and behavioral alterations in developing rats treated with 5,7-dihydroxytryptamine.

Intracisternal administration of 5,7-dihydroxytryptamine (5,7-DHT) to immature rats produced a marked reduction of brain norepinephrine and serotonin. Accompanying these reductions of brain amines were a decrease in body weight and alterations in behavior. After treatment with 5,7-DHT at 3 days of age, locomotor activity was significantly elevated at 14 days of age, but was reduced at 28 days of age. 5,7-DHT alone also induced a significant deficit in acquisition of the shuttle-box avoidance response and blocked body movements observed after decapitation. Treatment with either pargyline or desipramine before injection of 5,7-DHT eliminated the effect of 5,7-DHT on noradrenergic fibers while enhancing the effects of 5,7-DHT on brain serotonergic fibers. These treatments also minimized the deficits of 5,7-DHT on growth and on acquisition of the avoidance response and reversed the blockade of decapitation convulsions. However, animals pretreated with pargyline or desipramine before they received 5,7-DHT still demonstrated hyperactivity at 14 days of age equivalent to that observed in neonates that received only 5,7-DHT. Furthermore, a behavioral syndrome induced by 30 mg/kg of 5-hydroxytryptamine was markedly potentiated by all of the 5,7-DHT treatments which suggest that serotonin receptors were supersensitive.

5,7-Dihydroxytryptamine↗
PubMed1988

Effects of 5,7-dihydroxytryptamine lesions of the nucleus accumbens in rats responding on a concurrent schedule of food, water and intravenous morphine self-administration.

The role of serotonergic innervations of the nucleus accumbens in the processes maintaining intravenous self-administration was assessed in rats responding on a concurrent schedule of food, water and morphine presentations. Five rats were trained on a concurrent fixed-ratio schedule of food and water presentation. They were then implanted with intravenous jugular catheters and bilateral injection guide cannulae into the central medial nucleus accumbens, made physically dependent on morphine and allowed to choose between intravenous morphine, food and water deliveries. A three-lever choice procedure provided almost continuous access to the three reinforcers. Dose-effect curves were determined by the substitution of the daily dose of morphine (3.3 mg/injection) with other doses (0.83-13.2 mg/injection) or eliminating drug injections (extinction) for 24 hour periods. The behavioral effects of 24 hour food extinction probes were also determined. The rats subsequently received bilateral microinjections of either the vehicle or 5,7-dihydroxytryptamine (5,7-DHT) into the nucleus accumbens. Following the lesion, response independent infusions of morphine were delivered for 24 hours at the previous rate of self-injection. The animals were placed back on the concurrent schedule and morphine dose-effect curves were redetermined. The 5,7-DHT lesion resulted in a significant dose-related decrease in morphine self-administration, and little or no effect on responding maintained by food or water presentations. Serotonergic innervations of the nucleus accumbens appear to participate in the neuronal activity mediating intravenous morphine self-administration.

5,7-Dihydroxytryptamine↗
PubMed1988

[Effect of 5,7-dihydroxytryptamine on pain sensitivity and analgesic activity of morphine].

Electron microscopy of rats ultrathin sections from dorsal and central raphe nucleus and spinal cord after 5,7-dihydroxytryptamine intracisternal microinjection (200 micrograms) has revealed neurones and axonal terminals distruction, which associated with tail-flick hypoalgesia and blood pressure nociceptive reactions diminished. In this condition the morphine (2 mg/kg) analgesia and drug depressive effect on pain hemodynamic manifestations increase significantly.

5,7-Dihydroxytryptamine↗
PubMed1986

5,7-Dihydroxytryptamine lesions of crayfish serotonin-containing neurons: effect on the lateral giant escape reaction.

The crayfish's lateral giant escape response, a relatively simple behavioral reaction, is readily modulated in certain situations. For example, when a crayfish is restrained, its lateral giant (LG) fibers--command neurons that mediate the escape response--are strongly inhibited (Krasne and Wine, 1975). Previous work (Glanzman and Krasne, 1983) had suggested that serotonin (5-HT) might mediate this restraint-induced inhibition of the escape response. To test this possibility, we attempted to lesion serotonergic neurons in crayfish with the 5-HT neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT). We compared the levels of 5-HT-immunoreactive staining in nerve cords from 5,7-DHT-treated and from normal crayfish to assess 5,7-DHT's effectiveness. Levels of immunoreactive staining, as judged by ratings of the visibility of immunofluorescence, were significantly lower in nerve cords from crayfish that had received injections of 5,7-DHT (1.0-4.0 mg) than in nerve cords from normal crayfish. In addition, some serotonergic neurons in the neurotoxin-treated crayfish developed an abnormal brown pigmentation. To assess the behavioral consequence of central serotonergic lesions, we compared the responsiveness of escape in crayfish treated with 5,7-DHT (2.0-2.75 mg) and in normal crayfish. The threshold for firing the LGs was significantly lower in restrained neurotoxin-treated animals than in restrained normal animals. Furthermore, the responsiveness of the LGs in neurotoxin-treated crayfish approximated that in crayfish whose nerve cords had been severed between the thorax and abdomen, a procedure known to abolish restraint-induced inhibition (Krasne and Wine, 1975).(ABSTRACT TRUNCATED AT 250 WORDS)

5,7-Dihydroxytryptamine↗
PubMed1983

Effect of substance P on the 5,7-dihydroxytryptamine induced alteration of the postnatal development of central serotonin neurons.

Systemic treatment with the serotonin neurotoxin 5,7-dihydroxytryptamine [5,7-HT]in the neonatal stage leads to a permanent alteration of the postnatal development of the serotonin neurons in rat brain with denervation of distant nerve terminal projections and hyperinnervation in regions close to the serotonin perikarya. Intracisternal administration of substance P was found to counteract both the denervation and the hyperinnervation, as evaluated by measuring endogenous serotonin levels and [3H]-serotonin uptake in vitro. Furthermore, substance P was found to potentiate the reduction of serotonin induced by tryptophan hydroxylase inhibition with alpha-propyldopacetamide, indicating that substance P can produce an increase in serotonin utilization and turnover. The results suggest that substance P has a degeneration preventing and/or regrowth stimulatory effect on damaged serotonin neurons during ontogeny.

5,7-Dihydroxytryptamine↗
PubMed1984

[Morphological changes in the neurons of the rat nucleus raphe dorsalis following application of 5,7-dihydroxytryptamine. A golgi-rapid-impregnation study].

The effect of stereotactically applicated 5,7-dihydroxytryptamine on the demonstrability of the different neuron types of the nucleus raphe dorsalis of the rat was investigated by means of the Golgi-rapid-impregnation technique. Degenerative changes could be demonstrated on the polygonal neurons, only. Typical variations of the dendritic structure was shown on the fusiform neurons. The pyriform neuron typ was not affected.

5,7-Dihydroxytryptamine↗
PubMed1997

Serotonin depletion by 5,7-dihydroxytryptamine alters deutocerebral development in the lobster, Homarus americanus.

The olfactory and accessory lobes constitute prominent histological structures within the larval and mature lobster deutocerebrum, and both are associated with a dense innervation from paired serotonergic nerve cells, the dorsal giant neurons (DGNs). During development, the cell bodies of the DGNs are the first central somata to express serotonin (5-HT), and the onset of their 5-HT immunoreactivity coincides with the beginning of accessory lobe formation. In contrast, the olfactory lobe anlagen emerge much earlier and grow in the apparent absence of serotonin. The role of serotonergic input for the development of these brain structures was investigated in lobster embryos after serotonin had been depleted pharmacologically with the neurotoxin 5,7-dihydroxytryptamine. A approximately 90% reduction of serotonin was confirmed in eggs using high-performance liquid chromatography with electrochemical detection. Morphometric analyses suggested that serotonin depletion dramatically slowed the growth of olfactory and accessory lobes, although glomeruli differentiated at the normal time in both areas. The toxin exhibited a high degree of specificity for serotonergic neurons and associated target regions, and serotonin depletion persisted for at least 2 months following treatment. The goal of future experiments is to determine which of the cell types that innervate the olfactory and accessory lobes are affected by toxin treatment, thereby resulting in the retarded growth of these areas.

5,7-Dihydroxytryptamine↗
PubMed1997

Distribution of the 5-hydroxytryptamine2C receptor protein in adult rat brain and spinal cord determined using a receptor-directed antibody: effect of 5,7-dihydroxytryptamine.

A synthetic peptide, corresponding to the N-terminal decapeptide (+Y11C12) of the rat 5-hydroxytryptamine2C (5-HT2C) receptor protein was used to produce a sheep polyclonal antiserum. Western blot analysis showed that the resultant antibody G241 recognised two membrane proteins, one (55 kDa) approximating the molecular mass of the 5-HT2C receptor (52 kDa) and a second (63 kDa), which may be a glycosylated form of the receptor protein. HEK 293 cells transfected with human 5-HT2C cDNA displayed intense cell surface immunoreactivity with the 5-HT2C antiserum, which was completely prevented by incubating the antibody with the synthetic 5-HT2C peptide (10 microM), whilst neither non-immune serum nor untransfected cells displayed any immunoreactivity. A radioimmunoassay was developed to quantify the regional distribution of 5-HT2C-like immunoreactivity (LI) in the adult rat brain. The choroid plexus contained five-fold higher levels of 5-HT2C-LI than any brain region but high levels were found in the frontal cortex, septum, hypothalamus, and striatum, intermediate levels in the thalamus and midbrain, and lower levels in brainstem, cerebellum, and spinal cord. In rat cortical membranes, the B(max) value from [3H]-mesulergine binding was ten-fold lower than 5-HT2C-LI levels determined by radioimmunoassay, which may reflect measurement of internalised receptor protein by radioimmunoassay which is not detected with conventional 5-HT2C ligands. Ten days after depletion of 5-HT with the serotonergic neurotoxin 5,7-dihydroxytryptamine (5,7-DHT), there was a significant increase in 5-HT2C-LI in the choroid plexus and the ventral cervical spinal cord, suggesting that receptors therein are located post-synaptic to destroyed serotonergic nerve terminals. In contrast, the significant reduction in 5-HT2C-LI observed in the midbrain, brainstem, and dorsal thoracic spinal cord following 5,7-DHT implies that 5-HT2C receptors may be located on 5-HT nerve terminals in these regions.

5,7-Dihydroxytryptamine↗
PubMed1999

Effects of 5,7-dihydroxytryptamine depletion of tissue serotonin levels on extracellular serotonin in the striatum assessed with in vivo microdialysis: relationship to behavior.

Effects of i.c.v. administration of 5,7-dihydroxytryptamine (5,7-DHT) on biochemistry and behavior were studied in awake Sprague-Dawley rats. It was found that 5,7-DHT depletion of striatal tissue levels of serotonin (5-HT) does not diminish extracellular levels until substantial depletions occur. This finding is similar to those observed after 6-hydroxydopamine lesions of the brain dopamine systems. Although varying amounts of 5,7-DHT produced serotonin depletions in striatal tissue, decreases in extracellular levels were only observed at tissue depletions greater than 60% compared to saline-injected control subjects. Thus, the effects of serotonin lesions which produce only moderate depletions may not be the result of decreased extracellular serotonin, but instead may be the result of compensatory changes in remaining neurons which maintain normal extracellular serotonin concentrations. Different degrees of striatal serotonin depletion were associated with opposite behavioral effects. Moderate levels of serotonin depletion (50-75%) produced evidence of increased anxiety, while these effects were no longer seen in rats with more severe 5-HT depletions (>75%).

5,7-Dihydroxytryptamine↗
PubMed1975

Ultrastructural evidence for the uptake of 5,6-dihydroxytryptamine in the frog's gustatory cell.

The fungiform papillae of the frog were examined electron-microscopically after a single injection of 5,6-dihydroxytryptamine (5,6-DHT). Thirty minutes after 5.6-DHT injection, numerous vesicles partially occupied with dark material were found in the cytoplasm of gustatory cell processes. Three days after the drug treatment, the majority of vesicles were completely filled with dark material so that their limiting membrane became obscure, while the terminal portions of gustatory cells showed no evidence for fine structural alteration indicative of drug retention. In addition, clear vacuoles, suggesting a degenerative change induced by the uptake of the neurotoxic agent, occurred in the cytoplasm of gustatory cell processes. It is suggested that the uptake of 5.6-DHT in gustatory cells may reflect the presence of an indoleamine, probably 5-hydroxytryptamine (serotonin).

5,6-Dihydroxytryptamine↗
PubMed2002

Overexpression of S100beta in transgenic mice does not protect from serotonergic denervation induced by 5,7-dihydroxytryptamine.

Transgenic mice overexpressing S100beta were used to examine whether the chronic elevation of this protein alters the response to selective partial serotonergic lesions produced by bilateral intracerebroventricular injections of 5,7-dihydroxytryptamine (5,7-DHT). Basal levels of S100beta mRNA examined by in situ hybridization were two- to threefold higher throughout the brain in transgenic than in control mice, whereas 5-HT levels in forebrain were similar in both. After the 5,7-DHT-induced lesions, no differences were found in the S100beta mRNA levels in either normal or transgenic mice. At 5 and 60 days after the lesion, forebrain 5-HT levels were reduced by 56% and 35%, respectively, in control mice and by 51% and 35%, respectively, in the transgenic mice. Analysis of the 5-HT immunostaining showed a marked decrease of the immunoreactivity in various brain regions, which was comparable at the two intervals postlesion. One exception was the medial hypothalamus, where an almost complete disappearance of 5-HT immunoreactivity was observed in the medial region at 5 days after lesion, followed by a marked reinnervation 60 days later. These hypothalamic changes were seen in both controls and S100beta-overexpressing transgenic mice. Quantitative analysis of the density of 5-HT transporter sites using [(3)H]citalopram binding, a marker of serotonergic terminals, showed a marked decrease in different brain regions at both 5 and 60 days after 5,7-DHT injections. No difference in basal and postlesion levels of [(3)H]citalopram binding was seen between transgenic and control mice. In conclusion, this study demonstrates that constitutive overexpression of S100beta in transgenic mice does not modify serotonin levels during development, nor does it protect the serotonergic neurons from selective neurotoxicity or modify the serotonergic sprouting induced by partial lesion.

5,7-Dihydroxytryptamine↗
PubMed2005

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.

A high density of opioid receptor-like 1 (ORL1) receptor (also referred to as NOP receptor) is found in limbic areas and in regions containing monoamines, which are implicated in emotional activity and physiopathology of depression and anxiety. We aimed at defining precisely the localization of ORL1 receptors in dorsal raphe nucleus, by means of a lesion strategy and autoradiographic studies. In control rats, [3H]nociceptin and nociceptin-stimulated [35S]GTPgammaS bindings were found to be correlated in several brain regions. We performed in rats a selective destruction of serotoninergic neurons by surgical stereotaxic injection of 5,7-dihydroxytryptamine (5,7-DHT) in dorsal raphe nucleus. This led to a marked decrease in serotonin contents in striata and frontal cortices (about -60%) and in autoradiographic [3H]citalopram binding in posterior regions. In dorsal raphe nucleus, [3H]nociceptin binding was decreased to the same extent as [3H]citalopram binding, whereas it was unchanged in the other regions studied. Nevertheless, in the dorsal raphe, nociceptin-stimulated [35S]GTPgammaS binding was decreased to a lesser extent than [3H]nociceptin binding in 5,7-DHT-lesioned rats. The ratio between nociceptin-stimulated [35S]GTPgammaS binding and [3H]nociceptin binding was significantly increased in 5,7-DHT-lesioned rats compared with controls in this region. These data demonstrate 1) that ORL1 receptors are located on serotoninergic neurons in the dorsal raphe nucleus and 2) that, after a lesion, the functionality of remaining ORL1 receptors appears to be up-regulated, which could correspond to a compensatory mechanism.

5,7-Dihydroxytryptamine↗
PubMed2000

Serotonin release from mesencephalic raphe neurons grafted to the 5,7-dihydroxytryptamine-lesioned rat hippocampus: effects of behavioral activation and stress.

Transplants of fetal midbrain raphe neurons into the adult brain have been shown to promote recovery of complex behavioral deficits in several experimental models, but the mechanisms underlying these effects are only partially understood. In the present study, we have used a well-characterized model system to ascertain whether midbrain raphe graft can display behaviorally relevant changes in transmitter release and/or metabolism. Fetal mesencephalic raphe neurons were grafted unilaterally into the hippocampus previously deprived of its innate serotonergic innervation by intraventricular injections of 5,7-dihydroxytryptamine. The contralateral hippocampus remained as a nongrafted, lesioned control. Microdialysis probes were implanted in the hippocampus 5-7 months postgrafting. Under baseline conditions, extracellular levels of serotonin were similar to normal in the grafted hippocampi, but undetectable on the contralateral, nongrafted side. Levels of the serotonin metabolite, 5-hydroxyindoleacetic acid (5-HIAA), were markedly higher than normal in the grafted hippocampi, but dramatically reduced on the contralateral nongrafted side. Handling stimulation (gentle stroking of a rat's fur and tail for 15 min) induced a 64% increase in serotonin output in the intact rats and a small but significant 12% increase in the grafted animals. Non-noxious tail-pinch (15 min) enhanced serotonin release by 86% in the intact rats and 28% in the grafted ones. Extracellular 5-HIAA levels remained unchanged during both handling and tail-pinch in both the intact and the grafted rats. Forced immobilization of the rats for 15 min induced a transient 124% increase in extracellular serotonin levels in the intact rats and a significant 19% increase in the grafted animals, whereas swimming in temperate water (25-30 degrees C; 15 min) induced no detectable changes in serotonin output in any of the groups. 5-HIAA levels remained unchanged during forced immobilization, but were significantly reduced during the swimming session in both the intact (-38%) and grafted (-15%) animals. The present results indicate that median raphe grafts can become functionally integrated in the denervated host hippocampus and respond by altered indole output when the animal is exposed to different types of environmental challenges.

5,7-Dihydroxytryptamine↗
PubMed1975

Recovery of brain noradrenaline after 5,7-dihydroxytryptamine-induced axonal lesions in the rat.

Time-dependent changes in regional CNS noradrenaline (NA) concentration, 3H-NA uptake and fluorescence morphology of CNS NA neurons were analysed in the adult rat up to 6 months after intraventricular injection of 5,7-dihydroxytryptamine (5,7-DHT), and compared with the time-course of changes in brain and spinal cord indolamine neurons. Following a substantial depletion of both amines in all CNS regions (telodiencephalon, brainstem and spinal cord) at 10 days after 150 mug 5,7-DHT, brain NA--but not 5-HT--levels recovered to near-normal values in brainstem and forebrain (35% below the age-matched controls) within 4 months. This was accompanied by a total restoration of the initially decreased capacity of the brain tissue to accumulate 3H-NA in vitro. Within 10 days after 5,7-DHT, there was a disappearance of NA terminals from many telencephalic, diencephalic and lower brain stem nuclei, from the cerebral and cerebellar cortices, and the grey matter of the spinal cord, concomitant with the appearance of numerous distorted, highly fluorescent swellings along the non-terminal axons of the major noradrenergic projection pathways. The recovery of the NA levels was paralleled by a re-appearance of fluorescent fibres, signifying an intense sprouting and regrowth of the drug-lesioned axons, which eventually re-innervated some of the previously denervated telodiencephalic regions. Except for a permanent loss of some surface-near perikarya in group A1 (the main source of the bulbospinal projections) there was no evidence of a retrograde degeneration of noradrenergic cell bodies in the rat CNS. The results are compatible with the idea that 5,7-DHT mainly causes a lesion of NA axons at a distance from the cell bodies, and this is followed by sprouting and regrowth of axons from the lisioned neurites, and formation of new terminal-like fibres in some previously denervated telodiencephalic regions. These findings indicate that chemical axotomy of central NA neurons induced by 5,7-DHT is--in contrast to that induced by 6-hydroxydopamine--followed by extensive axonal regeneration.

5,6-Dihydroxytryptamine↗
PubMed1989

Immunohistochemical study on fetal raphe samples transplanted into the leptomeningeal tissue of 5,6-dihydroxytryptamine-treated adult rats.

Pieces of fetal midbrain raphe containing serotonergic and dopaminergic neurons were transplanted into the leptomeningeal tissue of adult host rats that had previously been denervated by treatment with 5,6-dihydroxytryptamine. One, 2 and 5 months after transplantation, the rate of neuronal survival in the grafted tissue and the extent of axonal outgrowth into the host brain were studied by use of serotonin and tyrosine hydroxylase (TH) immunohistochemistry. The survival rate of the grafts in the 1-month group was approximately 70%. Neurons containing either serotonin or catecholamine were demonstrated by means of immunocytochemical procedures in the grafts. Two and 5 months after transplantation, serotonin-immunoreactive nerve fibers were densely distributed throughout the graft tissue, while TH-immunoreactive fiber elements were restricted to an area near the somata of TH-positive neurons. Numerous serotonin-immunoreactive fibers derived from the transplant were found in the leptomeningeal tissue surrounding the graft, on the wall of neighboring blood vessels, and also in the adjacent parenchyma of the host brain. Outgrowing TH-immunoreactive nerve fibers were not observed in the host brain, although such elements occurred in the leptomeningeal tissue and the wall of the larger blood vessels. These results suggest that the serotonergic and catecholaminergic (dopaminergic) neurons located in transplants of the raphe nuclei show different patterns when reinnervating the host tissue.

5,6-Dihydroxytryptamine↗
PubMed1991

Differential recovery of adrenocortical responses to neural stimuli following administration of 5,7-dihydroxytryptamine into the hypothalamus.

In view of the role of serotonin in adrenocortical regulation, the effects of depletion of hypothalamic serotonin, using localized injections of the neurotoxin 5,7-dihydroxytryptamine into the hypothalamic paraventricular nucleus, on the rise in plasma corticosterone following afferent neural stimulation, were studied. The neurotoxin caused a significant reduction (p less than 0.001) in hypothalamic serotonin content of about 50% during the first month and about 30% up to two months later. Basal and ether stress-induced rises in plasma corticosterone levels were unaffected at all times after this treatment, but responses to stimulation of the sciatic nerve were reduced for up to four weeks (p less than 0.01), recovering at later times. Responses to photic and acoustic stimuli were almost entirely prevented up to four weeks following the treatment (p less than 0.001) but showed a gradual recovery to full, or almost full, adrenocortical responses at eight weeks, following acoustic and photic stimulation respectively. These results demonstrate a differential recovery of the adrenocortical responses, following the neurotoxin injection and indicate that different neural modalities require different 5-HT concentrations in the PVN for the expression of a full adrenocortical response.

5,7-Dihydroxytryptamine↗