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PubMed1985

Growth rate of a peripheral annulus defined by neurotoxic destruction in the goldfish retina.

Fifteen goldfish of similar size (6.8 cm in body length on the average) were reared in an aquarium (about 22 degrees C) for 5 months after neurotoxic destruction of retinal dopamine (DA) cells with intravitreal injection of 6-hydroxydopamine, and then further for 8 months after destruction of indoleamine-accumulating cells with 5,7-dihydroxytryptamine. By means of a histofluorescence technique for retinal wholemounts, the growth rate and the number of DA cells were estimated for a peripheral annulus which had been well defined by the successive neurotoxic destructions of monoamine-accumulating cells. As the fish grew from 8.4 to 11.6 cm in body length on the average over the 8-month period, the defined peripheral annulus of the retina was found to be enlarged radially by approximately 1.5 X and circumferentially by 1.3 X while the number of DA cells in the annulus remained unchanged.

5,7-Dihydroxytryptamine↗

PubMed1985

Retinal growth in carp of the same age: density and number of dopamine neurons.

Research has shown that an increase in the size of retina with fish growth is accompanied by a reduction in the density of monoamine neurons along with an increase in their cell number per retina. The age of fish, however, has not been considered in relation to the above. In the present study, juvenile carp (6.4 +/- 0.7 cm in body length), hatched 2 months earlier, were reared for 10 months under 2 different sets of conditions; one group was kept in a small aquarium at room temperature (RT, 9-26 degrees C), and the other was kept in a large aquarium in which the water temperature was constant (CT, 22 degrees C). The left eye of fish transferred into the RT aquarium was intravitreally injected with 5,7-dihydroxytryptamine (5,7-DHT; 1.0 microgram) to destroy indoleamine-accumulating (IA) neurons. The fish grew faster in the CT (16 +/- 1.6 cm) than in the RT aquarium (9.3 +/- 1.7 cm), resulting in a wide variation among fish of the same age. In fluorescent retinal flatmounts, the density of dopamine (DA) neurons was found to be lower, but their cell number per retina greater in the CT than in the RT group; these differences were statistically significant (P less than 0.001). The data suggest that the above parameters depend on the size of carp but not on their age. In the fish treated with 5,7-DHT and reared in the RT aquarium for 10 months, the growth zone of the retina was determined by circumferential addition of IA cells.(ABSTRACT TRUNCATED AT 250 WORDS)

5,7-Dihydroxytryptamine↗

PubMed1990

The role of serotonin in the development and environmental regulation of type II corticosteroid receptor binding in rat hippocampus.

Hippocampal concentrations of serotonin (5-HT) increase over the first two weeks of life, and show a peak on day 14. This pattern is very similar to the previously reported developmental changes in hippocampal type II corticosteroid receptor binding. We found that adult animals treated during the first days of life with the 5-HT neurotoxin, 5.7-dihydroxytryptamine, showed reduced hippocampal type II corticosteroid receptor binding. In addition, manipulations that resulted in increased hippocampal type II corticosteroid receptor binding, such as neonatal handling or exogenous thyroid hormone treatment also increased hippocampal 5-HT turnover. Finally, concurrent administration of the 5-HT2 receptor antagonist, ketanserin, blocked the effects of handling on hippocampal type II corticosteroid receptor binding. Taken together with the results of recent in vitro experiments, these data suggest that (a) 5-HT may be involved in the ontogenetic variation in hippocampal type II corticosteroid receptor binding, and (b) that increases in 5-HT activity may mediate the effects of environmental stimulation on hippocampal type II corticosteroid receptor binding.

5,7-Dihydroxytryptamine↗

PubMed1989

Evidence for the involvement of the central adrenergic system in the febrile response induced by interleukin-1 in rats.

We have studied the effect of noradrenaline- and serotonin-depleting agents on the febrile response induced by an intracerebroventricular (i.c.v.) injection of interleukin-1 (IL-1) in rats. Pretreatment with an injection into the lateral ventricle of the catecholamine-depleting agent, 6-hydroxydopamine (6-OHDA), abolished the febrile response induced by IL-1. Injection of 6-OHDA into the ventral noradrenergic ascending bundle (VNAB) did not affect the pyrogenic effect of IL-1. Pretreatment with the serotonin-depleting agent, 5,7-dihydroxytryptamine (5,7-DHT), did not inhibit the febrile response to IL-1. In addition, pretreatment with a beta-adrenergic blocker (propranolol) but not an alpha-adrenergic blocker (yohimbine) attenuated the fever induced by an i.c.v. injection of IL-1. These results suggest that the integrity of the central catecholaminergic system is important in mediating the IL-1-induced fever in rats. The central serotonergic system, as well as noradrenergic neurotransmission at the hypothalamus, do not appear to participate in this endogenous pyrogen-induced febrile response.

5,7-Dihydroxytryptamine↗

PubMed1983

Effect of local 6-OHDA and 5,6-DHT injections into the rat olfactory bulb on neophobia and learned aversion to a novel food.

This study investigated the role of the noradrenergic (NA) and the serotoninergic (5-HT) centrifugal fibers on the olfactory bulb (OB). For this purpose, behavioral responses largely depending on olfactory information were measured in rats after discrete bilateral injections into the OB with either 6-hydroxydopamine (6-OHDA) or 5,6-dihydroxytryptamine (5,6-DHT) solutions. The evaluation of the level of endogenous 5-HT in the OB was measured by high performance liquid chromatography. The NA fibers appeared lesioned after the 6-OHDA treatment only, whereas the 5-HT level was significantly reduced in 5,6-DHT treated bulbs only (34% of the control value). The animals were fed on usual stock-diet (S) and had the choice between S and a novel food (V) on neophobia test, and again on the following day after aversive conditioning (0.9 mEq/kg LiCl i.p.). The behavioral results showed that the drug administrations were followed by a significant effect in one case only: the intake of V was significantly enhanced in 6-OHDA treated animals during neophobia test. Thus, neophobia was reduced by 6-OHDA. The data are interpreted as follows: (1) the lesion of the bulbar NA or 5-HT fibers does not induce total anosmia; and (2) the NA innervation of the OB could play a role in the modulation of behavioral responses to biological odorants.

5,6-Dihydroxytryptamine↗

PubMed1983

Brain 5-hydroxytryptamine and learned resistance to punishment.

Rats can learn to persist in making a response that is punished. Brain 5-hydroxytryptamine (5-HT) systems are known to mediate acute responding to punishment. This work investigates 5-HT involvement in learned resistance to punishment. Forebrain 5-HT was depleted by intracerebral injection of 5,7-dihydroxytryptamine. Lesioned rats were fully able to learn resistance to punishment, although acute responding to punishment was impaired. Forebrain 5-HT does not mediate learned resistance to punishment.

5,7-Dihydroxytryptamine↗

PubMed1984

Brain monoaminergic control of male reproductive behavior. I. Serotonin and the post-ejaculatory refractory period.

The present experiment was performed to examine the role of serotonergic mechanisms in the control of copulation and the post-ejaculatory refractory period in the male rat. Disruption of central serotonergic systems in two separate groups of animals was achieved by: (1) selective electrolytic lesions of the midbrain raphe nuclei, or (2) localized intraventricular or intracerebral injection of a specific serotonergic neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT). A third group of animals was tested for sexual behavior following intraperitoneal injection of p-chlorophenylalanine (PCPA), an inhibitor of serotonin synthesis. Both electrolytic and neurochemical lesions localized in the dorsal raphe nucleus produced a highly significant shortening of the ejaculatory latency, and the post-ejaculatory refractory period. Disruption of serotonergic mechanisms following intraventricular injection of 5,7-DHT or systemic administration of PCPA also caused a significant reduction in the length of the refractory period. These results support the hypothesis that central serotonergic systems are normally inhibitory to certain facets of male copulatory behavior and suggest the existence of a serotonergic control system which normally exerts an inhibitory influence over the resumption of mating following ejaculation.

5,7-Dihydroxytryptamine↗

PubMed1984

Spontaneous and delayed spatial alternation following damage to specific neuronal elements within the nucleus medianus raphe.

Previous studies have shown that rats with electrolytic lesions of the nucleus medianus raphe (MR) show alterations in spontaneous alternation and in the acquisition of a delayed spatial alternation task. The current study was designed to investigate whether these changes are secondary to forebrain serotonin depletion or if they are due to the destruction of MR cells or fibers of passage within the region of the MR. To this end, rats were prepared with either an electrolytic lesion of the nucleus, or were given an intra-MR injection of either the serotonin neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) or the excitotoxin ibotenate. Rats were then tested for the presence of spontaneous alternation in a T-maze, and were subsequently also trained on a contingently-reinforced delayed alternation task. Only the group with electrolytic lesions showed significant response perseveration in the spontaneous alternation task, although both the electrolytic and ibotenate groups were impaired in acquiring the delayed alternation task. Rats with 5,7-DHT injections performed comparable to controls in both tasks despite the fact that forebrain serotonin levels in this group were reduced at least as much as in the other two lesioned groups. These results suggest that these behavioral effects of MR lesions are due to the destruction of non-serotonergic fibers and/or cells within the region of the nucleus.

5,7-Dihydroxytryptamine↗

PubMed1986

Chemical lesions of the nucleus accumbens septi in rats: effects on muricide and apomorphine-induced aggression.

To assess the influence of monoaminergic neurones in the nucleus accumbens septi (NAS) on muricidal and apomorphine-induced aggression, bilateral intraaccumbens injections of relevant neurotoxins were performed. Neurochemical effects in the mesolimbic area (NAS and tuberculi olfactorii) and striatal tissue were investigated using high performance liquid chromatography. 6-Hydroxydopamine (6-OHDA) with desipramine pretreatment significantly decreased mesolimbic dopamine (DA) metabolism, 5,7-dihydroxytryptamine (5,7-DHT) plus desipramine diminished serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA), while DSP-4 depleted noradrenaline (NA), 5-HT, 5-HIAA and tryptophan in the mesolimbic area. No significant biochemical changes were observed in the striatum. Behaviourally, 6-OHDA-treated rats were markedly more aggressive in the apomorphine-induced fighting test. Similarly, DSP-4 injections into the NAS (10 micrograms/1 microliter) enhanced this type of aggression. The 5,7-DHT lesion did not alter apomorphine-induced fighting. None of the neurotoxins induced muricidal behaviour. It is concluded that dopaminergic postsynaptic receptors in the NAS may be involved in the pro-aggressive effect of apomorphine. The results support the hypothesis that NA-containing neurones play an inhibitory role in apomorphine-induced aggression and suggest that such a DA-NA interaction might occur in the NAS.

5,7-Dihydroxytryptamine↗

PubMedDate not supplied

Intra-median raphe infusions of muscimol and the substance P analogue DiMe-C7 produce hyperactivity: role of serotonin neurons.

Injections into the midbrain median raphe nucleus (MR) of the metabolically stable substance P analogue, DiMe-C7, produce dose-dependent increases in locomotor activity (LMA). Ibotenic acid (8.0 micrograms in 2.0 microliter vehicle) lesions of the MR block the hyperkinetic effects of optimal doses of both DiMe-C7 (1.0 microgram in 0.5 microliter vehicle) and the GABAA agonist, muscimol (100 ng in 0.5 microliter vehicle). This observation indicates that the increases in LMA produced by intra-MR DiMe-C7 and muscimol infusion are not due to diffusion to sites outside the MR. Intra-MR administration of the selective serotonin (5-HT) neurotoxin, 5,7-dihydroxytryptamine (6.0 micrograms in 1.5 microliter vehicle), following pretreatment with the norepinephrine and dopamine reuptake inhibitor, nomifensine maleate (15 mg/kg, i.p.), blocked the hyperactivity induced by intra-MR infusions of DiMe-C7 (1.0 microgram) but not that of muscimol (100 ng). These observations suggest that the LMA effects of intra-MR DiMe-C7 and muscimol administration are mediated by different neural mechanisms. The LMA effects of DiMe-C7 depend on intact 5-HT neurons in the MR, whereas the effects of muscimol depend on intact non-5-HT MR cells.

5,7-Dihydroxytryptamine↗

PubMed1988

Selective increase of offensive behavior in the rat following intrahypothalamic 5,7-DHT-induced serotonin depletion.

Cerebral serotonin (5-HT) depletions usually increase aggressive behaviors and more specifically facilitate elicitation of offensive behaviors. In order to localize the brain structures involved in this effect, 5,7-dihydroxytryptamine (5,7-DHT), a neurotoxin of 5-HT neurons, was injected into the ascending serotonergic pathway within the lateral hypothalamus, thus depleting 5-HT only in the forebrain structures. The effects of such treatment on offensive and defensive as well as social and non-social behaviors were studied in resident rats confronted with untreated intruders. Pretreatment with desipramine protected noradrenergic neurons. The content of 5-HT fell to 25% of controls, whereas noradrenaline was maintained at 90% in the forebrain anterior to the injection site. Ethological analysis of both resident's and intruder's behavior showed that offensive items were increased in 5,7-DHT-treated residents, whereas defensive items were increased in their non-treated partners; non-social activities were unchanged. Control of mouse-killing behavior during a 2-h test in the same animals showed a clear increase in elicitation of killing in 5,7-DHT-injected rats. These results confirm that the inhibitory control of serotonin is exerted specifically on offensive aggression. They suggest that forebrain structures are involved in this control.

5,7-Dihydroxytryptamine↗

PubMed1994

Specific destruction of the serotonergic afferents to the suprachiasmatic nuclei prevents triazolam-induced phase advances of hamster activity rhythms.

Administration of Triazolam (Tz)--a short acting benzodiazepine (BZ)--induces permanent phase-shifts in locomotor activity of golden hamsters (Mesocricetus auratus). However, the target area(s) as well as the mechanism involved in the Tz-induced changes are not known. Previous results indicated that raphe nuclei (RN) would appear to be a likely site for Tz-induced phase shifts. Therefore, we specifically destroyed the 5-HT fibers connecting the RN with the SCN--the site of the endogenous mammalian clock--by microinjections of the selective neurotoxin 5,7 dihydroxytryptamine (5,7-DHT) at the level of SCN. Infusion of 5,7-DHT resulted in long lasting damage of the ascending serotonergic projection from RN to the hypothalamus. Subsequently, the phase-shifting effect of Tz was investigated. Only complete or almost complete depletion of the 5-HT input to the SCN was accompanied with a pronounced reduction of the phase shift together with a significant reduction of wheel-running activity during the 6 h following Tz injection. Our present results support the view that the 5-HT innervation of the SCN represents an essential link in the phase-shifting action following peripheral Tz injections.

5,7-Dihydroxytryptamine↗

PubMed1995

Probable involvement of serotonin in the increased permeability of the blood-brain barrier by forced swimming. An experimental study using Evans blue and 131I-sodium tracers in the rat.

The possibility that endogenous serotonin (5-hydroxytryptamine, 5-HT) participates in alteration of the blood-brain barrier (BBB) following short-term forced swimming (FS) exercise was examined in a rat model. Subjection of conscious young (age 8-9 weeks, 80-90 g) animals to continuous FS (at a water temperature of 30 +/- 1 degrees C) for 30 min, increased the permeability of the BBB to Evans blue albumin (EBA) and 131I-sodium in six and nine brain regions, respectively. The EBA staining was noted in posterior cingulate cortex, parietal, occipital cortices, cerebellar vermis, medial lateral cerebellar cortices and dorsal surface of hippocampus. In addition to these brain regions, the BBB permeability to 131I-sodium was further extended to caudate nucleus, thalamus and hypothalamus. This effect of FS on the BBB permeability was absent in adult (age 24-30 weeks, 300-400 g) animals. Measurement of 5-HT showed a profound increase of plasma and brain in young rats by 180% and 250%, respectively, from the control group. Adult animals showed only a minor increase in brain and plasma 5-HT levels. In young animals, pretreatment with p-CPA (a 5-HT synthesis inhibitor) and indomethacin (a prostaglandin synthesis inhibitor) prevented the FS induced increase in BBB permeability and 5-HT levels. Destruction of serotonergic neurons with 5,7-dihydroxytryptamine (5,7-DHT) reduced the breakdown of the BBB and attenuated the brain 5-HT level without affecting the plasma 5-HT. Cyproheptadine, ketanserin (5-HT2 receptor antagonists) and vinblastine (a vesicular transport inhibitor) prevented the increased permeability of the BBB alone. The plasma and brain 5-HT continued to remain high. These observations suggest that (i) 5-HT plays an important role in the breakdown of BBB permeability in FS, (ii) this effect of 5-HT on BBB permeability is mediated by 5-HT2 receptors, and (iii) FS induced increase in BBB permeability is age dependent.

5,7-Dihydroxytryptamine↗

PubMed1985

Up-regulation of thyrotropin-releasing hormone (TRH) receptors in rat spinal cord after codepletion of serotonin and TRH.

Immunohistochemical evidence indicates the coexistence of serotonin and TRH in many raphe neurons. We examined the biochemical changes in TRH receptors after destruction of the serotonergic pathways by 5,7-dihydroxytryptamine (5,7-DHT). 2 weeks after an intracerebroventricular injection of 5,7-DHT, rats were killed, and specific brain regions were dissected on ice. Serotonin levels in the CNS of lesioned rats was reduced by 50-85% in all regions, with the highest reduction in the spinal cord and hippocampus. Immunoreactive TRH was reduced in the spinal cord by 70%, but other brain regions contained normal levels of TRH. TRH receptor binding was increased by 40% in the spinal cord of lesioned rats, but appeared unchanged in rostral brain regions in which no decrease in TRH content was detected. Scatchard plots of TRH receptor binding in the spinal cord indicated that the increased binding after 5,7-DHT administration reflected an increased receptor number. These findings suggest that biochemical up-regulation of TRH receptors occurs in the spinal cord following depletion of TRH.

5,7-Dihydroxytryptamine↗

PubMed1985

The role of vagal afferents and carbon dioxide in the respiratory response to thyrotropin-releasing hormone.

Rats treated neonatally with pargyline and 5,7-dihydroxytryptamine to decrease central serotonin-containing neurons have an accentuated respiratory response to i.c.v. thyrotropin-releasing hormone (TRH). Since these treated rats also evidence an elevated PaCO2, we sought to evaluate the importance of CO2 in determining the magnitude of the respiratory response to TRH. Neonatal treatment with capsaicin or acute vagotomy also produced adult animals whose basal PaCO2 was elevated and whose respiratory response to TRH was greater than that seen in control rats with lower PaCO2 values. In normal rats, however, administration of CO2 immediately before and after TRH administration does not alter the subsequent response to TRH. Thus, it appears that TRH facilitates the processing of CO2-dependent afferent impulses, and that CO2 does not alter disposition or pharmacokinetics of TRH.

5,7-Dihydroxytryptamine↗

PubMed1988

Studies on the physiological role and mechanism of action of neuropeptide Y in the regulation of luteinizing hormone secretion in the rat.

It has been recently shown that intraventricular or systemic injection of neuropeptide Y (NPY) can produce a decrease in plasma luteinizing hormone (LH) levels in castrated rats of both sexes. In order to evaluate the physiological role of NPY in the regulation of LH secretion in the female rat, we proceeded to immunoneutralization experiments using specific antibodies to NPY. Injection of 0.5 ml antiserum to NPY produce a 20-fold increase of LH plasma levels, whereas injection of preimmune serum did not modify the plasma concentrations of LH. To investigate the possibility that catecholamines or serotonin might be involved in the effect of NPY in LH secretion, castrated rats were treated with alpha-methylparatyrosine (alpha-MPT), an inhibitor of catecholamine biosynthesis, or received an i.c.v. injection of the neurotoxin 5-7-dihydroxytryptamine (5,7-DHT) prior to the intraventricular injections of NPY. The pretreatment with alpha-MPT could not prevent the decrease of plasma LH induced by NPY injection whereas the pretreatment with 5,7-DHT reversed the effect of NPY injection. The anatomical connection between LH-releasing hormone (LHRH) and NPY neuronal systems were also investigated using double immunostaining technique. It appeared that NPY endings are in apposition to LHRH cell bodies in the preoptic area in proximity to the organum vasculosum of the lamina terminalis (OVLT).(ABSTRACT TRUNCATED AT 250 WORDS)

5,7-Dihydroxytryptamine↗

PubMed1996

Dual effect of serotonin on formalin-induced nociception in the rat spinal cord.

To examine the role of the descending serotonergic system in the regulation of spinal nociceptive processing, the effects of serotonin (5-HT) and selective ligands for 5-HT receptor subtypes on persistent nociception were investigated. Formalin (5% formaldehyde) injected into the plantar region of the rat hindpaw induced two phases of aversive responses such as licking and biting. Intrathecal administration of selective 5-HT3 receptor antagonists, granisetron (0.1-100 pmol/rat) and ondansetron (1-1000 pmol/rat), reduced the second phase of the formalin-induced aversive responses without affecting the first one. The antinociceptive effect of granisetron (100 pmol/rat) was abolished when 5-HT was depleted from the lumbar cord by pretreatment with 5,7-dihydroxytryptamine (5,7-DHT). In the 5,7-DHT-treated rats, intrathecal administration of 1-(m-chlorophenyl)-biguanide, a selective 5-HT3 receptor agonist, facilitated the aversive responses in the second phase whereas that of 8-OH-DPAT, a selective 5-HT1A receptor agonist, suppressed them. Intrathecal administration of 5-HT showed a dual effect on the second phase of the aversive responses in the 5,7-DHT-treated rats; 5-HT inhibited the aversive responses when administered at a low dose (0.1 nmol/rat) but facilitated them at a high dose (1 nmol/rat). In addition, the inhibitory and facilitatory effects of intrathecal 5-HT were blocked by its co-administration with NAN190, a 5-HT1A receptor antagonist, and granisetron, respectively. These results suggest that 5-HT suppresses formalin-induced nociception in the spinal cord via the 5-HT1A receptor and facilitates it via the 5-HT3 receptor.

5,7-Dihydroxytryptamine↗

PubMed1988

Regulation of striatal prodynorphin mRNA levels by the raphe-striatal pathway.

Peptides derived from proenkephalin and prodynorphin are known to be located in striatal projection neurones. Anatomical studies have shown the presence of a major serotonergic projection from the dorsal raphe nucleus to the striatum, although the function of this pathway is unknown. We have used in situ nucleic acid hybridization to investigate a possible role of this serotonergic innervation in the regulation of striatal opioid gene expression. The levels of proenkephalin mRNA and prodynorphin mRNA were determined in rat striatum and nucleus accumbens. Destruction of the dorsal raphe nucleus by microinjection of 5,7-dihydroxytryptamine failed to affect the levels of proenkephalin mRNA in any region. However, the levels of prodynorphin mRNA were significantly reduced in the medial nucleus accumbens and caudomedial striatum. This implies that activity in the raphe-striatal serotonin pathway mediates a tonic and selective enhancement of prodynorphin gene expression in the striatal target cells. This is in contrast to the tonic suppression of proenkephalin gene expression mediated by the mesostriatal dopamine pathway.

5,7-Dihydroxytryptamine↗