SEARCH · PubMed Health

Results for “Dihydroxytryptamines”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,045 records · Page 58Linked to original sources

PubMed1998

Cocaine and fluoxetine induce the expression of the hVH-5 gene encoding a MAP kinase phosphatase.

A novel class of immediate early genes that encode enzymes of the MAP kinase phosphatase family has recently been described. These enzymes are dual-specificity protein phosphatases and some show tissue-specific distribution, like the hVH-5 gene (homologue of vaccinia virus H1 phosphatase gene clone 5), which is expressed predominantly in the adult brain. In this paper, we investigated whether the hVH-5 gene is induced by psychostimulants in rat brain, as has been demonstrated for immediate early genes encoding transcription factors. Using in situ hybridization, we found that i.p. injection of cocaine, amphetamine and caffeine induced hVH-5 mRNA expression within 40 min in the nucleus accumbens (NAc), caudate putamen, frontal cortex and hippocampus, with a maximal effect in the NAc. The cocaine-induced hVH-5 gene induction involves the serotonergic system, since it was abolished in the NAc by lesioning serotonergic raphé projections with 5,7-dihydroxytryptamine. Moreover, the effect of cocaine was fully mimicked by the selective serotonin uptake inhibitor fluoxetine. In contrast to what has been described for c-fos and egr-1 immediate early genes, we found that hVH-5 mRNA expression in the NAc and hippocampus was as significant after repeated cocaine injections for 10 days as after a single injection. The considerable and prolonged induction of the MAP kinase phosphatase hVH-5 gene by psychostimulant drugs in postmitotic brain cells, particularly in the NAc, could indicate that MAP kinase substrates are involved in the reinforcing properties of drugs of abuse.

5,7-Dihydroxytryptamine↗

PubMed2002

Anxiogenic effect of median raphe nucleus lesion in stressed rats.

Serotonin (5-HT) neurons located in the median raphe nucleus (MRN) may have a role in the development of behavioral changes to stress. The objective of the present work was to investigate the effects of a selective lesion of 5-HT neurons located in the MRN in previously stressed male Wistar rats submitted to the elevated plus maze (EPM). In an initial experiment, the animals (n=20-22) were submitted to one (acute) or seven (chronic) daily restraint stress periods (2 h) and tested in the EPM 24 h later. Results showed that acute restraint caused a significant decrease in the number of entries into the open arms, as compared to nonstressed controls. This effect disappeared when the animals were submitted to chronic restraint. In the next set of experiments, animals (n=6-8) received, 1 week before the behavioral studies, intra-MRN injection of 5,7-dihydroxytryptamine (5,7-DHT; 8 microg/1 microl). Neurochemical analysis showed that this treatment significantly decreases 5-HT and 5-hydroxy-indoleacetic acid (5-HIAA) levels in the hippocampus, but not in the striatum. No difference between lesioned and sham-operated animals in EPM performance was found in nonstressed animals or in those submitted to acute restraint. In chronically restrained animals, however, lesioned rats showed a significant decrease in the number of entries and time spent in the open arms. These results suggest that lesions of 5-HT neurons located in the MRN cause anxiogenic-like behavior in animals that have been chronically restrained.

5,7-Dihydroxytryptamine↗

PubMed2003

The serotonergic modulation of synaptic plasticity in the rat hippocampo-medial prefrontal cortex pathway.

The ability of the serotonergic (5-HTergic) system to affect the hippocampo-medial prefrontal cortex (mPFC) synaptic properties was examined in rats with lesions of 5-HTergic neurons. Intracerebroventricular injections of 5,7-dihydroxytryptamine (5,7-DHT) resulted in selective depletion of 5-HT and 5-hydroxyindoleacetic acid in the cerebral cortex, hippocampus and raphe regions. The 5,7-DHT-lesioned rat had no changes in basal synaptic transmission in the hippocampo-mPFC pathway. Conversely, we observed the augmentation of short-term synaptic plasticity, i.e. paired-pulse facilitation, when compared with sham-operated rats in this pathway. The magnitude of long-term potentiation (LTP) was significantly augmented in 5,7-DHT-lesioned rats. This augmentation of hippocampo-mPFC LTP had a significant correlation with the degree of cortical 5-HT levels. These results suggest that the 5-HTergic system may modulate plastic properties at the hippocampal-mPFC synapses in vivo.

5,7-Dihydroxytryptamine↗

PubMed1985

The effect of adrenalectomy and corticosterone on homotypic collateral sprouting of serotonergic fibers in hippocampus.

Lesioning of serotonergic (5-HT) fibers using 5,7-dihydroxytryptamine (5,7-DHT) in one of the two median raphe-hippocampal pathways induced homotypic sprouting from the other. We have utilized this model with the horseradish peroxidase (HRP) tracing technique to test the effects of an adrenal corticosteroid-corticosterone on homotypic sprouting in female adult rats. Removal of the adrenal glands does not interfere with the 5,7-DHT destruction of 5-HT fibers observed at 3 days. However, the animals without circulating adrenal steroids do not show the increase of the HRP-labeled cells normally seen 21 days after the 5,7-DHT lesions. Furthermore, s.c. implantation of corticosterone pellets was able to completely restore homotypic sprouting of 5-HT fibers in the hippocampus.

5,7-Dihydroxytryptamine↗

PubMed1999

Suppression of serotonin hyperinnervation does not alter the dysregulatory influences of dopamine depletion on striatal neuropeptide gene expression in rodent neonates.

Sixty days following neonatal dopamine depletion (>98%) with 6-hydroxydopamine, preprotachykinin and preprodynorphin mRNA levels were significantly reduced (67 and 78% of vehicle controls, respectively) in the anterior striatum as determined by in situ hybridization while preproenkephalin mRNA expression was elevated (133% of vehicle controls). Suppression of the serotonin hyperinnervation phenomenon in the dopamine-depleted rat with 5,7-dihydroxytryptamine yielded no significant alterations in reduced striatal preprotachykinin (66%) or preprodynorphin (64%) mRNA levels, while preproenkephalin mRNA expression remained significantly elevated (140%). These data suggest that striatal serotonin hyperinnervation does not contribute to the development of dysregulated striatal neuropeptide transmission in either direct or indirect striatal output pathways following neonatal dopamine depletion.

5,7-Dihydroxytryptamine↗

PubMed1999

Organization of the corticotectal projection in hamsters with neonatally elevated levels of serotonin in the superior colliculus.

A previous study from this laboratory showed that elevated serotonin (5-HT) levels in the hamsters superior colliculus (SC), induced by a single subcutaneous injection of 5,7-dihydroxytryptamine (5,7-DHT) at birth, resulted in an abnormally widespread distribution of the uncrossed retinotectal projection. The present study investigated whether the corticotectal projection in such animals was altered. Adult normal and 5,7-DHT-treated hamsters were injected with horseradish peroxidase (HRP) into occipital cortex and processed for anterograde tracing of corticotectal terminals in the SC. Quantitative analysis showed that normal and 5,7-DHT-treated hamsters were not significantly different in total labeling or in the gradient of labeling density within the SC. These data indicate that corticotectal axons achieve normal terminal fields after neonatal elevation of 5-HT in the SC.

5,7-Dihydroxytryptamine↗

PubMed1999

Nucleus reticularis gigantocellularis and nucleus raphe magnus in the brain stem exert opposite effects on behavioral hyperalgesia and spinal Fos protein expression after peripheral inflammation.

Previous findings indicate that the brain stem descending system becomes more active in modulating spinal nociceptive processes during the development of persistent pain. The present study further identified the supraspinal sites that mediate enhanced descending modulation of behavior hyperalgesia and dorsal horn hyperexcitability (as measured by Fos-like immunoreactivity) produced by subcutaneous complete Freund's adjuvant (CFA). Selective chemical lesions were produced in the nucleus raphe magnus (NRM), the nuclei reticularis gigantocellularis (NGC), or the locus coeruleus/subcoeruleus (LC/SC). Compared to vehicle-injected animals with injection of vehicle alone, microinjection of a serotoninergic neurotoxin 5,7-dihydroxytryptamine into the NRM significantly increased thermal hyperalgesia and Fos protein expression in lumbar spinal cord after hindpaw inflammation. In contrast, the selective bilateral destruction of the NGC with a soma-selective excitotoxic neurotoxin, ibotenic acid, led to an attenuation of hyperalgesia and a reduction of inflammation-induced spinal Fos expression. Furthermore, if the NGC lesion was extended to involve the NRM, the behavioral hyperalgesia and CFA-induced Fos expression were similar to that in vehicle-injected rats. Bilateral LC/SC lesions were produced by microinjections of a noradrenergic neurotoxin, DSP-4. There was a significant increase in inflammation-induced spinal Fos expression, especially in the ipsilateral superficial dorsal horn following LC/SC lesions. These results demonstrated that multiple specific brain stem sites are involved in descending modulation of inflammatory hyperalgesia. Both NRM and LC/SC descending pathways are major sources of enhanced inhibitory modulation in inflamed animals. The persistent hyperalgesia and neuronal hyperexcitability may be mediated in part by a descending pain facilitatory system involving NGC. Thus, the intensity of perceived pain and hyperalgesia is fine-tuned by descending pathways. The imbalance of these modulating systems may be one mechanism underlying variability in acute and chronic pain conditions.

5,6-Dihydroxytryptamine↗

PubMed1999

Pharmacological characteristics and regulation of 5-HT receptor-stimulated phosphoinositide hydrolysis in the rat spinal cord.

In slices from immature rat spinal cord, both 5-hydroxytryptamine (5-HT) and the 5-HT2A/C receptor agonists (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) and alpha-methyl-5-HT (alpha-Me-5-HT) stimulate phosphoinositide (PI) hydrolysis. PI breakdown is also increased by the 5-HT3 receptor agonist 2-Me-5-HT but not by phenylbiguanide. The effect of either 5-HT or DOI is blocked by selective 5-HT2A receptor antagonists such as spiperone and ketanserin and more markedly by mixed 5-HT2 receptor antagonists, such as ritanserin, methysergide and mesulergine, with higher affinity at the 2C subtype. The effect of 2-Me-5-HT is blocked by 5-HT2 and not by 5-HT3 receptor antagonists, indicating that 5-HT3 receptors do not directly or indirectly take part in PI hydrolysis in the spinal cord. Moreover, lesion with neonatal capsaicin of thin primary afferents to the dorsal spinal cord enhances inositol phosphate formation stimulated by 5-HT or DOI but not by 2-Me-5-HT. This lesion also increases 5-HT2A and 5-HT2C receptor density. After neonatal injection of 5,7-dihydroxytryptamine, which results in a marked loss of 5-HT content in the cord, 5-HT and 5-HT2 receptor agonists also enhance PI breakdown without a concomitant change in receptor number. The results suggest that the 5-HT-stimulated PI response in the rat spinal cord is associated only with the 5-HT2 receptor class, in particular with the 5-HT2C subtype.

5,7-Dihydroxytryptamine↗

PubMed2000

Repeated electroconvulsive shock promotes the sprouting of serotonergic axons in the lesioned rat hippocampus.

This study reports the effect of repeated electroconvulsive shock on the sprouting of 5-hydroxytryptamine neurons in the partly lesioned rat dorsal hippocampus. We have adopted a 5-hydroxytryptamine homotypic collateral sprouting model to examine whether electroconvulsive shock administration altered the rate of 5-hydroxytryptamine axonal reinnervation of the dorsal hippocampus. The 5-hydroxytryptamine innervation of hippocampus originates from the median raphe via the cingulum bundle and the fimbria-fornix. Lesioning of the cingulum bundle has previously been shown to cause sprouting of intact 5-hydroxytryptamine afferents originating from the unharmed fimbria-fornix. Rats were unilaterally injected with the 5-hydroxytryptamine neurotoxin, 5,7-dihydroxytryptamine, into the right cingulum bundle and 5-hydroxytryptamine immunoreactivity in the dorsal hippocampus was investigated 1, 3, 6 and 12weeks after the injection. The lowest level of 5-hydroxytryptamine-immunoreactivity in the hippocampus was detected at three weeks after the lesion. At six weeks, 5-hydroxytryptamine immunoreactive fibres started to reappear, and at 12weeks the level of 5-hydroxytryptamine immunoreactivity was similar to that observed on the unlesioned side. Based on this time-course, six weeks was chosen as the time-point to investigate the action of a course of repeated electroconvulsive shock administrations. Repeated electroconvulsive shock (five shocks over 10days) doubled the number of sprouting 5-hydroxytryptamine-immunoreactive fibres and significantly increased levels of the 5-hydroxytryptamine metabolite, 5-hydroxyindoleacetic acid. The present data provide the first direct evidence that electroconvulsive shock enhances 5-hydroxytryptamine axon sprouting in the partly lesioned hippocampus. This is an effect which may contribute to the therapeutic effect of electroconvulsive therapy in major depression.

5,7-Dihydroxytryptamine↗

PubMed2001

Reorganization of the corticotectal projections introduced by neonatal monocular enucleation in the Monodelphis opossum and the influence of serotoninergic depletion.

The influence of neonatal serotoninergic lesion (performed with s.c. injection of 5,7-dihydroxytryptamine) on the plasticity of the developing corticotectal projection was studied in the gray short-tailed opossum (Monodelphis domestica). As a first step, the placement and density of neurons projecting from the visual cortical areas to the superior colliculus was established in the adult opossum. Injections of retrogradely transported fluorescent dyes into the superior colliculus of intact three-month-old animals labeled neurons of cortical layer V. In this species, there are three visual areas: the striate area and two secondary areas, the laterally placed peristriate area and the medial visual area. The population of the labeled neurons was denser in peristriate and medial visual areas than in the striate area. Secondly, the influence of neonatal monocular enucleation on the extent of this projection was investigated, alone or in combination with a serotoninergic lesion. Injection of dyes into the superior colliculi of three-month-old animals that were unilaterally enucleated on the second postnatal day also labeled neurons of cortical layer V. However, the density of the cortical neurons projecting to the superior colliculus contralateral to the remaining eye was much lower. This reduction was most profound in the striate visual area. No significant modifications of this projection were found on the side ipsilateral to the remaining eye. In another group of opossums, unilateral enucleation on the second postnatal day was combined with serotoninergic lesion. Brains of some of the treated pups were immunostained for serotonin on the fifth postnatal day. At this age, 70-80% of serotoninergic axons in the brain were missing. However, in about three weeks these axons had regrown, and their density in the neocortex was approximately the same as in the control animals. We conclude that severe reduction of the serotoninergic innervation during the early postnatal period did not influence the plastic changes induced in the corticotectal projection by unilateral enucleation.

5,7-Dihydroxytryptamine↗

PubMed1999

Regulation of the transmitter phenotype of rostral and caudal groups of cultured serotonergic raphe neurons.

We have studied the regulation of survival and serotonergic markers by neurotrophins and several trophically active cytokines in neurons cultured from the embryonic rat raphe region under defined conditions. At embryonic day 14, saturating concentrations of brain-derived neurotrophic factor, neurotrophin-3, neurotrophin-4 and basic fibroblast growth factor elicited a two- to 2.5-fold increase in numbers of tryptophan hydroxylase- and serotonin-immunoreactive neurons over a four-day culture period. Transforming growth factor beta-1 and glial cell line-derived neurotrophic factor were less potent, while fibroblast growth factor-5 was only marginally effective. Distinct responses to different factors were noted depending on embryonic age and regional origin of serotonergic neurons. Thus, brain-derived neurotrophic factor augmented numbers of tryptophan hydroxylase-positive neurons at embryonic day 16 by a factor of seven, but only 1.5- to two-fold when cultures were established from day 13 or 14 embryos. In cultures of rostral serotonergic groups (B4-B9), numbers of tryptophan hydroxylase-positive neurons decreased in the absence of factors, whereas numbers of tryptophan hydroxylase-immunoreactive neurons in cultures from caudal serotonergic groups (B1-B3) increased during a 12-day culture period. There was no evidence that serotonergic neurons undergo apoptosis (as visualized by terminal deoxynucleotidyl transferase dUTP nick end labeling) or proliferate (as visualized by 5-bromodeoxyuridine incorporation) in culture. Numbers of serotonergic neurons also increased when cultures were treated with a brief 24-h pulse of brain-derived neurotrophic factor, supporting the notion that changes in numbers of serotonergic neurons reflected alterations of phenotype rather than cell death or proliferation. The ability of cells to specifically take up the serotonin analog 5,7-dihydroxytryptamine was also up-regulated by brain-derived neurotrophic factor in both rostral and caudal raphe cultures. Lability of the serotonergic phenotype was further suggested by the observation that ciliary neurotrophic factor fully prevented the brain-derived neurotrophic factor-mediated increase in tryptophan hydroxylase-positive neurons. The effect of ciliary neurotrophic factor was dependent on the presence of astrocytes. We conclude that serotonergic neurons show spatially and temporally distinct responses to neurotrophic factors, which seem to have a profound influence of the transmitter phenotype rather than on survival.

5,7-Dihydroxytryptamine↗

PubMed2000

c-fos expression, behavioural, endocrine and autonomic responses to acute social stress in male rats after chronic restraint: modulation by serotonin.

The effects in male rats of serotonin depletion (using the neurotoxin 5,7-dihydroxytryptamine) on the cross-sensitization of an acute social stress (defeat by a larger resident male) by previous repeated restraint stress (10 days, 60 min per day) was studied. Previous restraint increased freezing responses during social defeat in sham-operated rats, but this was not observed in those with depleted serotonin (83% or more in different regions of the brain). In contrast, neither heart rate (tachycardia) nor core temperature responses (hyperthermia) were accentuated in previously restrained rats (i.e. neither showed heterotypical sensitization), and neither adapted to repeated restraint (there is a hypothermic core temperature response during restraint). Corticosterone levels, which did adapt, nevertheless did not show accentuated responses to social defeat in previously restrained rats, though samples could only be taken 60 min after defeat. c-fos expression in the central nucleus of the amygdala 60 min after social defeat was increased by previous restraint. No other areas examined in the hypothalamus (e.g., paraventricular nucleus) or brainstem (e.g., solitary nucleus) showed differences related to previous restraint. Serotonin depletion reduced the expression of c-fos in the frontal cortex, lateral preoptic area, medial amygdala, central gray, medial and dorsal raphe, and locus coeruleus after social stress, but this was not altered by previous restraint. These results show that serotonin depletion has selective effects on the cross-sensitization of responses in previously stressed rats to a heterotypical stressor.

5,7-Dihydroxytryptamine↗

PubMed2002

Dual 5-HT mechanisms in basolateral and central nuclei of amygdala in the regulation of the defensive behavior induced by electrical stimulation of the inferior colliculus.

Regulatory mechanisms in the basolateral nucleus of the amygdala (BLA) serves as a filter for unconditioned and conditioned aversive information that ascend to higher structures from the brainstem whereas the central nucleus (CeA) is the main output for the resultant defense reaction. We have shown that neural substrates in the inferior colliculus are activated by threatening stimuli of acoustic nature and have important functional links with the amygdala. In this work, we examined the influence of lesions with 5,7-dihydroxytryptamine (5,7-DHT) of these nuclei of amygdala on the aversive responses induced by electrical stimulation of the inferior colliculus. Thus, rats were implanted with an electrode in the CeA of the inferior colliculus for the determination of the thresholds of alertness, freezing and escape responses. Each rat also bore a cannula implanted in the BLA or CeA for injection of 5,7-DHT (8.0 microg/0.8 microl) or its vehicle. The data obtained show that CeA lesions increase the thresholds of aversive responses whereas BLA lesions decrease the thresholds of these responses. From this evidence it is suggested that defensive behavior induced by activation of the neural substrates of aversion in the inferior colliculus seems to depend on the integrity of the amygdala. BLA regulates the input and CeA functions as the output for these aversive states generated at brainstem level. It is likely that aversive information ascending from the inferior colliculus may receive either inhibitory or excitatory influences of 5-HT mechanisms in the BLA or CeA, respectively.

5,7-Dihydroxytryptamine↗

PubMed2003

Neurotransmitter release and its presynaptic modulation in the rat hippocampus after selective damage to cholinergic or/and serotonergic afferents.

UNLABELLED: Male Long-Evans rats sustained injections of 5,7-dihydroxytryptamine (5,7-DHT) into the fimbria-fornix and the cingular bundle or/and intraseptal injections of 192 IgG-saporin to induce serotonergic or/and cholinergic hippocampal denervations; Sham-operated rats served as controls. Four to ten weeks after lesioning, we measured (i). the electrically evoked release of acetylcholine ([3H]ACh), noradrenaline ([3H]NA) and serotonin ([3H]5-HT) in hippocampal slices in the presence of drugs acting on auto- or heteroreceptors, (ii). the nicotine-evoked release of NA and (iii). the choline acetyltransferase (ChAT) activity and the concentration of monoamines in homogenates. Saporin lesions reduced the accumulation of [3H]choline, the release of [3H]ACh and the ChAT activity, but increased the concentration of NA and facilitated the release of [3H]NA evoked by nicotine. 5,7-DHT lesions reduced the accumulation and the release of [3H]5-HT, the concentration of 5-HT, and also facilitated the release of [3H]NA evoked by nicotine. Accumulation and electrically evoked release of [3H]NA were not altered by either lesion. The combination of both toxins resulted in an addition of their particular effects. The 5-HT(1B) receptor agonist, CP 93129, and the muscarinic agonist, oxotremorine, reduced the release of [3H]ACh in control and 5,7-DHT-lesioned rats; in rats injected with saporin, their effects could not be measured reliably. CP 93129 and the alpha(2)-adrenoceptor agonist, UK 14304, reduced the release of [3H]5-HT in all groups by about 65%. IN CONCLUSION: (i). selective neurotoxins can be combined to enable controlled and selective damage of hippocampal transmitter systems; (ii). 5-HT exerts an inhibitory influence on the nicotine-evoked release of NA, but partial serotonergic lesions do not influence the release of ACh at a presynaptic level and (iii). presynaptic modulatory mechanisms involving auto- and heteroreceptors may be conserved on fibres spared by the lesions.

5,7-Dihydroxytryptamine↗

PubMed1999

Plasticity of 5-hydroxytryptamine(1B) receptors during postnatal development in the rat visual cortex.

The distribution of 5-hydroxytryptamine1A and 5-hydroxytryptamine1B receptors in the visual cortex was studied by quantitative autoradiography during postnatal development. Overall, receptor densities increased throughout development, but exhibited regional rearrangements, particularly in the case of 5-hydroxytryptamine1B receptors. Neonatal treatment with 5,7-dihydroxytryptamine, which causes selective degeneration of serotoninergic neurons, had no effect on the density of 5-hydroxytryptamine1A receptors in the visual cortex. However, a transient increase in 5-hydroxytryptamine1B at postnatal days 10-12 was observed after this treatment, suggesting a regulation of postsynaptic receptors. Neonatal enucleation resulted in a marked increase in 5-hydroxytryptamine1B binding sites in all layers of the visual cortex by P16, whereas it had no effect upon 5-hydroxytryptamine1A binding sites. These results show that both receptor subtypes do not exhibit striking transient features in the visual cortex during postnatal development, but rather undergo discrete reorganizations. 5-Hydroxytryptamine1B receptors show changes in density after either neonatal degeneration of serotoninergic neurons or enucleation, indicating that the serotoninergic system involving this receptor subtype can exhibit some postnatal plasticity in the visual cortex.

5,7-Dihydroxytryptamine↗

PubMedDate not supplied

Centrifugal innervation of the rat retina.

Centrifugal fibers innervating the retina have been shown in all classes of vertebrate, except for mammals where conventional tract-tracing methods have not been able to unmistakably demonstrate their existence. In a previous study, a unilateral, intravitreal injection of 5,7-dihydroxytryptamine was used to reveal indoleamine-accumulating centrifugal fibers which were visualized by an immunoreaction against serotonin. In the present study, I employed a modification of this method to stain retinopetal neurons in the rat. Terminals were located preferentially in the outer retina; labeled fibers could be traced back along an ipsilateral pathway to somata in the dorso-caudal portions of the chiasm or the medio-lateral preoptic area, and thence towards the suprachiasmatic nuclei. The unique beaded appearance of the fibers distinguishes them from retinal ganglion cell axons. The labeling of central cell bodies strongly suggests that they possess terminals in the retina. Thus, at least some mammalian retinas receive centrifugal innervation. This indoleamine-accumulating retinopetal pathway may be involved in retinal melatonin synthesis, coordination of circadian rhythms, and interocular phenomena.

5,7-Dihydroxytryptamine↗

PubMedDate not supplied

Serotonin synthesis and accumulation by neurons of the anuran retina.

Serotonin-synthesizing and serotonin-accumulating neurons were studied in the retinas of Xenopus laevis and Bufo marinus. All previously identified cell types exhibiting serotonin-like immunoreactivity (SLI) were labeled by intravitreal injection of 5,7-dihydroxytryptamine (5,7-DHT). They included two amacrine cell types (large and small) in both species, and one bipolar cell type in Xenopus. Incubation of retinas in culture medium in the ambient light reduced SLI in amacrine cells and enhanced the labeling in bipolar cells. After incubation, some photoreceptor cell bodies and large numbers of outer segments also displayed SLI in both species. Incubation with the serotonin-uptake inhibitor, fluoxetine, reduced immunolabeling in bipolar cells and outer segments to the level in the untreated retinas. Both large SLI and 5,7-DHT-accumulating amacrine cells in Xenopus and Bufo were labeled with an antibody raised against phenylalanine hydroxylase (PH), which binds to tryptophan 5-hydroxylase, one of the synthesizing enzymes for serotonin. Small SLI and 5,7-DHT-accumulating amacrine cells in both species represented two populations, one with and the other without PH-like immunoreactivity (PH-LI). The anti-PH antibody failed to label any SLI or 5,7-DHT-accumulating bipolar cells in Xenopus. These observations indicate that all large and some small SLI amacrine cells in the retinas of Xenopus and Bufo synthesize serotonin, while other small SLI amacrine, bipolar and photoreceptor cell bodies, and outer segments only accumulate serotonin.

5,7-Dihydroxytryptamine↗

PubMedDate not supplied

Increased serotonin in the developing superior colliculus affects receptive-field size of retinotectal afferents but not that of postsynaptic neurons.

Administration of a single subcutaneous dose of 5,7-dihydroxytryptamine (5,7-DHT) to newborn hamsters results in a significant increase in the density of serotoninergic (5-HT) fibers in the superficial layers of the superior colliculus (SC) and marked abnormalities in the uncrossed retinotectal projection when these animals reach adulthood (Rhoades et al., 1993). The present study was undertaken to determine whether elevation of 5-HT in the developing SC altered the visual representation in SC. Multi-unit recordings from SC cells demonstrated that the overall organization of the visual map in the superficial SC laminae was normal and that the receptive-field sizes for unit clusters were unchanged in the 5,7-DHT-treated animals. However, when a combination of CNQX and MK-801 was directly applied to the SC to block postsynaptic activity, the receptive fields of unit clusters (presumably retinotectal axon terminals) in the 5,7-DHT treated animals were significantly larger than those in the normally reared hamsters. These results are consistent with the conclusions that elevation of 5-HT levels in the developing SC reduces the postnatal refinement of the crossed retinotectal axons, and that mechanisms operating within the SC may act to maintain normal sizes for the receptive fields of its constituent neurons.

5,7-Dihydroxytryptamine↗