Number Of Serotoninergic Neurons Research Articles

Bisphenol A interferes with first shell formation and development of the serotoninergic system in early larval stages of Mytilus galloprovincialis

Bisphenol A-BPA, a widespread plastic additive, is an emerging contaminant of high concern and a potential endocrine disruptor in mammals. BPA also represents a potential threat for aquatic species, especially for larval stages. In the marine bivalve Mytilus galloprovincialis, BPA has been previously shown to affect early larval development and gene transcription. In this work, the effects of BPA (0.05–0.5–5 μM) were further investigated at different times post fertilization (24–28–32–48 hpf). BPA induced concentration-dependent alterations in deposition of the organic matrix and calcified shell at different larval stages, as shown by double calcofluor/calcein staining, resulting in altered phenotypes at 48hpf. Transcription of Tyrosinase-TYR, that plays a key role in remodelling of the shell organic matrix, and of HOX1, a member of homeobox genes involved in larval shell formation and neurogenesis, were evaluated by In Situ Hybrydization-ISH. BPA altered the spatial pattern of expression of both genes, with distinct effects depending on the concentration and developmental stage. Moreover, BPA affected the time course of mRNA levels for TYR from 24 to 48hpf. BPA impaired development of serotonin-5-HT-immunoreactive neurons at different times pf; at 48hpf, the reduction in the number of serotoninergic neurons was associated with developmental delay and downregulation of the 5-HT receptor-5-HTR. All the effects were observed from the lowest concentration tested, corresponding to detectable BPA levels in contaminated coastal waters. These data demonstrate that BPA interferes with key processes occurring during the first developmental stages of mussels, thus representing a potential threat for natural populations.

The Serotoninergic Neuron System in the CNS of the Common Snail: Morphology, Ontogeny, Control of Behavior

We report here studies of the morphology of the serotoninergic neuron system, which modulates defensive behavior, in the CNS of the common snail. Only one neuron, Pd4, projects to the pleural and parietal ganglia. Stimulation of this neuron evokes the same effects as stimulation of the whole group of modulatory neurons. In juvenile animals, the number of serotoninergic neurons and the relative sizes of these neurons were smaller than in adult animals, which may underlie the age-related differences in defensive behavior.

Chronic administration of 13- cis-retinoic acid does not alter the number of serotoninergic neurons in the mouse raphe nuclei

The synthetic retinoid 13- cis-retinoic acid (13- cis-RA), prescribed for the treatment of severe nodular acne, has been linked to an increased incidence of depression. Chronic treatment studies in rodents have shown that 13- cis-RA induces an increase in depression-related behaviours and a functional uncoupling of the hippocampus and dorsal raphe nucleus (DRN). Changes in the number of serotoninergic neurons in the DRN have been reported in depressed human patients. Given that retinoids have apoptotic effects, we hypothesized that a decrease in the number of serotoninergic neurons in the DRN or median raphe nucleus (MRN) would lead to decreased serotoninergic tone and in turn to the behavioural changes seen with 13- cis-RA administration. Here, we used immunolabelling and unbiased stereological methods to estimate the number of serotonin (5-hydroxytryptamine, 5-HT) neurons in the MRN and DRN of vehicle control and 13- cis-RA-treated adult mice. In the MRN, the number of 5-HT immunolabelled cells was 1815±194 in control, compared with 1954±111 in 13- cis-RA treated tissues. The number of 5-HT immunolabelled cells was much higher in the DRN, with 7148±377 cells in the control, compared with 7578±424 in the 13- cis-RA treated group. Further analysis of the DRN revealed that there were no changes in the number of 5-HT neurons within distinct subregions of the DRN. Similarly, changes in the density of serotoninergic neurons or in the volume of the MRN or DRN were not observed in 13- cis-RA treated animals. These data show that apoptotic actions of 13- cis-RA do not occur in vivo at drug concentrations that induce changes in depression-related behaviour and functional uncoupling of the DRN and hippocampus. The potential pro-depressant behavioural and molecular effects associated with chronic administration of 13- cis-RA may result from changes in serotoninergic activity rather than changes in the number of serotoninergic neurons.

Effects of β-amyloid protein on serotoninergic, noradrenergic, and cholinergic markers in neurons of the pontomesencephalic tegmentum in the rat

The effects on serotoninergic, noradrenergic and cholinergic markers on neurons of the pontomesencephalic tegmentum nuclei were studied in rats following local administration of fibrillar β-amyloid peptide (Aβ1–40) into the left retrosplenial cortex. Focal deposition of Aβ in the retrosplenial cortex resulted in a loss of serotoninergic neurons in the dorsal and median raphe nuclei. The dorsal raphe nucleus showed a statistically significant reduction of 31.7% in the number of serotoninergic neurons and a decrease (up to 17.38%) in neuronal density in comparison with the same parameters in uninjected controls. A statistically significant reduction of 50.3%, together with a significant decrease of 53.94% in the density of serotoninergic neurons, was also observed in the median raphe nucleus as compared with control animals. Furthermore, a significant reduction of 35.07% in the number of noradrenergic neurons as well as a statistically significant decrease of 56.55% in the density of dopamine-β-hydroxylase-immunoreactive neurons were also found in the locus coeruleus as compared with the corresponding hemisphere in uninjected controls. By contrast, a reduction of 24.37% in the number of choline acetyltransferase-positive neurons and a slight decrease (up to 22.28%) in the density of cholinergic neurons, which were not statistically significant, was observed in the laterodorsal tegmental nucleus in comparison with the same parameters in control animals. These results show that three different neurochemically defined populations of neurons in the pontomesencephalic tegmentum are affected by the neurotoxicity of Aβ in vivo and that Aβ might indirectly affect serotoninergic, noradrenergic and cholinergic innervation in the retrosplenial cortex.

Early desensitization of somato-dendritic 5-HT1A autoreceptors in rats treated with fluoxetine or paroxetine.

Electrophysiological and autoradiographic approaches were used to assess possible changes in 5-hydroxytryptamine (serotonin) 5-HT1A receptors in the rat dorsal raphe nucleus after a subchronic treatment with fluoxetine or paroxetine, two specific serotonin reuptake inhibitors with antidepressant properties. Fluoxetine or paroxetine were injected daily (5 mg/kg, i.p.) for various time periods up to 21 days. Electrophysiological recordings performed 24 h after the last injection showed that the potency of the 5-HT1A receptor agonist, 8-OH-DPAT, to depress the firing of serotoninergic neurons in the dorsal raphe nucleus within brain stem slices was significantly reduced as early as after a 3-day treatment with either drug. The proportion of recorded neurons showing desensitization of somatodendritic 5-HT1A autoreceptors increased along the treatment from approximately 40% on the 3rd day to 60-80% on the 21st day. At no time during the treatment, was the specific binding of [3H]8-OH-DPAT (agonist radioligand) or [3H]WAY-100 635 (antagonist radioligand) to 5-HT1A receptors modified in the dorsal raphe nucleus or in other brain areas, suggesting that neither the density nor the coupling of these receptors to G-proteins were probably altered in rats injected with fluoxetine or paroxetine for up to 21 days. These results show that adaptive desensitization of somatodendritic 5-HT1A autoreceptors within the dorsal raphe nucleus can already be detected after a 3-day treatment with selective serotonin reuptake inhibitors. Rather than the desensitization per se, it may be the progressive increase in the number of serotoninergic neurons with desensitized 5-HT1A autoreceptors which plays a critical role in the (slowly developing) antidepressant action of these drugs.

Serotoninergic projections from the raphe nuclei to the preoptic area in sheep as revealed by immunohistochemistry and retrograde labeling.

A retrograde tracer, fluorogold, was injected into the sheep preoptic area in order to demonstrate the origin of the serotoninergic fibers observed in this area. Within the raphe nuclei, retrogradely fluorogold-labeled neurons were observed mainly in the median raphe nucleus (B8), groups B6/B5, and in the area lateral to the nucleus interpeduncularis (group S4), but not in the dorsal raphe nucleus. About 50% of these fluorogold-containing neurons were immunostained with a specific antiserum raised against serotonin. Double-labeled neurons (serotonin-immunoreactive and fluorogold containing neurons) represented less than 20% of the whole number of serotoninergic neurons. We concluded that a few serotoninergic neurons in the median raphe nucleus and in groups B5/B6 and S4 project to the preoptic area. Moreover, these nuclei contained non-serotoninergic neurons which project to the same area. These results give new information on the serotoninergic innervation of the preoptic area in the sheep.

Localization of biogenic amines and monoamine oxidase in the rabbit hippocampus

Comparison of the localization of monoamines and monoamine oxidase in the rabbit hippocampus shows that most pyramidal and all granular neurons contain no monoamines. Up to 1% of pyramidal and about 3% of polymorphic neurons are noradrenergic, and some of the latter are basket cells. Their terminals, containing both noradrenalin and monoamine oxidase, are in contact with the bodies and processes of the pyramidal and granular neurons. Single serotoninergic polymorphic neurons are found in sectors H1 and H2 of the cornu ammonis and in sector H5 of the fascia dentata of the hippocampus; they have few terminals. Noradrenergic afferents enter the cornu ammonis in the external bundle of the alveus and in the septal tract, which runs along the inner surface of the fimbria. Noradrenergic terminal plexuses surround the bodies of the pyramidal cells and are concentrated at the level of the apical dendrites of the pyramids and at the base of the granular neurons of the fascia dentata. Convergence of noradrenergic and serotoninergic terminals is found on some pyramidal, granular, and polymorphic neurons. The high concentration of serotonin in the hippocampus despite the minimal number of serotoninergic neurons can be explained by the large number of serotonin-containing stellate cells of nonneural nature. They are localized on groups of pyramidal neurons in sectors H1 and H2 and also on blood vessels. Individual variations are found in the number of serotonin-containing neurons in the hippocampus and in the number and distribution of serotonin-containing stellate cells.