Number Of Serotonin-positive Cells Research Articles

Effects of stress contagion on anxiogenic- and orofacial inflammatory pain-like behaviors with brain activation in mice.

The conditions of stress contagion are induced in bystanders without direct experiences of stressful events. This study determined the effects of stress contagion on masseter muscle nociception in mice. Stress contagion was developed in the bystanders after cohabitating with a conspecific mouse subjected to social defeat stress for 10 days. On Day 11, stress contagion increased anxiety- and orofacial inflammatory pain-like behaviors. The c-Fos and FosB immunoreactivities evoked by masseter muscle stimulation were increased in the upper cervical spinal cord, while c-Fos expressions were increased in the rostral ventromedial medulla, including the lateral paragigantocellular reticular nucleus and nucleus raphe magnus in stress contagion mice. The level of serotonin in the rostral ventromedial medulla was increased under stress contagion, while the number of serotonin positive cells was increased in the lateral paragigantocellular reticular nucleus. Stress contagion increased c-Fos and FosB expressions in the anterior cingulate cortex and insular cortex, both of which were positively correlated with orofacial inflammatory pain-like behaviors. The level of brain-derived neurotrophic factor was increased in the insular cortex under stress contagion. These results indicate that stress contagion can cause neural changes in the brain, resulting in increased masseter muscle nociception, as seen in social defeat stress mice.

Bisphenol A (BPA)-Induced Changes in the Number of Serotonin-Positive Cells in the Mucosal Layer of Porcine Small Intestine-the Preliminary Studies.

Bisphenol A (BPA) is a substance used in the production of plastics which has a negative impact on many internal organs. Because BPA is normally toxic for the gastrointestinal (GI) tract, the intestine is especially vulnerable to the adverse effects of this substance. The aim of this investigation was to study the influence of two doses of BPA (0.05 mg and 0.5 mg/kg body weight/day) on the number of mucosal cells in the porcine small intestine and containing serotonin (5-hydroxytryptamine, 5-HT). During the experiment, it was demonstrated that both applied BPA doses caused an increase in the number of 5-HT-positive cells located in the mucosal layer of the duodenum, jejunum, and ileum. These changes may be connected with the direct impact of BPA on the intestinal mucosa, the pro-inflammatory and immunomodulatory properties of this substance, and/or the influence of BPA on the neurochemical characterization of nervous structures supplying the intestine.

Prenatal sodium arsenite affects early development of serotonergic neurons in the fetal rat brain

Prenatal arsenite exposure has been associated with developmental disorders in children, including reduced IQ and language abnormalities. Animal experiments have also shown that exposure to arsenite during development induced developmental neurotoxicity after birth. However, the evidence is not enough, and the mechanism is poorly understood, especially on the exposure during early brain development. This study assessed effects of sodium (meta) arsenite shortly after exposure on early developing fetal rat brains.Pregnant rats were administered 50mg/L arsenite in their drinking water or 20mg/kg arsenite orally using a gastric tube, on gestational days (GD) 9–15. Fetal brains were examined on GD16.Pregnant rats administered 20mg/kg arsenite showed reductions in maternal body weight gain and food consumption during treatment, but not with 50mg/L arsenite. Arsenite did not affect fetal development, as determined by body weight, mortality and brain size. Arsenite also did not induce excessive cell death or affect neural cell division in any region of the fetal neuroepithelium. Thyrosine hydroxylase immunohistochemistry revealed no difference in the distribution of catecholaminergic neurons between fetuses of arsenite treated and control rats. However, reductions in the number of serotonin positive cells in the fetal median and dorsal raphe nuclei were observed following maternal treatment with 20mg/kg arsenite. Image analysis showed that the serotonin positive areas decreased in all fetal mid- and hind-brain areas without altering distribution patterns. Maternal stress induced by arsenite toxicity did not alter fetal development. These results suggest that arsenite-induced neurodevelopmental toxicity involves defects in the early development of the serotonin nervous system.

NUMBER OF SEROTONIN POSITIVE CELLS AND ACUTE CELLULAR REJECTION IN THE EARLY PERIOD AFTER SMALL BOWEL TRANSPLANTATION IN PIGS

Small bowel transplantations (SBT) are being increasingly performed to treat patients with irreversible intestinal failure or short-bowel syndrome. Histologic evaluation of small bowel allograft biopsies is important for the diagnosis of acute cellular rejection (ACR). Serotonin (5-hydroxytriptamin) is a biogenous amine of which up to 95% is present in the enterochromaffin cells of the gastrointestinal tract. The aim of our study was to analyze rejection and number of serotonin positive cells in the intestinal graft biopsy samples early after SBT in pigs. 24 pigs were used and divided into 4 groups. Group A, autologous SBT (n = 3) as a control group; group B, allogeneic SBT with tacrolimus monotherapy (n = 7); group C, allogeneic SBT immunosuppressed with tacrolimus and sirolimus (n = 8); and group D, without immunosuppression (n = 6). Observation period was 30 days. Mucosal biopsies were obtained on days 0, 3, 5, 7, 10, 14, 20, 28 after transplantation. ACR was classified according to standardized grading schema on a scale of indeterminate, mild, moderate, and severe. Serotonin positive cells were quantified as the number of positive cells in 20 high power fields. There were no significant differences in the number of serotonin positive cells and different grades of ACR. In our experiment the number of serotonin positive cells was not a sensitive marker of ACR in the early period after small bowel transplantation.

Cell-specific expression of glucose-dependent-insulinotropic polypeptide is regulated by the transcription factor PDX-1.

Glucose-dependent insulinotropic polypeptide (GIP) is a potent stimulator of insulin secretion and comprises an important component of the enteroinsular axis. GIP is synthesized in enteroendocrine K-cells located principally in the upper small intestine. The homeobox-containing gene PDX-1 is also expressed in the small intestine and plays a critical role in pancreatic development and in the expression of pancreatic-specific genes. Previous studies determined that the transcription factors GATA-4 and ISL-1 are important for GIP expression. In this study, we demonstrate that PDX-1 is also involved in regulating GIP expression in K-cells. Using immunohistochemistry, we verified the expression of PDX-1 protein in the nucleus of GIP-expressing mouse K-cells and evaluated the expression of PDX-1, serotonin, and GIP in wild-type and PDX-1(-/-) mice at 18.5 d after conception. Although we demonstrated a 97.8% reduction in the number of GIP-expressing cells in PDX-1(-/-) mice; there was no statistical difference in the number of serotonin-positive cells. Additionally, PDX-1 transcripts and protein were detected in a GIP-expressing neuroendocrine cell line, STC-1. Electromobility shift assays using STC-1 nuclear extracts demonstrated the specific binding of PDX-1 protein to a specific regulatory region in the GIP promoter. Using chromatin immunoprecipitation analysis, we demonstrated binding of PDX-1 to this same region of the GIP promoter in intact cells. Lastly, overexpression of PDX-1 in transient transfection assays led to a specific increase in the activity of GIP/Luc reporter constructs. The results of these studies indicate that the transcription factor PDX-1 plays a critical role in the cell-specific expression of the GIP gene.

Altered serotonin immunoreactivities in the left colon of patients with colonic inertia.

BACKGROUND: Serotonin is an important positive regulator of colonic motility and transit. Its quantity and distribution in the left colon could be abnormal in patients with colonic inertia (CI) and contribute to the disease. AIM: To evaluate serotonin positive cells and immuno-reactivities in the mucosa, submucosa and muscularis propria of the left colon from patients with CI was compared to a control group. PATIENTS AND METHODS: Nineteen patients who underwent subtotal colecotomy for CI were assessed. The control group consisted of 15 patients who underwent left hemicolectomy for colonic cancer; histologically normal tissue specimens were used. Immunohistochemical staining for serotonin was performed. In the mucosa, the average number of serotonin positive cells per microscopic field (200 x ) was determined. The positively stained area (square pixels) in the mucosa, submucosa and muscularis propria per microscopic field (200 x ) was calculated utilizing a computer image analysis program. RESULTS: In the mucosa, both the number of serotonin positive cells and positively stained area were significantly higher in the patient group than in controls (P < 0.05). The difference in serotonin positive area in the submucosa in the CI group compared to the control group was not statistically significant. There was a very significant correlation between the serotonin positive area in the submucosa and muscularis propria in controls (r=0.65, p < 0.01), but not in patients with CI. CONCLUSION: The increased serotonin level in patients with CI may contribute to the disease or be an adaptive response to some other pathology. The lack of a positive correlation in serotonin levels between the submucosa and muscularis propria in CI patients suggests that the coordinated distribution of serotonin may be disrupted in CI.

Coexistence of proguanylin (1–15) and somatostatin in the gastrointestinal tract

In order to identify proguanylin-secreting cells, we have raised an antiserum against the synthetic fragment of human proguanylin (1-15) and have examined the proguanylin-positive cells in the human and rat gastrointestinal tract by immunohistochemical methods. Numerous proguanylin (1-15)-immunoreactive cells were found in the gastrointestinal tract. They were either pyramidal or spindle shaped in the stomach. Spindle-shaped cells, frequently possessing long slender processes, were located at the base of the pyloric epithelium and did not extend to the lumen. In the duodenum and jejunum, these cells were mostly pyramidal in shape and often had a slender process towards the lumen. The immunostaining was completely blocked by the human proguanylin (1-15) fragment. Paneth and goblet cells were negative against this antiserum. The number of serotonin-positive cells was much larger than that of proguanylin-positive cells in all the segments tested. The number of proguanylin-positive cells decreased from the jejunum to the ileum and very few cells were observed in the colon. In contrast to serotonin-positive cells, most somatostatin-positive cells were also positive for proguanylin. Thus, proguanylin (1-15) or its related protein appears to coexist with somatostatin in intestinal endocrine D cells which may be a source of circulating proguanylin. Proguanylin, like somatostatin, may also regulate intestinal function as a local regulator.