Immunoreactivity of glutamine synthetase in satellite glia around various subpopulations of lumbar dorsal root ganglia neurons in adult rats treated with monosodium glutamate.

Satellite glial cells (SGCs), involved inter alia in glutamate (Glu) metabolism, form a glial sheath around sensory neurons of dorsal root ganglia (DRGs). SGCs show a presence of glutamine synthetase (GS) which transform uptaken Glu into glutamine (Gln). In DRGs, this aminoacid is used mainly by small neurons which are able to synthetize substance P (SP) that play a crucial role in nociception. The aim of the study was to define the influence of monosodium glutamate (MSG) on GS immunoreactivity in satellite glia around various subpopulations of neurons including SP immunopositive cells in DRGs of adult rats. The studies were carried out on lumbar DRGs slides in rats which received subcutaneous injection of saline solution (control group) or 4 g/kg b. w. of MSG (MSG group). Immunofluorescence reactions were conducted with use of anti-GS and anti-SP antibodies. Administration of MSG to adult rats increased the GS immunoexpression in SGCs. In rats receiving MSG, a number of small neurons with GS-immunopositive glial sheath was not altered when compared to control individuals, whereas there was a statistically significant increase of GS immunoexpression in SGCs around large and medium neurons. Moreover, in these animals, a statistically significant increase in the number of small SP-positive neurons with GS-positive glial sheath was observed. SP is responsible for transmission of pain, thus the obtained results may be useful for further research concerning the roles of glia in nociceptive pathway regulation.

Maternal acrylamide exposure changes intestinal epithelium, immunolocalization of leptin and ghrelin and their receptors, and gut barrier in weaned offspring.

Acrylamide (ACR) is an amide formed as a byproduct in many heat-processed starchy-rich foods. In utero ACR exposure has been associated with restricted fetal growth, but its effects of postnatal functional development of small intestine is completely unknown. The current study investigated the time- and segment-dependent effects of prenatal ACR exposure on morphological and functional development of small intestine in weaned rat offspring. Four groups of pregnant female Wistar rats were exposed to ACR (3 mg/kg b.w./day) for 0, 5, 10 and 15 days during pregnancy. Basal intestinal morphology, immunolocalization of gut hormones responsible for food intake and proteins of intestinal barrier, activity of the intestinal brush border disaccharidases, apoptosis and proliferation in intestinal mucosa were analyzed in offspring at weaning (postnatal day 21). The results showed that in utero ACR exposure disturbs offspring gut structural and functional postnatal development in a time- and segment-depended manner and even a short prenatal exposure to ACR resulted in changes in intestinal morphology, immunolocalization of leptin and ghrelin and their receptors, barrier function, activity of gut enzymes and upregulation of apoptosis and proliferation. In conclusion, prenatal ACR exposure disturbed the proper postnatal development of small intestine.

Investigation of structural and neurobiochemical differences in brains from high-performance and native hen breeds.

Selection of livestock has not only led to changes in the level of their performance but also modified their behavior. As a result, within a single species, we have to deal with different behaviors of different breeds. In our study, we assumed that the different behaviors within a species are due to differences in the morphology and physiology of behavior-related systems. Two breeds of hens were used as a model: the highly reactive, fearful and high-performance Leghorn breed and proactive, unselected Green-legged Partridge breed. The higher reactivity and fearfulness of Leghorn hens in comparison to the Green-legged Partridge breed may be related to the greater number of neurons in the paraventricular nucleus and anterior hypothalamus and the higher content of zinc and iron in the brain, as these elements are involved in neuronal conduction and myelination processes. The reactive behaviours of Green-legged Partridge hens may be associated with the lower number of neurons in the paraventricular nucleus and the anterior hypothalamus and the higher concentration of dopamine and copper ions in the brain. The analyses confirmed the hypothesis of the existence of interbreed differences in the morphology and physiology of behaviour-related systems, which most probably emerged through unintentional and correlated selection towards high production performance. Consequently, attention should be drawn that the selection of a given genotype (breed) towards a specific environment could lead to creation of highly specialised lines that may not achieve homeostasis in every maintenance system.

The Effects of Prenatal Supplementation with ß-Hydroxy-ß-Methylbutyrate and/or Alpha-Ketoglutaric Acid on the Development and Maturation of Mink Intestines Are Dependent on the Number of Pregnancies and the Sex of the Offspring.

Prenatal and postnatal supplementation with ß-hydroxy-ß-methylbutyrate (HMB) and alpha-ketoglutaric acid (AKG) affects the development and maturation of offspring. Both substances have the potential to stimulate cell metabolism via different routes. However, parity affects development and may alter the effects of dietary supplementation. This study aimed to evaluate the effect of gestational supplementation with HMB and/or AKG to primiparous and multiparous minks on the structure and maturation of the offspring's small intestine. Primiparous and multiparous American minks (Neovison vison), of the standard dark brown type, were supplemented daily with HMB (0.02 g/kg b.w.) and/or AKG (0.4 g/kg b.w.) during gestation (n = 7 for each treatment). Supplementation stopped when the minks gave birth. Intestine samples were collected from 8-month-old male and female offspring during autopsy and histology and histomorphometry analysis was conducted (LAEC approval no 64/2015). Gestational supplementation had a long-term effect, improving the structure of the offspring's intestine toward facilitating absorption and passage of intestinal contents. AKG supplementation affected intestinal absorption (enterocytes, villi and absorptive surface), and HMB affected intestinal peristalsis and secretion (crypts and Goblet cells). These effects were strongly dependent on parity and offspring gender. Present findings have important nutritional implications and should be considered in feeding practices and supplementation plans in animal reproduction.

Reactivity of astrocytes in hippocampal CA1 area in rats after administration of habanero peppers.

INTRODUCTION: Astrocytes react to microenvironmental changes. Their reactivity is manifested by an increase in glial fibrillary acidic protein (GFAP) and S100b protein levels, hypertrophy and hyperplasia. The aim of the study was to analyse immunoreactive GFAP (GFAP-IR) and S100b (S100b-IR) astrocytes of hippocampal CA1 area in adult rats intragastrically (i.g.) treated with habanero peppers. MATERIAL AND METHODS: Brains from 10 control rats (group C) and 10 rats receiving oil suspension of habanero fruits for 7 days (group I-7) or 28 days (group II-28) were used. Antibodies against GFAP and S100b were used for immunohistochemistry. Morphology and distribution of astrocytes was evaluated under light microscope and their density was quantitatively analysed. RESULTS: In the CA1 hippocampal area of group II-28 rats, GFAP-IR cells with numerous, branched processes were observed. S100b-IR astrocytes had delicate, single processes in comparison with cells without processes observed in groups I-7 and C. In groups I-7 and II-28, GFAP-IR astrocytes' density significantly increased in SR - stratum radiatum of hippocampal CA1 area. In group I-7, a density of cells with the expression of S100b was significantly increased in SO - stratum oriens layer. In group II-28, the density of S100b-IR astrocytes was decreased. CONCLUSIONS: Habanero peppers administrated to rats, especially for a longer time, caused reactive changes in the astrocytes in hippocampal CA1 area, and thus these glial cells may protect neurons against excitotoxic damage.

Effects of monosodium glutamate treatment on calretinin-immunoreactive neurons in hippocampus of postnatal rats.

INTRODUCTION: Calretinin (CR) is a protein, which is present in GABAergic neurons and belongs to the calcium-binding proteins family. It may reduce the excitotoxicity phenomenon through its Ca2+ buffering properties. This phenomenon is due to the increase of calcium ions levels caused by the excess of glutamate­the main excitatory neurotransmitter. The aim of the study was to investigate alterations of calretinin-immunoreactivity in neurons of hippocampal CA1 region and dentate gyrus with hilus in 10 day-old rats treated with monosodium glutamate (MSG). MATERIAL AND METHODS: Ten 7 day-old Wistar rats were used. The MSG-group consisted of 5 MSG-treated rats at a dose of 4 g/kg b.w. for 3 consecutive days and the second group consisted of 5 control animals. After euthanasia the brains containing hippocampus were dissected and embedded in paraffin blocks. The immunohistochemical peroxidase-antiperoxydase reaction was performed on tissue sections. The morphometric analyses of CR-immunopositive neurons: density, percentage ratio to the density of all cells and an assessment of digital immunostaining intensity were performed. RESULTS: The distribution of the CR-immunoreactive neurons in the hippocampus was irregular. In the MSG-group there were single cells, which were more intensely stained than in control animals. Some of cells contained processes of different length. The density of CR-immunopositive cells and their percentage ratio to the density of all cells did not change significantly after MSG treatment. However, there was a statistically significant increase in the staining intensity of CR-immunopositive cells. CONCLUSIONS: The obtained results indicate that CR-positive cells in P7-P10 rats are only slightly affected by MSG in CA1 region and dentate gyrus with hilus of the hippocampus.

Effects of aspartame metabolites on astrocytes and neurons.

Aspartame, a widespread sweetener used in many food products, is considered as a highly hazardous compound. Aspartame was discovered in 1965 and raises a lot of controversy up to date. Astrocytes are glial cells, the presence and functions of which are closely connected with the central nervous system (CNS). The aim of this article is to demonstrate the direct and indirect role of astrocytes participating in the harmful effects of aspartame metabolites on neurons. The artificial sweetener is broken down into phenylalanine (50%), aspartic acid (40%) and methanol (10%) during metabolism in the body. The excess of phenylalanine blocks the transport of important amino acids to the brain contributing to reduced levels of dopamine and serotonin. Astrocytes directly affect the transport of this amino acid and also indirectly by modulation of carriers in the endothelium. Aspartic acid at high concentrations is a toxin that causes hyperexcitability of neurons and is also a precursor of other excitatory amino acid - glutamates. Their excess in quantity and lack of astrocytic uptake induces excitotoxicity and leads to the degeneration of astrocytes and neurons. The methanol metabolites cause CNS depression, vision disorders and other symptoms leading ultimately to metabolic acidosis and coma. Astrocytes do not play a significant role in methanol poisoning due to a permanent consumption of large amounts of aspartame. Despite intense speculations about the carcinogenicity of aspartame, the latest studies show that its metabolite - diketopiperazine - is cancirogenic in the CNS. It contributes to the formation of tumors in the CNS such as gliomas, medulloblastomas and meningiomas. Glial cells are the main source of tumors, which can be caused inter alia by the sweetener in the brain. On the one hand the action of astrocytes during aspartame poisoning may be advantageous for neuro-protection while on the other it may intensify the destruction of neurons. The role of the glia in the pathogenesis of many CNS diseases is crucial.