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PubMed2006

Effect of ketanserin and amphetamine on nigrostriatal neurotransmission and reactive oxygen species in Parkinsonian rats. In vivo microdialysis study.

5-HT(2A/2C) receptors are one of the most important in controlling basal ganglia outputs. In rodent models of Parkinson's disease (PD) blockade of these receptors increases locomotion and enhances the actions of dopamine (DA) replacement therapy. Moreover, previously we established that 5-HT(2A/2C) antagonist attenuate DA D(1) agonist mediated vacuous chewing movements (VCMs) which are considered as an animal representation of human dyskinesia. These findings implicate 5-HT neuronal phenotypes in basal ganglia pathology, and promote 5-HT(2) antagonists as a rational treatment approach for dyskinesia that is prominent in most instances of PD replacement therapy. In the current study we determined whether ketanserin (KET) and/or amphetamine (AMPH) affected dopaminergic neurotranssmision in intact and fully DA-denervated rats. Moreover, we looked into extraneuronal content of HO. of the neostriatum after AMPH and/or KET injection, assessed by HPLC analysis of dihydroxybenzoic acids (2,3- and 2, 5-DHBA) - spin trap products of salicylate. Findings from the present study demonstrated that there are no substantial differences in extraneuronal HO. generation in the neostriatum between control and parkinsonian rats. KET did not affect DA release in the fully DA-denervated rat's neostriatum and also did not enhance HO. production. As 5-HT(2A/2C) receptor-mediated transmission might prove usefulness not only in addressing motor complications of PD patients (dyskinesia) but also in addressing non-motor problems such depression and/or L-DOPA evoked psychosis, the findings from the current study showed that the use of 5-HT(2A/2C) receptor antagonists in Parkinson's disease does not impend the neostriatal neuropil to be damaged by these drugs. We concluded that 5-HT(2A/2C) receptor antagonists may provide an attractive non-dopaminergic target for improving therapies for some basal ganglia disorders.

Amphetamine↗

PubMed1996

Control of growth hormone synthesis.

A large body of research, primarily in the rodent and human species, has elucidated many of the details regarding the control of GH synthesis and release. Cell type-specific transcriptional control has been identified as the main mechanism of the somatotroph-specific expression of GH. The recent detailed analysis in rodents and humans of a highly specific transcriptional activator protein, PIT-1, has opened several new areas of study. This is especially true for research in the farm animal species, where PIT-1 has been cloned and its binding elements on the GH gene are being investigated in a number of economically important species. Genetic and biochemical analyses of PIT-1 and other GH regulators have shown the central role of PIT-1 not only in the cell-autonomous stimulation of GH gene transcription, but also in the participation of PIT-1 in the response at the GH gene to exogenous hormones such as RA and TH. PIT-1 has been implicated in the proliferative development of the pituitary itself, in the maintenance of anterior pituitary cell types once cell types are defined, and in the mechanism by which the hypothalamic signal for GH release is transduced. However, PIT-1 by itself does not activate the GH gene, so that additional unknown factors exist that need to be identified to fully understand the cell type-specific activation of the GH gene. In addition, GH gene regulatory elements acting through well-characterized systems such as TH have seemingly different effects; the specific context of the regulatory elements relative to the promoter elements appear to be crucial. These contextual details of GH gene regulation are not well understood for any species and need to be further studied to be able to make predictions for particular elements and regulatory mechanisms across species. The regulation of the pulsatile secretion of GH by GHRH and SRIH is reasonably well understood after the cloning and analysis of the two releasing factors and their receptors. Modification or manipulation of the pathways involved in the regulation of GH secretion is a potential means of enhancing the lean tissue growth of meat animals. However, further understanding of the systems controlling the in vivo release of GH is needed before such manipulations are likely to be productive. Several other research questions regarding the control of GH expression and release remain to be answered. What is the biochemical connection between exogenous signal transduction (i.e., GRH/GHRH-R, TR, ER, RAR) and PIT-1 at the GH gene? Are there additional coactivators or repressors of GH that respond to cAMP levels? Do ubiquitous regulatory factors such as GHF-3 and Zn-15, identified thus far only in the rat, exist in humans or livestock? Zn-15 is expected to be found in many mammalian species, because its recognition sequence between the PIT-1 binding sites is highly conserved across mammals (Figure 2). What is the mechanism causing GH levels to drop during aging? Does PIT-1 expression decrease during the lifespan of animals? Is it possible to increase GH gene expression within target tissues by directing the expression of PIT-1 to these tissues via transgenesis, or are other factors limiting in peripheral tissues so that the lack of PIT-1 expression is not the deciding factor? Finally, is there genetic variation in the expression of GHRH and/or SRIH or in their respective receptors? These questions are relevant to and could be investigated in several of the livestock species.

Animals↗

PubMed2000

Identification and chromosomal localisation by fluorescence in situ hybridisation of human gene of phosphoinositide-specific phospholipase C beta(1).

Members of phosphoinositide-specific phospholipase C (PLC) families are central intermediary in signal transduction in response to the occupancy of receptors by many growth factors. Among PLC isoforms, the type beta(1) is of particular interest because of its reported nuclear localisation in addition to its presence at the plasma membrane. It has been previously shown that both the stimulation and the inhibition of the nuclear PLCbeta(1) under different stimuli implicate PLCbeta(1) as an important enzyme for mitogen-activated cell growth as well as for murine erythroleukaemia cell differentiation. The above findings hinting at a direct involvement of PLCbeta(1) in controlling the cell cycle in rodent cells, and the previously reported mapping of its gene in rat chromosome band 3q35-36, a region frequently rearranged in rat tumours induced by chemical carcinogenesis, prompted us to identify its human homologue. By screening a human foetal brain cDNA library with the rat PLCbeta(1) cDNA probe, we have identified a clone homologous to a sequence in gene bank called KIAA 0581, which encodes a large part of the human PLCbeta(1). By using this human cDNA in fluorescence in situ hybridisation on human metaphases, it has been possible to map human PLCbeta(1) on chromosome 20p12, confirming the synteny between rat chromosome 3 and human chromosome 20 and providing a novel locus of homology between bands q35-36 in rat and p12 in man. Since band 20p12 has been recently reported amplified and/or deleted in several solid tumours, the identification and chromosome mapping of human PLCbeta(1) could pave the way for further investigations on the role exerted both in normal human cells and in human tumours by PLCbeta(1), which has been shown to behave as a key signalling intermediate in the control of the cell cycle.

Animals↗

PubMed1987

Towards global control of cystic and alveolar hydatid diseases.

Control programmes against Echinococcus granulosus in its dog-sheep transmission cycle (Fig. 1) have been successful in many parts of the world'. In contrast, the related E. multilocularis presents a much more complex problem for control authorities. Unlike E. granulosus, the life cycle of E. multilocularis predominantly involves sylvatic hosts (e.g. rodents and foxes) (Fig. 2) and the control of wild life echinococcosis presents a formidable challenge to ecologists and epidemiologists. This review contrasts the two parasites, explaining why E. granulosus in its domestic dog-sheep life cycle has been so responsive to control, and examines the prospects for control of E. multilocularis.

Journal Article↗

PubMed1992

Dietary obesity in nine inbred mouse strains.

The effect of 7 wk consumption of a diet containing 32.6% of kilocalories as fat [condensed milk (CM) diet] on body composition and energy intake was evaluated in nine strains of inbred mice (AKR/J, C57L/J, A/J, C3H/HeJ, DBA/2J, C57BL/6J, SJL/J, I/STN, and SWR/J). Control animals were fed a high-carbohydrate diet containing 11.6% of energy as fat (Purina Rodent Chow diet). Relative to Chow diet controls, the CM diet significantly increased carcass lipid content in six strains (AKR/J, C57L/J, A/J, C3H/HeJ, DBA/2J, and C57BL/6J), but had no or a marginal effect on adiposity in three strains of mice (SJL/J, I/STN, and SWR/J). The obesity produced by the CM diet in six strains was not due to hyperphagia. Only one of six (AKR/J) of the strains that increased adiposity on the CM diet consumed more energy than controls during the 7 wk of the experiment. The identification of inbred mouse strains that are sensitive to dietary obesity, vs. others that are resistant, provides a useful tool to pursue the metabolic and genetic basis of this trait in the mouse.

Animal Feed↗

PubMed1993

Mechanisms of tolerance in the copper-loaded rat liver.

The aim of this study was to contribute to the understanding of the pathogenesis of copper-induced damage and subsequent recovery and tolerance to copper in the copper-loaded rat liver. Male Wistar rats were allocated randomly into groups of four, fed a pelleted diet containing 1500 mg/g copper, and killed at 1, 5, 6, 10, and 15 weeks. Two additional groups were treated as follows: (a) 5 weeks copper loading followed by 5 weeks with normal rodent diet (group 5-0), (b) 5 weeks copper loading followed by 5 weeks normal diet and 5 weeks of copper reloading (group 5-0-5). Control rats were fed a normal rodent diet that contained 18 mg/kg of copper. Tissues were collected for histology, histochemistry, immunocytochemistry, and copper analysis by atomic absorption spectrophotometry and X-ray microanalysis. In the rats continuously fed the high copper diet, copper concentration rose to 444 +/- 32 micrograms/g of liver (wet weight) by Week 1 and to 726 +/- 170 micrograms/g at Week 5, decreasing to 417 +/- 9 micrograms/g at Week 15. X-ray microanalysis and dot mapping microanalysis demonstrated copper within the nucleus, nucleolus, and lysosomes of these continuously loaded rats. Recovery with unloading of liver copper was demonstrated by both qualitative and quantitative methods in group 5-0 (41.32 +/- 19 micrograms/g). Recovery and tolerance were associated with a reduction in nucleolar copper. Copper tolerance was demonstrated in group 5-0-5 and in continuously copper-loaded rats by Weeks 10 and 15. Copper tolerance was reflected by a change in intracellular levels and distribution of copper and an efficient copper unloading mechanism.

Adaptation, Physiological↗

PubMed1999

Sex-dependent differences in the activities of acetylsalicylic acid-esterases in mouse kidneys.

Acetylsalicylic acid (ASA), the most used drug worldwide, is hydrolyzed to salicylic acid and acetate by esterases present in tissues of several species including humans. Sex differences in drug metabolism by rodent liver are documented in the literature. In this paper we report a difference in the activities of the esterases (ASA-esterase I and II) in the kidneys of male and female mice. In this species there is no difference between males and females in liver ASA-esterases (ASA-esterase I: males 38.5 +/- 7.9 (N = 5) and females 31.6 +/- 7.6 (N = 5) nmol of salicylic acid formed min-1 mg protein-1, P > 0.05; ASA-esterase II: males 77.3 +/- 17.4 (N = 5) and females 61.4 +/- 15.1 (N = 5) nmol of salicylic acid formed min-1 mg protein-1, P > 0.05). However, in the kidneys males presented a much higher enzyme activity than females (ASA-esterase I: males 25.2 +/- 6.3 (N = 5) and females 6.8 +/- 0.6 (N = 5) nmol of salicylic acid formed min-1 mg protein-1, P < 0.0002; ASA-esterase II: males 79.8 +/- 10.1 (N = 5) and females 13.0 +/- 1.1 (N = 5) nmol of salicylic acid formed min-1 mg protein-1, P < 0.0001). The difference between sexes observed in mouse kidneys could serve as a model to study the molecular basis of this sex difference and also to determine the possible involvement of pituitary and gonadal hormones in this difference in ASA-esterase activities since these hormones control the sex differences in rodent liver enzyme activity.

Animals↗

PubMed2003

Kynurenate production by cultured human astrocytes.

In the rodent brain, astrocytes are known to be the primary source of kynurenate (KYNA), an endogenous antagonist of both the glycine(B) and the alpha7 nicotinic acetylcholine receptor. In the present study, primary human astrocytes were used to examine the characteristics and regulation of de novo KYNA synthesis in vitro. To this end, cells were exposed to KYNA's bioprecursor L-kynurenine, and newly formed KYNA was recovered from the extracellular milieu. The production of KYNA was stereospecific and rose with increasing L-kynurenine concentrations, reaching a plateau in the high microM range. In an analogous experiment, astrocytes also readily produced and liberated the potent, specific glycine(B) receptor antagonist 7-chlorokynurenate from L-4-chlorokynurenine. KYNA synthesis was dose-dependently reduced by L-leucine or L-phenylalanine, two amino acids that compete with L-kynurenine for cellular uptake, and by aminooxyacetate, a non-specific aminotransferase inhibitor. In contrast, KYNA formation was stimulated by 5 mM pyruvate or oxaloacetate, which act as co-substrates of the transamination reaction. Aglycemic or depolarizing (50 mM KCl or 100 microM veratridine) conditions had no effect on KYNA synthesis. Subsequent studies using tissue homogenate showed that both known cerebral kynurenine aminotransferases (KAT I and KAT II) are present in astrocytes, but that KAT II appears to be singularly responsible for KYNA formation under physiological conditions. Taken together with previous results, these data suggest that very similar mechanisms control KYNA synthesis in the rodent and in the human brain. These regulatory events are likely to influence the neuromodulatory effects of astrocyte-derived KYNA in the normal and diseased human brain.

Aminooxyacetic Acid↗

PubMed1991

Increased UDP-GlcNAc:Gal beta 1-3GaLNAc-R (GlcNAc to GaLNAc) beta-1, 6-N-acetylglucosaminyltransferase activity in metastatic murine tumor cell lines. Control of polylactosamine synthesis.

Malignant transformation of rodent cell lines by polyoma virus and by activated ras genes is associated with increased UDP-GlcNAc:Man alpha-R beta-1,6-N-acetylglucosaminyltransferase V (GlcNAc-transferase V) activity and it product -GlcNAc beta 1-6Man alpha 1-6Man beta 1-branched Asn-linked oligosaccharides. In this report, we have compared beta 1-6GlcNAc branching of core O- and N-linked oligosaccharides in three experimental models of malignancy, namely (a) rat2 fibroblasts and their malignant T24H-ras-transfected counterpart; (b) benign SP1 mammary carcinoma cells and two metastic sublines of SP1; and (c) the metastatic MDAY-D2 lymphoma cell line and its poorly metastatic glycosylation mutant KBL-1. In addition to the previously reported increase in GlcNAc-transferase V activity, UDP-GlcNAc:Gal beta 1-3GalNAc alpha-R (GlcNAc to GalNAc) beta-1,6-N-acetylglucosaminyltransferase (core 2 GlcNAc-transferase, EC 2.4.1.102) activity was found to be elevated by 70% in the malignant rat2 and SP1 cell lines while several other glycosyltransferase activities were not significantly different. The action of core 2 GlcNAc-transferase followed by beta 1-4Gal-transferase provides an N-acetyllactosamine antenna that can be extended with polylactosamine (i.e. repeating Gal beta 1-4GlcNAc beta 1-3) provided UDP-GlcNAc:Gal beta-R beta 1-3GlcNAc-transferase (GlcNAc-transferase) (i)) activity is present. Polylactosamine content in microsomal membrane glycoproteins was quantitated by labeling the GlcNAc termini resulting from the action of Escherichia freundii endo-beta-galactosidase with bovine galactosyltransferase/UDP-[3H] Gal. Glycopeptidase F- sensitive and -insensitive fractions were measured to assess the N- and O-linked components. In the SP1 tumor model, the metastatic sublines showed increased core 2 GlcNAc-transferase and GlcNAc-transferase V activities but no change in GlcNAc-transferase (i) activity, yet polylactosamine was increased in both O- and N-linked oligosaccharides. In rat2 cells, down-regulation of GlcNAc-transferase (i) following transformation was associated with decreased polyactosamine even though core 2 GlcNAc-transferase and GlcNAc-transferase V were elevated in the cells. Finally, a 3-fold decrease in GlcNAc-transferase V in KBL-1, the glycosylation mutant of MDAY-D2 cells, resulted in complete loss of polylactosamine in N-linked but no change in O-linked polylactosamine content. These results suggest that, provided GlcNAc-transferase (i) is not limiting, the beta 1-6-branching enzymes core 2 GlcNAc-transferase and GlcNAc-transferase V regulate the levels of polyactosamine in O- and N-linked oligosaccharides, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Sugars↗

PubMed1999

Short-term leptin infusion does not affect circulating levels of LH, testosterone or cortisol in food-restricted pubertal male rhesus macaques.

OBJECTIVES: Although the adipocyte protein leptin has been implicated in the control of reproductive function in rodents, its role in primate reproductive physiology is poorly understood. Because primates in puberty show nighttime LH secretion and there is considerable evidence that the fertile state requires adequate nutrition, we reasoned that animals on the verge of reproductive competence would respond to leptin infusions by secreting LH. Food restriction reduces circulating leptin levels and slows or stops the GnRH pulse generator. Therefore, we examined the endocrine effects of leptin infusions in food-restricted male pubertal primates during the night when they normally secrete LH. In addition, we investigated the effect of leptin on in vitro testosterone production by Leydig cells. SUBJECTS: Four pubertal male rhesus macaques (Macaca mulatta), 4-5.5 kg in weight (2.5-4-year-old) were examined in this study. Leydig cells from adult male rats were to investigate in vitro effects of leptin. DESIGN: To document that animals had entered puberty, blood samples were collected from each of the four animals at 15-minute intervals for 15 h both during the day and at night. Since at this age animals secrete LH mainly at night, blood samples were collected at 15-minute intervals from each of the four animals on two separate occasions for 15 h between 1500 and 0600h. During the experiment, animals were feeding from 0800 to 0830h, cages were completely cleaned of food at 0900h and the afternoon meal was not given to individual animals on the day they were studied. One of the studies served as the control (food restricted group) and during the other, 2 mg (n = 4) or 0.3 mg (n = 3) of recombinant human leptin was administered intravenously during 2000-0100h (food restricted plus leptin group). Blood samples (1 ml) were collected through the indwelling catheter and immediately transferred from the plastic syringe into chilled glass tubes containing 10 microl 14% EDTA. The samples were centrifuged at 5-h intervals and the plasma withdrawn and stored frozen at - 20 degrees C in polypropylene vials until assays were performed. MEASUREMENTS: Bioactive LH was determined and testosterone, cortisol and leptin were measured by radioimmunoassay. RESULTS: During daytime experiments in these animals, LH pulses were sometimes observed late in the day and generally continued for 12-15 h. Food-restricted pubertal males showed delayed or absent LH pulses. Short-term leptin administration to food-restricted male rhesus macaques had no effect on LH, testosterone, or cortisol levels either during or after the infusion. Leptin also had no direct effect on basal or LH-stimulated testosterone production in Leydig cells. CONCLUSIONS: Our data support the notion that leptin is not the missing signal for the acute suppression of reproductive hormones secretion in food-restricted primates.

Animals↗

PubMed2006

Results of a 90-day safety assurance study with rats fed grain from corn borer-protected corn.

The results of a 90-day rat feeding study with grain from MON 810 corn (YieldGard Cornborer -- YieldGard Cornborer is a registered trademark of Monsanto Technology, LLC) that is protected against feeding damage from corn and stalk boring lepidopteran insects are presented. Corn borer protection was accomplished through the introduction of cry1Ab coding sequences into the corn genome for in planta production of a bioactive form of Cry1Ab protein. Grain from MON 810 and its near-isogenic control was separately formulated into rodent diets at levels of 11% and 33% (w/w) by Purina Mills, Inc. (PMI). All diets were nutritionally balanced and conformed to PMI specifications for Certified LabDiet (PMI Certified LabDiet 5002 is a registered trademark of Purina Mills, Inc.) 5002. There were a total of 400 rats in the study divided into 10 groups of 20 rats/sex/group. The responses of rats fed diets containing MON 810 were compared to those of rats fed grain from conventional corn varieties. Overall health, body weight, food consumption, clinical pathology parameters (hematology, blood chemistry, urinalysis), organ weights, and gross and microscopic appearance of tissues were comparable between groups fed diets containing MON 810 and conventional corn varieties. This study complements extensive agronomic, compositional and farm animal feeding studies with MON 810 grain, confirming that it is as safe and nutritious as grain from existing commercial corn varieties.

Animals↗

PubMed2005

Results of a 90-day safety assurance study with rats fed grain from corn rootworm-protected corn.

The results of a 90-day rat feeding study with YieldGard (YieldGard Rootworm Corn is a registered trademark of Monsanto Technology, LLC.) Rootworm corn (MON 863) grain that is protected against feeding damage caused by corn rootworm larvae are presented. Corn rootworm-protection was accomplished through the introduction of a cry3Bb1 coding sequence into the corn genome for in planta production of a modified Cry3Bb1 protein from Bacillus thuringiensis. Grain from MON 863 and its near isogenic control were separately formulated into rodent diets at levels of 11% and 33% (w/w) by Purina Mills, Inc. Additionally, six groups of rats were fed diets containing grain from different conventional (non-biotechnology-derived) reference varieties. The responses of rats fed diets containing MON 863 were compared to those of rats fed grain from conventional corn varieties. All diets were nutritionally balanced and conformed to Purina Mills, Inc. specifications for Certified LabDiet 5002. There were a total of 400 rats in the study divided into 10 groups of 20 rats/sex/group. Overall health, body weight gain, food consumption, clinical pathology parameters (hematology, blood chemistry, urinalysis), organ weights, gross and microscopic appearance of tissues were comparable between groups fed diets containing MON 863 and conventional corn varieties. This study complements extensive agronomic, compositional and farm animal feeding studies with MON 863 grain, confirming that it is as safe and nutritious as existing conventional corn varieties.

Animals↗

PubMed2000

Skilled forelimb reaching for pasta guided by tactile input in the rat as measured by accuracy, spatial adjustments, and force.

Rats are capable of reaching for food with a single forelimb, but since they locate the target of their reach using olfaction, it is unclear how they adjust their limb movement to compensate for errors. Although it is thought that their reaching movement is ballistic and can only be adjusted by trial and error, whether they can use haptic cues to aid in locating and identifying a target has not been examined. The present study addressed this question by allowing rats to reach through a slot for rigidly held pieces of uncooked pasta of varying thickness, which could be oriented vertically or horizontally from different points around the slot and which were attached to a force transducer. The tasks required that animals not only adjust their reach and grasp to the target's location but also identify the target based on its texture. Acquisition curves were made of head orientation, limb transport trajectories, number of attempts per success, paw orientation, breaking direction and force of the grasp. A haptic discrimination test used pasta and similar sized metal rods with different tactile properties as discriminanda. The results indicated that whereas postural orientation and limb transport trajectory were not modified as a function of target orientation, paw orientation and grasp force did vary as a function of the sensory qualities of the target object, and the rats could make a haptic discriminative choice of a target object. The results show that the rat is capable of adjusting paw movements using haptic information, suggesting that somatosensory features of sensorimotor control of limb and paw movements in carnivores and primates are shared by rodents. This commonality points to a conservation of motor control in mammals, explains some of the idiosyncratic features of rat reaching behavior, and confirms that rodents provide a good model for investigating sensorimotor functions.

Animals↗

PubMed1978

[Life cycle of Frenkelia. IV. Pathomorphological findings in the organs of experimentally infected bank voles].

In 1975 the buzzard (Buteo buteo) was found to be the final host of Frenkelia clethrionomyobuteonis. After this discovery it became possible to investigate systematically the pathomorphology of the infection in the intermediate host, the bank vole (Clethrionomys glareolus). Fifty bank voles were infected orally with a suspension of sporocysts recovered from the faeces of experimentally infected buzzards. Each rodent receive 7000 sporocysts. Six controls each were given a faecal suspension from a non-infected buzzard. The voles were killed between 1 and 140 days after infection and examined histologically. Between the 5th and 8th day of the infection during the schizogonic multiplication of the parasite a focal necrosis of liver cells and of the liver parenchyma is observed followed by a reversible resorptive inflammation associated with siderophagia and the occurrence of giant cells. The spleen was spodogenously enlarged up to twice its normal size. There also was haemosiderosis of the bone marrow, the liver and the spleen up to 25 days after infection. At the same time the erythropoiesis in the bone morrow, the spleen and in the lymph nodes increased; there also was a lymphoid hyperplasia in spleen and lymph nodes. About 10 days after infection a reversible infiltration with lymphocytes and plasma cells developed in the liver, heart and brain. This infiltration was again detectable as perivascular and meningeal reactions in the brain after the 49th day after infection. The second asexual multiplication of the parasite was seen histologically in the grey and white matter of the central nervous system after the 18th day of infection. The developing cysts increased in size continuously thereby compressing the surrounding nervous tissue. Disseminated focal necrosis with resorptive inflammatory components was prominent in the parenchyma of the brain after the 49th day of infection. It was possible to differentiate between damage in single organs and systemic pathological lesions. The lesions in single organs were directly connected with the development of parasitic stages in the liver (schizonts) and in the brain (cysts). The generalized lesions occurred in the haemopoietic system after an impairment of the blood during the first asexual multiplication. They also occurred in the immunocytic systems after the first and during the second asexual multiplication and during the relatively late cystic phase of the parasite in the brain. The pathogenesis of the disintegration of blood cells is not clear. The immunocytic reaction can be considered an immunological response of the host against the parasite. The effect of the development of the cysts on the function and structure of the central nervous system is expected to lead to an increasing impairment of the motility of the intermediate host.

Animals↗

PubMed1996

Respiratory rhythm generation in a precocial rodent in vitro preparation.

In vitro preparations for studying the neural control of respiration consisting of brainstem and spinal cord regions isolated from the newborn (PO-P1) precocial rodent, Acomys cahirinus (spiny mouse) are described. Spiny mice have a longer gestation period (39 days) than laboratory rats (22 days) and mice (20 days) and thus are born in a considerably more mature state. We sought to determine if in vitro preparations isolated from spiny mice would spontaneously generate a respiratory motor pattern and thus offer a more mature in vitro model than previously established altricial rodent models. Brain stem-spinal cords isolated from newborn spiny mice, unlike comparable Sprague-Dawley preparations, did not generate a sustained respiratory rhythm. However, spiny mice medullary slice preparations consisting of respiratory rhythm centres generated a stable spontaneous respiratory rhythm. Moreover, spiny mice and Sprague-Dawley medullary preparations responded in a similar fashion to excitatory amino acid, glycine, TRH and, mu-opioid receptor agonists and antagonists. Thus, considering the extended period of fetal development and the maturity of the spiny mouse at birth, medullary slice preparations isolated from this precocial rodent will compliment altricial models for the study of developmental and general neuronal mechanisms underlying respiratory control.

Animals↗

PubMed2005

Fetomaternal cross talk in the placental vascular bed: control of coagulation by trophoblast cells.

Humans and rodents exhibit a peculiar type of placentation in which zygote-derived trophoblast cells, rather than endothelial cells, line the terminal maternal vascular space. This peculiar aspect of the placental vasculature raises important questions about the relative contribution of fetal and maternal factors in the local control of hemostasis in the placenta and how these might determine the phenotypic expression of thrombophilia-associated complications of pregnancy. Using genomewide expression analysis, we identify a panel of genes that determine the ability of fetal trophoblast cells to regulate hemostasis at the fetomaternal interface. We show that spontaneous differentiation of trophoblast stem cells is associated with the acquisition of an endothelial cell-like thromboregulatory gene expression program. This program is developmentally regulated and conserved between mice and humans. We further show that trophoblast cells sense, via the expression of protease activated receptors, the presence of activated coagulation factors. Engagement of these receptors results in cell-type specific changes in gene expression. Our observations define candidate fetal genes that are potential risk modifiers of maternal thrombophilia-associated pregnancy complications and provide evidence that coagulation activation at the fetomaternal interface can affect trophoblast physiology altering placental function in the absence of frank thrombosis.

Animals↗

PubMedDate not supplied

Ultrastructural changes in limb distal nerves of rats with alcoholism and/or malnutrition before and after dietary correction.

To study peripheral nerves changes in chronic alcoholism and in malnutrition, we examined ultrastructurally the distal nerve branches of the digits of rats treated with four different dietary schemes, as follows: controls (n = 22), fed standard rodent diet plus water ad libitum; alcoholism (n = 12), fed the standard diet and 2-12% ethanol in drinking water; malnutrition (n = 21), fed with corn tortillas instead of standard diet; and alcoholism and malnutrition combined (n = 22). After 10 months under these conditions, a proportion of animals from each group were sacrificed. The remaining rats of the malnutrition and alcoholism alone groups were deferred a standard diet. The combined alcohol + malnutrition group was subdivided into standard diet, malnutrition and ethanol. After a further 4 months under these new conditions, the animals were sacrificed. Ultrastructural examination of limb distal nerve branches showed that glycogen-like particles were more common in malnourished animals, whereas remyelinating axons were more numerous in ethanol-treated rats. Bands of regeneration were present in both groups, but were more common in animals treated with ethanol. These features decreased significantly when the respective nutritional factor was reversed. The results confirm that ethanol plays a definitive role in the development of alcoholic neuropathy and that malnutrition accentuates, the histopathological abnormalities.

Alcoholism↗

PubMed1984

The use of cell surface antigens to characterize and select for fragments of human chromosomes retained by interspecies hybrids.

We have used a mouse cell transformant generated by human chromosome-mediated gene transfer (CMGT) to explore the use of cell surface antigens in the identification of fragments of human chromosomes retained by somatic cell hybrids. The transformed line, 21-30b, contained an intact rear-ranged human chromosome, and could be shown by isozyme analysis to contain genetic material from chromosomes 9 and X. By using the transformant as an immunogen in mice, it was also possible to produce antiserum to human-specific surface antigens. Using genetically characterized human X rodent hybrid lines, the genes controlling expression of these antigens could be localized to 11per----11p13, segregating concordantly with surface antigen S3. These conclusions were possible despite the fact that the presence of chromosome 11 in the transformant was not detectable by the presence of chromosome specific isozyme LDH-A or surface antigens W6/34 and 4F2. Finally, the fluorescence-activated cell sorter (FACS) was used to fractionate the transformant cells into antigen positive and negative subpopulations. This resulted in the isolation and characterization of four additional chromosome rearrangements involving interspecies chromosome translocations. This work demonstrates the value of chromosome-specific surface antigens and the FACS in the evaluation of human chromosome fragments retained by interspecies hybrids.

Animals↗