Biomedical subjects

Eva Fekete

Publications and source records attributed to Eva Fekete.

7 recordsLinked to original sources

PubMed2006

Chronic ethanol exposure impairs neuronal nitric oxide synthase in the rat intestine.

BACKGROUND: Nitric oxide (NO), synthesized by neuronal (nNOS), endothelial (eNOS), and inducible (iNOS) nitric oxide synthases, plays an essential role in the physiological functions of the gastrointestinal (GI) tract. Chronic ethanol intake has been shown to interfere with several of these physiological functions, leading to the pathological alterations observed in alcoholic individuals. Our aim therefore was to investigate the effects of chronic ethanol consumption on NOS isoforms in different GI segments. METHODS: Rats received either 20% aqueous ethanol solution or water for 8 weeks. Tissue samples of the duodenum, jejunum, ileum, and colon of the rats were used for measurement of the NOS activity, protein content, and nNOS immunohistochemistry. Anti-HuC/D immunohistochemistry was used to determine the total number of neurons. RESULTS: Measurement of the physiological constitutive NOS (cNOS) activity revealed a 20 times higher activity in the colon than in the small intestine and after chronic ethanol treatment demonstrated a significant decrease in the jejunum, ileum, and colon, while in the duodenum it remained unchanged compared with the control group. The physiological iNOS activity was higher in the ileum and colon than in the duodenum and jejunum, and these levels were not significantly affected by ethanol. Neuronal nitric oxide synthase immunohistochemistry revealed a significant decrease in the numbers of immunostained cells in all investigated intestinal segments, while the total number of myenteric neurons remained constant. The nNOS protein content measured by Western blotting indicated a significant decrease in the colon after ethanol consumption, while in other intestinal segments change was not detectable. CONCLUSIONS: This study has demonstrated for the first time that chronic ethanol consumption has a differential effect on NOS activity, NOS protein content, and the number of nitrergic neurons in different intestinal segments, suggesting that chronic ethanol administration affects the NO pathways in the enteric nervous system.

Animals↗

PubMed2005

Multiple calmodulin mRNAs are selectively transported to functionally different neuronal and glial compartments in the rat hippocampus. An electron microscopic in situ hybridization study.

The ultrastructural distribution of the calmodulin (CaM) mRNAs transcribed from the three CaM genes was studied in the CA1 region of the adult rat hippocampus by means of electron microscopic in situ hybridization. Digoxigenin-labeled CaM gene-specific riboprobes were detected with nanogold-anti-digoxigenin antibody conjugate. The CaM mRNAs were differentially distributed in both the neuronal and glial cell compartments. The greatest difference in neuronal distribution of the CaM mRNAs was found in the dendrites, where the mRNAs transcribed from the CaM I and III genes were much more abundant than the CaM II mRNA. The neuronal perikarya were heavy labeled for all the CaM mRNAs. Interestingly, the myelinated axons and axon terminals also contained small amounts of nanogold particles for all the CaM mRNAs, which diminished with increasing distance from the soma. Most of the synaptic profiles, however, contained labeling only in the postsynaptic region. The CaM mRNAs were differentially distributed in the glial cells. While the glial cell somata were only lightly labeled, surprisingly concentrated labeling was present in the perisynaptic and perivascular astrocytic processes. In general, the CaM II mRNA was the least represented in the glial processes. Only a very low CaM gene expression was observed in the endothelial and resting microglial cells. These results provide ultrastructural evidence for differential targeting of the multiple CaM mRNA transcripts to the intracellular compartments and suggest their microdomain-specific regulation.

Animals↗

PubMed2004

CreA-mediated carbon catabolite repression of beta-galactosidase formation in Aspergillus nidulans is growth rate dependent.

Carbon catabolite repression by the CreA-transcriptional repressor is widespread in filamentous fungi, but the mechanism by which glucose triggers carbon catabolite repression is still poorly understood. We investigated the hypothesis that the growth rate on glucose may control CreA-dependent carbon catabolite repression by using glucose-limited chemostat cultures and the intracellular beta-galactosidase activity of Aspergillus nidulans, which is repressed by glucose, as a model system. Chemostat cultures at four different dilution rates (D = 0.095, 0.068, 0.045 and 0.015 h-1) showed that formation of beta-galactosidase activity is repressed at the two highest Ds, but increasingly derepressed at the lower Ds, the activity at 0.015 h-1 equalling that in derepressed batch cultures. Chemostat cultures with the carbon catabolite derepressed A. nidulans mutant strain creADelta4 revealed a dilution-rate independent constant beta-galactosidase activity of the same range as that found in the wild-type strain at D = 0.015 h-1. Two other enzymes--isocitrate lyase, which is almost absent on glucose due to a CreA-independent mechanism; and galactokinase, which is formed constitutively and independent of CreA--were measured as controls. They were formed at constant activity at each dilution rate, both in the wild-type strain as well as in the carbon catabolite derepressed mutant strain. We conclude that the growth rate on glucose is a determinant of carbon catabolite repression in A. nidulans, and that below a certain growth rate carbon catabolite derepression occurs.

Aspergillus nidulans↗

PubMed2004

Effects of angiotensin II and AIII microinjections into the zona incerta after intra- and extracellular fluid loss.

Our recent results showed that angiotensin II or III (AII, AIII) microinjected into the zona incerta (ZI) significantly increased water intake. The most effective doses of AII and AIII were also defined. The two neuropeptides had their effects differently on drinking via different receptors. AII bound to AT(1) that was blocked by AT(1) receptor antagonist Losartan and the effect of AIII was eliminated by prior application of AT(2) receptor antagonist PD 123319. After different hydrational challenges, the effects of AII and AIII in the ZI have never been experimented, however. In the present experiments, the previously defined effective doses of AII (100 ng) or AIII (200 ng) were microinjected into the ZI after different types of challenges: (1). lowered thirst motivation when animals ingested approximately 40% of their daily fluid need during the consequent 60-min-daily-drinking period before the injection, (2). 48-h water deprivation, (3). intracellular dehydration and (4). extracellular dehydration. In all of the cases, incertally injected AII increased the animals' water ingestion. While Losartan could block these effects, PD 123319 was ineffective. Experiments were repeated by AIII, but in none of the cases differences were experienced between the groups. The finding that following hydrational challenges water intake increased only after AII injections and it could be blocked only by Losartan suggests that AII and AT(1) receptor play a pivotal role in the ZI in maintaining the body water balance.

Angiotensin II↗

PubMed2003

Angiotensin II and III microinjections into the zona incerta influence drinking behavior.

Different doses of angiotensin II (AII) or angiotensin III (AIII) microinjections into the zona incerta have been studied on drinking of rats in separate experiments during the consequent 60-min-daily-drinking period. Also, the dipsogen power of only the effective dose of AII and AIII was compared to vehicle treated rats. After, angiotensin receptor (AT(1), AT(2)) antagonists on AII or AIII induced drinking were tested. In the first and second experiments only the 100 ng AII and the 200 ng AIII increased water intake significantly. In the third experiment the AII started its dipsogen effect earlier, at the 5 min measuring time, compared to the AIII. Both effects kept on lasting parallel from the 10 min on. Considering the antagonist pre-treatments in the fourth experiment, animals were injected with 90 ng losartan, an AT(1) antagonist, 180 ng PD 123319 or 200 ng CGP 42112, both AT(2) antagonists, respectively. Both AII and AIII increased water consumption. The effect of AII could be blocked by losartan, but not by PD 123319 or CGP 42112. On the other hand, the effect of AIII could not be blocked by losartan, but by both the PD 123319 and CGP 42112. Since, the effects of AII, AIII and angiotensin antagonists have not been tested in the zona incerta, the finding that water intake increased after AII or AIII injections and it could be blocked only by either of the antagonists suggests that AT(1) and AT(2) receptors play partially different roles in the regulation of water intake.

Angiotensin II↗

PubMed2002

Gastrin-releasing peptide microinjected into the amygdala inhibits feeding.

Bombesin (BN)-like peptides including gastrin-releasing peptide (GRP) are known to inhibit feeding. In the amygdaloid body BN receptors have been found in moderate to high densities. The central part of the amygdala (ACE) is essentially involved in the regulation of feeding and body weight. In the present experiments GRP was injected into the ACE and liquid food intake, general behavioural activity, as well as core temperature, were examined in male CFY rats. Food intake was measured every 5 min for 30 min and at the 40th and the 60th min following GRP or vehicle microinjections. Bilateral application of 50, 100 or 150 ng GRP resulted in transient inhibition of food intake while bilateral injection of 25 or 300 ng GRP did not modify feeding. Effect of GRP was eliminated by prior application of BN receptor antagonist [Leu(13)-psi(CH(2)NH)-Leu(14)]BN. After GRP or vehicle treatments animals were video-monitored and food intake, the first meal latency (FML), intermeal intervals (IMI), the time spent feeding (FT), grooming, resting and exploration were analysed at 5-min intervals for 30 min. However, FML did not change after GRP, the first IMI increased and intake, FT and intake/FT significantly decreased during the first 5 min. Duration of resting gradually increased after GRP and animals spent less time with exploration after GRP treatment than after vehicle injection. These differences were significant during the 25-30-min period. In body temperature, no significant changes were observed. Our results show that GRP in the ACE inhibits feeding and that GRP may decrease the efficiency of eating and may act as a satiety signal.

Amygdala↗

PubMed2002

Differential calmodulin gene expression in the rodent brain.

Apparently redundant members of the calmodulin (CaM) gene family encode for the same amino acid sequence. CaM, a ubiquitous cytoplasmic calcium ion receptor, regulates the function of a variety of target molecules even in a single cell. Maintenance of the fidelity of the active CaM-target interactions in different compartments of the cell requires a rather complex control of the total cellular CaM pool comprising multiple levels of regulatory circuits. Among these mechanisms, it has long been proposed that a multigene family maximizes the regulatory potentials at the level of the gene expression. CaM genes are expressed at a particularly profound level in the mammalian central nervous system (CNS), especially in the highly polarized neurons. Thus, in the search for clear evidence of the suggested differential expression of the CaM genes, much of the research has been focused on the elements of the CNS. This review aims to give a comprehensive survey on the current understanding of this field at the level of the regulation of CaM mRNA transcription and distribution in the rodent brain. The results indicate that the CaM genes are indeed expressed in a gene-specific manner in the developing and adult brain under physiological conditions. To establish local CaM pools in distant intracellular compartments (dendrites and glial processes), local protein synthesis from differentially targeted mRNAs is also employed. Moreover, the CaM genes are controlled in a unique, gene-specific fashion when responding to certain external stimuli. Additionally, putative regulatory elements have been identified on the CaM genes and mRNAs.

Animals↗