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M Kiraly

Publications and source records attributed to M Kiraly.

17 recordsLinked to original sources
PubMed2003

Early olfactory involvement in Alzheimer's disease.

BACKGROUND: In Alzheimer's disease (AD) the olfactory system, including the olfactory bulb, a limbic paleocortex is severely damaged. The occurrence of early olfactory deficits and the presence of senile plaques and neurofibrillary tangles in olfactory bulb were reported previously by a few authors. The goal of the present study was to analyze the occurrence of AD-type degenerative changes in the peripheral part of the olfactory system and to answer the question whether the frequency and severity of changes in the olfactory bulb and tract are associated with those of the cerebral cortex in AD. MATERIAL AND METHODS: In 110 autopsy cases several cortical areas and the olfactory bulb and tract were analyzed using histo- and immunohistochemical techniques. Based on a semiquantitative analysis of cortical senile plaques, neurofibrillary tangles and curly fibers, the 110 cases were divided into four groups: 19 cases with severe (definite AD), 14 cases with moderate, 58 cases with discrete and 19 control cases without AD-type cortical changes. RESULTS: The number of cases with olfactory involvement was very high, more than 84% in the three groups with cortical AD-type lesions. Degenerative olfactory changes were present in all 19 definite AD cases, and in two of the 19 controls. The statistical analysis showed a significant association between the peripheral olfactory and cortical degenerative changes with respect to their frequency and severity (P < 0.001). Neurofibrillary tangles and neuropil threads appear in the olfactory system as early as in entorhinal cortex. CONCLUSION: The results indicate a close relationship between the olfactory and cortical degenerative changes and indicate that the involvement of the olfactory bulb and tract is one of the earliest events in the degenerative process of the central nervous system in AD.

Adult↗
PubMed2001

A gene expression map for Caenorhabditis elegans.

We have assembled data from Caenorhabditis elegans DNA microarray experiments involving many growth conditions, developmental stages, and varieties of mutants. Co-regulated genes were grouped together and visualized in a three-dimensional expression map that displays correlations of gene expression profiles as distances in two dimensions and gene density in the third dimension. The gene expression map can be used as a gene discovery tool to identify genes that are co-regulated with known sets of genes (such as heat shock, growth control genes, germ line genes, and so forth) or to uncover previously unknown genetic functions (such as genomic instability in males and sperm caused by specific transposons).

Algorithms↗
PubMed2001

Genome-wide analysis of developmental and sex-regulated gene expression profiles in Caenorhabditis elegans.

We have constructed DNA microarrays containing 17,871 genes, representing about 94% of the 18,967 genes currently annotated in the Caenorhabditis elegans genome. These DNA microarrays can be used as a tool to define a nearly complete molecular profile of gene expression levels associated with different developmental stages, growth conditions, or worm strains. Here, we used these full-genome DNA microarrays to show the relative levels of gene expression for nearly every gene during development, from eggs through adulthood. These expression data can help reveal when a gene may act during development. We also compared gene expression in males to that of hermaphrodites and found a total of 2,171 sex-regulated genes (P < 0.05). The sex-regulated genes provide a global view of the differences between the sexes at a molecular level and identify many genes likely to be involved in sex-specific differentiation and behavior.

Aging↗
PubMed2000

Opposite regulation of calbindin and calretinin expression by brain-derived neurotrophic factor in cortical neurons.

Regulation of calbindin and calretinin expression by brain-derived neurotrophic factor (BDNF) was examined in primary cultures of cortical neurons using immunocytochemistry and northern blot analysis. Here we report that regulation of calretinin expression by BDNF is in marked contrast to that of calbindin. Indeed, chronic exposure of cultured cortical neurons for 5 days to increasing concentrations of BDNF (0.1-10 ng/ml) resulted in a concentration-dependent decrease in the number of calretinin-positive neurons and a concentration-dependent increase in the number of calbindin-immunoreactive neurons. Consistent with the immunocytochemical analysis, BDNF reduced calretinin mRNA levels and up-regulated calbindin mRNA expression, providing evidence that modifications in gene expression accounted for the changes in the number of calretinin- and calbindin-containing neurons. Among other members of the neurotrophin family, neurotrophin-4 (NT-4), which also acts by activating tyrosine kinase TrkB receptors, exerted effects comparable to those of BDNF, whereas nerve growth factor (NGF) was ineffective. As for BDNF and NT-4, incubation of cortical neurons with neurotrophin-3 (NT-3) also led to a decrease in calretinin expression. However, in contrast to BDNF and NT-4, NT-3 did not affect calbindin expression. Double-labeling experiments evidenced that calretinin- and calbindin-containing neurons belong to distinct neuronal subpopulations, suggesting that BDNF and NT-4 exert opposite effects according to the neurochemical phenotype of the target cell.

Animals↗
PubMed1991

Ion channels involved in the presynaptic hyperexcitability induced by herpes virus suis in rat superior cervical ganglion.

Rat superior cervical ganglia infected with herpes virus suis (pseudorabies virus) display a spontaneous bursting activity of still unknown origin. Previous intracellular recordings from the ganglionic neurons combined with pharmacological studies showed that the postganglionic action potentials are induced by acetylcholine release spontaneously from the preganglionic nerve. In this study we investigated whether the acetylcholine release is caused by mechanisms which are dependent on action potentials spontaneously generated on the preganglionic nerve or by mechanisms which occur without any changes in the excitability of presynaptic fibers. Simultaneous intra- and extracellular recordings from the ganglion cells and from the preganglionic nerve, respectively, were performed 32-38 h after the inoculation of herpes virus suis (strain Aujeszky) into the anterior chamber of one eye of the rat. Tetrodotoxin, well known to prevent the generation of action potentials by blocking the fast sodium channels, completely and reversibly abolished, whereas the potassium channel blockers 4-aminopyridine and apamin, enhanced the spontaneous, bursting activity at pre- and postsynaptic levels. The nicotinic receptor antagonist hexamethonium abolished the postsynaptic discharges and reduced the preganglionic activity by 50%. Pre- and postsynaptic electrical activities were suppressed in low calcium Krebs' solution, demonstrating that extracellular calcium is required not only for acetylcholine release but also for triggering the presynaptic action potentials. It is concluded that in the infected ganglia the spontaneous acetylcholine release is due to the generation of action potentials in the preganglionic nerve. Voltage-gated sodium and calcium channels contribute to the presynaptic electrogenesis, while the latter appears to be damped by the activation of voltage- and calcium-dependent potassium channels. Possible factors as well as mechanisms inducing such an increase in excitability are discussed.

4-Aminopyridine↗
PubMed1989

Neuroneuronal interconnections in the rat superior cervical ganglion; possible anatomical bases for modulatory interactions revealed by intracellular horseradish peroxidase labelling.

Electrophysiologically identified neurons of rat superior cervical ganglion were intracellularly injected with horseradish peroxidase and processed for light and electron microscopic observation. At light microscope level, neurons could be classified according to their dendritic arborization pattern in the vicinity of the soma into radiate, tufted and intermediate types. Upon electrical stimulation of the internal and external carotid nerves it was observed that radiate and intermediate neurons sent their axons into one or the other of these nerve trunks, whereas a majority of tufted neurons gave no response to stimulation of either of these postganglionic nerves. Electron microscopic exploration of horseradish peroxidase-labelled neurons revealed a surprisingly high prevalence of interconnectivity between ganglionic neurons. These contacts were both dendrosomatic and dendrodendritic, and were a universal feature of the labelled neurons explored. Twenty-two of the 23 labelled cells were found to receive direct dendritic appositions on their somata, and 13 of these 23 cells were seen each to send their dendrites into contact with at least one unlabelled neuronal soma. Dendrodendritic contacts were observed for 87% of the labelled neurons, and most of the cells (80%) were seen to form triadic contacts which included two dendrites and a preganglionic nerve ending. All these figures represent minimum incidences. None of the dendrosomatic or dendrodendritic appositions observed was overtly synaptic although several morphological features indicated the possibility of somatic and or dendritic release and uptake at sites of apposition. It is suggested that the observed appositions provide anatomical substrates for modulatory interactions between the ganglionic neurons, possibly involving slow potentials or the switching of metabolic pathways.

Animals↗
PubMed1986

Biochemical and electrophysiological evidence of functional vasopressin receptors in the rat superior cervical ganglion.

Binding of radioactive vasopressin--but not of oxytocin--was detected by autoradiography and by labeling of membranes obtained from the rat superior cervical ganglion. In both instances binding could be displaced by V1 (smooth muscle-type) but not by V2 (kidney-type) agonists, indicating that the ganglionic vasopressin receptors are similar to those present on hepatocytes and vascular smooth muscle. In accordance with the V1 character of the receptors, vasopressin activated the turnover of membrane inositol lipids, and this effect was abolished by a structural analogue known to act as a vasopressor antagonist. A possible physiological role of vasopressin was suggested by intracellular recordings obtained from ganglion cells in vitro. Vasopressin induced a reduction in the amplitude of the fast excitatory postsynaptic potential evoked by electrical stimulation of the preganglionic nerve. This reduction in ganglionic transmission was antagonized by the same synthetic structural analogue that blocked the effect of vasopressin on inositol lipids. This study provides evidence for the presence of functional vasopressin receptors in a rat sympathetic ganglion and thus suggests that vasopressin may play a role in peripheral autonomic function.

Animals↗
PubMed1985

Neurohypophysial peptides depress cholinergic transmission in a mammalian sympathetic ganglion.

The actions of arginine-vasopressin (AVP) and oxytocin (OXT) were investigated in the rat superior cervical ganglion (SCG). At micromolar concentrations AVP decreased the amplitude of fast excitatory postsynaptic potentials (f-EPSPs) evoked by preganglionic stimulation and in many cells depolarized the postsynaptic membrane. Both effects were reversibly abolished by a potent vasopressor antagonist. The peptide decreased the frequency of spontaneous miniature EPSPs and the quantal content of the f-EPSPs without affecting the sensitivity of the ganglion cells to acetylcholine. OXT exerted the same effects as AVP but was less powerful. It was concluded that neurohypophysial peptides exert a dual pre- and post-synaptic action mediated by specific receptors.

Action Potentials↗
PubMed1985

Immunohistochemical and biochemical detection of serotonin in the guinea pig celiac-superior mesenteric plexus.

Serotonin (5-HT) in the guinea pig celiac-superior mesenteric plexus was quantitatively measured by HPLC and visualized by an immunohistochemical method. Preincubation of the ganglia in a Krebs solution containing L-tryptophan and pargyline markedly elevated the content of 5-HT and K+ solution caused a release of 5-HT into the incubation medium. 5-HT immunoreactivity was localized to dense but unevenly distributed nerve fibers throughout the plexus and to small diameter cells commonly referred to as small intensely fluorescent cells. These findings provide evidence of an extensive network of 5-HT-containing neural elements in the guinea pig prevertebral ganglia.

Animals↗
PubMed1984

Evidence for a serotonin-mediated slow excitatory potential in the guinea-pig coeliac ganglia.

The nature of the putative transmitter(s) mediating the non-cholinergic excitatory post-synaptic potential (e.p.s.p.) described in the preceding paper was investigated by means of electrophysiological, pharmacological and immunohistochemical methods. Serotonin (1-10 microM) when applied by superfusion caused a slow depolarization that closely mimicked the synaptic response in about 60% of the coeliac neurones that exhibited a non-cholinergic e.p.s.p. The serotonin depolarization evoked in low-Ca2+, high-Mg2+ solution or in a Krebs solution containing cholinergic antagonists was quantitatively similar to that elicited in normal Krebs solution. When compared in the same neurones the membrane resistance change during the course of the serotonin depolarization and of the non-cholinergic e.p.s.p., as well as their respective responses to conditioning polarization, were similar. The non-cholinergic e.p.s.p. was reversibly abolished during serotonin-induced depolarization; the blockade persisted when the membrane potential was restored to the resting level by hyperpolarizing current. The serotonin depolarization as well as the non-cholinergic e.p.s.p. were reversibly suppressed by cyproheptadine (20-50 microM), a serotonin antagonist, and enhanced by fluoxetine (30-50 microM), a serotonin reuptake inhibitor. On the other hand, pre-treating the ganglia with L-tryptophan (50 microM), a precursor of serotonin, preferentially augmented the synaptically induced response. A portion of the neurones (15%) were depolarized by substance P (1 microM) which also reversibly desensitized the non-cholinergic e.p.s.p. elicited in these neurones. The remaining neurones (25%) were insensitive to either serotonin or substance P, and the non-cholinergic e.p.s.p.s elicited in these cells were likewise not appreciably affected by these two agents. Furthermore, cyproheptadine, fluoxetine and L-tryptophan had no significant effect on the non-cholinergic e.p.s.p.s elicited in serotonin-insensitive neurones. Using the immunohistofluorescent techniques, dense but unevenly distributed serotonin immunoreactive nerve fibres could be observed surrounding many coeliac neurones. Immunoreactivity was not observed in the ganglia incubated with antisera pre-absorbed with excess serotonin. Collectively our results suggest that serotonin is the mediator of non-cholinergic e.p.s.p.s. elicited in about 60% of coeliac neurones sampled in this study, and that in the remaining neurones the slow depolarization may be generated by substance P and/or some unknown transmitter(s).

Action Potentials↗
PubMed1983

Serotonin mediates a slow excitatory potential in mammalian celiac ganglia.

Neuropharmacological and histochemical evidence presented here indicates that serotonin (5-HT) is the transmitter mediating one of the postsynaptic potentials in the guinea pig celiac ganglion. Repetitive nerve stimulation elicited in celiac neurons, in addition to the nicotinic fast excitatory postsynaptic potential (EPSP), a slow EPSP that was resistant to cholinergic antagonists. Application of 5-HT caused a depolarization with membrane characteristics similar to those of the slow EPSP; furthermore, the latter was reversibly suppressed by 5-HT. The slow depolarization evoked by either nerve stimulation or 5-HT was augmented by fluoxetine, a 5-HT reuptake blocker, and depressed by cyproheptadine, a 5-HT receptor blocker; in addition, tryptophan, a precursor of 5-HT, enhanced differentially the slow EPSP. Lastly, histochemical study revealed dense networks of 5-HT immunoreactive nerve fibers encircling many ganglionic neurons.

Action Potentials↗
PubMed1983

Capsaicin causes release of a substance P-like peptide in guinea-pig inferior mesenteric ganglia.

The effects of capsaicin (0.5-100 microM) on neurones of the isolated inferior mesenteric ganglia (i.m.g.) of the guinea-pig were investigated by means of intracellular recording techniques. When applied to neurones of the i.m.g. that exhibited a slow non-cholinergic excitatory potential (Dun & Jiang, 1982), capsaicin caused in the large majority of these cells a long lasting depolarization accompanied by intense neuronal discharges. During and immediately following the depolarization, repetitive presynaptic stimulation consistently failed to elicit the non-cholinergic depolarization; a partial recovery was observed in relatively few neurones. The fast (nicotinic) excitatory post-synaptic potentials (e.p.s.p.s) were not suppressed by capsaicin in any of these cells. The membrane potential, input resistance and the amplitude of fast e.p.s.p.s in neurones of the i.m.g. that generated no detectable non-cholinergic depolarizations were not affected by capsaicin. Post-synaptic membrane sensitivity to exogenous application of substance P was not altered following capsaicin superfusion even though the latter effectively abolished the non-cholinergic depolarization in the same neurones. Superfusing the i.m.g. with a Ca-free Krebs solution markedly attenuated or abolished the depolarizing effect of capsaicin whereas tetrodotoxin (1 microM) was without effect. Capsaicin was without effect in a few neurones that generated a non-cholinergic depolarization; the latter was not desensitized by bath application of substance P. Capsaicin caused no appreciable effects in neurones of the bullfrog sympathetic ganglia; thus, the fast and slow post-synaptic potentials including the late slow e.p.s.p. the transmitter of which is the peptide luteinizing hormone-releasing hormone (Jan & Jan, 1982) were not affected. The results suggest that the depolarizing effect of capsaicin in neurones of the guinea-pig i.m.g. is due to a selective release of ganglionic substance P or a substance P-like peptide in a Ca-dependent manner, and that the non-cholinergic potentials elicited in capsaicin-insensitive neurones may be generated by a transmitter(s) other than substance P.

Action Potentials↗
PubMed1982

Alteration of the electrophysiological activity in sympathetic ganglia infected with a neurotropic virus. I. Presynaptic origin of the spontaneous bioelectric activity.

The bioelectric activity of the rat superior cervical ganglion (SCG) infected with pseudorabies virus (PRV) was examined in vitro 30-38 h after inoculation. Simultaneous intra- and extracellular recordings on the internal (ICN) and external carotid nerves (ECN) revealed a synchronized spontaneous activity. This synchronization can be ascribed either to the functional organization of the ganglion or to the mechanism of initiation itself. In the infected ganglia two categories of cells were observed: cells displaying abnormal spontaneous discharges, and silent cells whose electrophysiological behavior was similar to control cells. Spontaneously active cells showed intermittent spiking and bursting activity. The discharge pattern was associated with the firing rate of the emitting cell: sporadically active cells emitted single spikes whereas highly active cells fired bursts of action potentials (APs). Long lasting intracellular recordings demonstrated that the cells undergo gradual changes evolving from sporadic on to high activity. Spontaneous APs usually rode on prepotentials similar to the excitatory postsynaptic potentials (EPSPs). A comparative study of spontaneous prepotentials and orthodromically evoked EPSPs in the same cell demonstrated that the spontaneous prepotentials are real synaptic potentials. No pace-maker potentials were observed. The passive and active electrical membrane properties of spontaneously active neurons were not different from those of silent cells or control cells impaled in uninfected ganglia. D-Tubocurarine abolished the spontaneous activity in the whole ganglion. Ortho- and antidromic electrical stimulations of suprathreshold intensity elicited an evoked response in neurons displaying spontaneous activity, followed by a delayed burst whose shape was similar to the spontaneous burst of the cell. Stimuli of subthreshold intensities induced this delayed burst independently from the evoked response. We conclude that the spontaneous bioelectrical activity is of presynaptic, but not necessarily of preganglionic origin. The possible existence of a cholinergic intraganglionic pathway revealed by the viral infection is discussed.

Action Potentials↗