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S Komoly

Publications and source records attributed to S Komoly.

12 recordsLinked to original sources
PubMed1992

Insulin-like growth factor I gene expression is induced in astrocytes during experimental demyelination.

To investigate insulin-like growth factor I (IGF-I) and IGF-I receptor gene expression during experimental demyelination and myelin regeneration, young mice were fed cuprizone (( bis(cyclohexanone) oxaldihydrazone )). This copper-chelating agent produces demyelination in the corpus callosum and superior cerebellar peduncles, and when treatment is stopped, there is rapid remyelination. At intervals during cuprizone treatment and recovery, brain sections were hybridized with specific probes and immunostained with antibodies to determine the localization and relative amounts of IGF-I and IGF-I receptor mRNAs and peptides. In untreated littermates, IGF-I and IGF-I receptor mRNAs and peptides were not detected in white matter. In cuprizone-treated mice, high levels of both IGF-I mRNA and peptide were expressed by astrocytes in areas of myelin breakdown. Astrocyte IGF-I expression decreased rapidly during recovery and oligodendroglial expression of myelin-related genes increased. In severely demyelinated areas, immature oligodendroglia exhibited a transient increase in IGF-I receptor mRNA and peptide immunoreactivity during early recovery. This highly specific pattern of IGF-I induction in astrocytes during demyelination and the expression of the IGF-I receptor in regenerating oligodendrocytes during recovery suggest that IGF-I functions in the regulation of oligodendrocyte and myelin metabolism in vivo.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1992

Hypercortisolemia inhibits yohimbine-induced release of norepinephrine in the posterolateral hypothalamus of conscious rats.

Chronic hypercortisolemia attenuates yohimbine (YOH)-induced increments in plasma levels of the sympathetic neurotransmitter norepinephrine (NE). The present study used in vivo microdialysis to study the effects of hypercortisolemia on YOH-induced release of NE in the brain. Cortisol (25 mg/kg.day) or saline was infused sc into rats for 7 days via an osmotic minipump. Microdialysate and plasma concentrations of NE and its metabolites dihydroxyphenylglycol and methoxyhydroxyphenylglycol were measured before and after YOH (1 mg/kg, iv) administration in conscious animals, with microdialysate and plasma collections beginning 20-24 h after probe implantation. Chronic cortisol treatment resulted in attenuated NE, dihydroxyphenylglycol, and methoxyhydroxyphenylglycol responses in both microdialysate and plasma. The results indicate that YOH increases central neural as well as peripheral release, reuptake, turnover, and metabolism of NE and that hypercortisolemia suppresses these responses.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1991

Simultaneous measurement of plasma and brain extracellular fluid concentrations of catechols after yohimbine administration in rats.

The present study examined whether systemic injection of the alpha 2 adrenoceptor blocker, yohimbine, affects concentrations of norepinephrine (NE) and its metabolites in extracellular fluid in the brain and in blood. Microdialysis probes were inserted into the posterior hypothalamus, medulla, and caudate/putamen in rats. Microdialysate and arterial blood were sampled after intravenous administration of yohimbine. In the hypothalamus yohimbine produced significant increases in extracellular fluid concentrations of NE, its intraneuronal metabolite, dihydroxyphenylglycol (DHPG), and methoxyhydroxyphenylglycol (MHPG), a major neuronal and extraneuronal metabolite of NE. The increases in these levels were small or absent in the caudate/putamen, where dopamine is the primary catecholamine transmitter. During systemic infusion of tracer amounts of [3H]NE, little if any radioactive NE or DHPG appeared in the microdialysate, whereas substantial levels of [3H]MHPG were present and increased as plasma [3H]MHPG levels rose. The results support the view that alpha 2 adrenoceptor blockade in the brain increases hypothalamic and medullary release, reuptake, and metabolism of NE. The findings cannot be explained by disruption of the blood-brain barrier for catecholamines by insertion of the microdialysis probes. Enhanced sympathetic outflow and peripheral release of NE when alpha 2 adrenoceptors are blocked appears to be attended by enhanced central NE release, presumably as a result of presynaptic alpha 2 adrenoceptor blockade at noradrenergic terminals in the brain. This is consistent with the hypothesis that central noradrenergic NE release is regulated by presynaptic alpha 2 adrenoceptors.

Animals↗
PubMed1991

Distribution of protein kinase C isozymes in rat optic nerves.

Light (LM) and electron (EM) microscopic immunocytochemical methods were used to study the distribution of protein kinase C (PKC) isozymes in adult rat optic nerves. In cryostat and vibratome sections examined by LM, type II (beta) isozyme was localized almost exclusively in the axons. In the EM, immunoreaction products were found to associate with microtubules and neurofilaments. The inner surface of axonal membranes were occasionally stained. Analysis of PKC isozyme composition of the optic nerves by using immunoblot techniques revealed that type II (beta) isozyme accounted for approximately 80% of the total immunoreactivity. By contrast, type III (alpha) isozyme, which accounted for the remaining 20% of PKC, was found mainly in the astrocytes. Astrocytic processes next to blood vessels and between myelinated axons were stained. In the EM, immunoreaction products were found in the cytoplasm and along astroglial filaments. Segments of plasma membranes also were stained; but nuclei were unstained. Adult glial cells were not stained by an antibody to type II (beta) isozyme except for the occurrence of a few punctate cytoplasmic densities in occasional astrocytes. Very faint or no immunostaining was observed in sections treated with a monoclonal antibody to type I (gamma) isozyme. Immunoblot analyses also did not reveal this subspecies. The absence of type I (gamma) isozyme in optic nerves is not due to a down-regulation of the enzyme during development. In developing (5 and 11 day) rats, immunoreactivity of protein kinase C was very faint or absent. After 15 days, reaction products of both type III (alpha) and type II (beta) isozymes were found throughout the nerve. These findings suggest that type II (beta) isozyme may be involved in axonal transport whereas type III (alpha) isozyme may play a role in some astrocyte functions in mature optic nerves.

Aging↗
PubMed1991

Cerebral ischemia induces transient intracellular redistribution and intranuclear translocation of the raf proto-oncogene product in hippocampal pyramidal cells.

In this report we describe changes in the intracellular redistribution of raf serine/threonine protein kinase (product of the raf proto-oncogene family) in hippocampal neurons following cerebral ischemia in Mongolian gerbils. For immunohistochemical localization studies polyclonal antisera specific for each of the A, B, and Raf-1 isotypes of raf, as well as a pan-raf antisera, were employed. Of these, only sera recognizing B-raf, as well as the general v-raf (raised against the conserved C-terminal region) were positive, indicating that B-raf is the major isotype in this neuronal region. Three different ischemic models were used (repeated 3 times for two min and single 5 or 15 min occlusions, of the common carotid arteries) to demonstrate that ischemic insult causes redistribution of raf protein kinase into the cell nucleus of hippocampal neurons. Increased amounts of raf protein in the nuclei of pyramidal cells following ischemia was confirmed by Western blot analysis of isolated nuclear fractionations. Moreover, an elevation in the level of nuclear raf protein also was detected in the contralateral (i.e. non-occluded hemisphere) neurons of CA1 and CA3 subfields 4 days after the ischemic insult indicating a possible transsynaptic increase in the amount of raf protein along with redistribution. The intranuclear translocation of the immunoreactive material started from the perinucleolar rim and with time extended throughout the nucleus. Enhanced levels and altered redistribution of the raf polypeptide in the nuclei of pyramidal cells of the CA3 subfield appears to be reversible and returns to the normal level 12 days following the ischemic insult.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1991

Sclerosis multiplex in gypsies.

MS rarely occurs in gypsies in Hungary despite the high DR2 frequency. When it does occur, it has special features more resembling that of Asians than Central Europeans. In order to find correlation between the clinical observations and the immunogenetical data, the distribution of DQw1 subtypes was investigated by means of Eco RV - DQ beta RFLP in DR2 positive healthy gypsies and Hungarians, as well asin DR2-positive Hungarian and unselected gypsy MS patients. DQw6 correlated with MS susceptibility in Hungarians. This allotype was completely absent in healthy DR2-positive gypsies. DR2-positive gypsy MS patients, however, carried DQw6. No correlation of complement allotypes with the occurrence of MS was found in Hungarians, while a striking elevation of C4 Q0 occurred in gypsy MS patients compared with healthy individuals in the gypsy group. The absence of the DR2, DW2, DQw6 haplotype, and the frequency of C4A Q0 in healthy gypsies seems to be associated with the low MS prevalence, but genes outside this region might also influence the MS susceptibility.

Alleles↗
PubMed1990

[Herpes zoster infection with acute urinary retention].

The history of a young female patient is presented. She developed urine retention of sudden onset as a complication of herpes zoster infection manifested in the sacral dermatomes. Symptomatic and antiviral treatments were introduced with full recovery of bladder function. The correct diagnosis of this rare and benign complication of herpes zoster infection can help to avoid unnecessary and invasive examinations.

Acyclovir↗
PubMed1989

Cerebrospinal fluid (CSF) investigations in migraine.

A normal cell count as well as normal CSF pressure levels were found in both classic and common migraine patients during and between attacks. Total protein content was significantly lower in the migraine patients than in the controls, but no changes were found in the CSF protein fractions. The CSF 5-hydroxyindoleacetic acid level of the migraine patients proved to be higher than in the controls, whereas the homovanillic acid concentration was within the control limits.

Adult↗
PubMed1987

Decrease in oligodendrocyte carbonic anhydrase activity preceding myelin degeneration in cuprizone induced demyelination.

Both immunohistochemical and biochemical evidence is presented to show for the first time that carbonic anhydrase II (CA II) activity falls in the brain of mice in cuprizone (bis(cyclohexanone)oxalyldihydrazone) induced demyelination well before demyelination develops. This fall began during the first week, whereas the first signs of myelin degeneration induced by cuprizone did not appear until 3 weeks and demyelination in the superior cerebellar peduncle in the mouse took 6-8 weeks to develop. The findings suggest that oligodendrocyte CA II activity is essential either for the survival of oligodendrocytes or for the maintenance of central myelin.

Animals↗
PubMedDate not supplied

Myasthenia gravis: demonstration of membrane attack complex in muscle end-plates.

The membrane attack complex (MAC) assembles from C5b-9 complement components and has neoantigenic properties. Antihuman-MAC rabbit immunserum was applied in order to localize the MAC in myasthenic muscles. Using the indirect immunoperoxidase method MAC was demonstrated at the motor end-plates in eleven myasthenic patients who underwent thymectomy. This result provides direct evidence of antibody-dependent complement-mediated injury of acetylcholine receptors in myasthenia gravis.

Adolescent↗