Search PubMed⌕ Search

Biomedical subjects

E Hansson

Publications and source records attributed to E Hansson.

At least 55 records · Page 3Linked to original sources
PubMed1997

Glutamate induced astroglial swelling--methods and mechanisms.

Glutamate (Glu) plays an important role in the early development of brain injuries caused by ischemia, i.e. stroke, or brain trauma. Glu induces a rapid astroglial swelling which, in turn, deranges the composition of neuroactive substances in the extracellular space. We report that Glu can induce astroglial cell swelling by interaction with metabotropic Glu receptors (mGluRs). Furthermore, the Na(+)-K(+)-2Cl- cotransporter, a Na(+)-K(+) ATPase, and the Na(+)-dependent electrogenic Glu carrier seem to be involved in this Glu-induced astroglial cell swelling. Two methods for studying cell swelling arc described. One is based on variations in the signal emitted by the fluorescent probe fura-2/AM when excited at its isosbestic point. These variations were shown to be directly proportional to variations in intracellular volume. Relative changes in cell volume and intracellular calcium concentration could be detected simultaneously in single astroglial cells. The other method used permits the cell volume to be calculated in relative terms with the aid of image processing techniques.

Animals↗
PubMed1996

Development of the urodynamic pattern in infants with myelomeningocele.

OBJECTIVE: To study changes in the urodynamic pattern during the first year of life in patients with myelomeningocele (MMC) and to correlate these to deleterious effects on the upper urinary tract. PATIENTS: methods Thirty-four infants with MMC were investigated using cystometry, micturating cystourethrography and urography at 1, 4 and 10 months of age. RESULTS: Detrusor contractility was characterized by an increase in activity, with hyper-reflexia in 45% initially, increasing to 65% at the 4-month investigation. During the same period, the number of infants with areflexia decreased from 25% to 12%. Between 4 and 10 months, there were only minor changes in detrusor contractility. The number of patients with poorly compliant bladders also increased between the first and fourth month. The number of patients with elevated outlet resistance increased only slightly during the first year, from 32% of all infants at the initial investigation to 40% at the 10-month follow-up. Vesico-ureteric reflux was detected in 12 of the patients during the year, with five already diagnosed at the first investigation. Almost all refluxes were cured with clean intermittent catheterization, with additional pharmacological therapy in two patients; one patient required a vesicostomy. CONCLUSIONS: This study indicates that detrusor activity, and to some extent outlet resistance, change during the first year of life in infants with MMC. The changes were mainly increases in activity and occurred mostly between the first and fourth months of age. There was a strong correlation between the occurrence of reflux and poor compliance, hypercontractility and outlet obstruction.

Humans↗
PubMed1996

Bladder exstrophy in Sweden--a long-term follow-up study.

A retrospective review of all new cases of bladder exstrophy in Sweden in 1970 through 1989 is presented. The aim was to evaluate management of the malformation in Sweden and possibly identify factors that might improve the outlook. The incidence was 1:33,500 births. Records were reviewed of the 61 children (37 males and 24 females) treated at Sweden's four specialist centers of pediatric surgery. There was one perinatal death. Primary management was mainly early bladder closure (within 72 hours), late closure or perinatal urinary diversion. Subsequent measures included augmentation cystoplasty, bladder neck reconstruction, provision of continent urinary reservoir and penile reconstruction. The follow-up time was 4-19 years. In 15 cases renal scarring developed, though with impairment of total function in only three. Ten patients achieved continence, defined as 3-hour dry intervals, of whom four had urinary reservoirs with continent stoma. Urinary tract infections were recorded during follow-up in 43% of the surviving patients, though the true incidence of infection presumably was higher. To improve management of bladder exstrophy in sparsely populated Sweden, a nation-wide strategy of ongoing interhospital collaboration has been adopted. Results will be continuously presented.

Adolescent↗
PubMed1995

Effect of external K+, Ca2+, and Ba2+ on membrane potential and ionic conductance in rat astrocytes.

1. The purpose of this study was (a) to identify if astrocytes show a similar non-Nernstian depolarization in low K+ or low Ca2+ solutions as previously found in human glial and glioma cells, and (b) to analyze the influence of the K+ conductance on the membrane potential of astrocytes. 2. The membrane potential (Em) and the ionic conductance were studied with whole-cell patch-clamp technique in neonatal rat astrocytes (5-9 days in culture) and in human glioma cells (U-251MG). 3. In 3.0 mM K+ Em was -75 +/- 1.0 mV (mean +/- SEM, n = 39) in rat astrocytes and -79 +/- 0.7 mV (n = 5) in U-251MG cells. In both cell types Em changed linearly to the logarithm of [K+]0 between 3.0 and 160 mM K+ free medium caused astrocytes to hyperpolarize to -93 +/- 2.7 mV (n = 21) and U-251MG cells to depolarize to -27 +/- 2.1 mV (n = 3). 4. The I-E curve did not show inward rectification in astrocytes at this developmental stage. The slope conductance (g) exhibited only a small decrease (-19%) in K+ free solution and no significant change in 160 mM K+. 5. Ba2+ (1.0 mM) depolarized astrocytes to -45 +/- 2.9 mV (n = 11), decreasing the slope conductance (g) by 42.4 +/- 8.3% (n = 11). Ca2+ free solution depolarized astrocytes to -53 +/- 3.4 mV (n = 12) and resulted in a positive shift of the I-E curve, increasing g by 15.3 +/- 8.2% (n = 8). 6. Calculations indicated that a block of K+ channels explains the depolarizing effect of Ba2+. The effects of K+ free or Ca2+ free solutions on Em can be explained by a transformation of K+ channels to non-specific leakage channels. That astrocytes show a different reaction to low K+ than glioma cells can be related to the lack of inwardly rectifying K+ channels in astrocytes at this developmental stage.

Animals↗
PubMed1995

Astrocytes in glutamate neurotransmission.

Astrocytes maintain ionic, amino acid neurotransmitter, and water homeostasis in the extracellular space of the brain. The anatomy of the cells, with their network formation and their capacity to react to and produce humoral and long-distance, slow-speed transfer of information within the syncytium, makes them appear to be a class of cells able to produce integrated responses to multiple stimuli. Impairment of the control by astroglia over the extracellular milieu, e.g., glutamate (Glu) concentration, could lead to disturbances in the neuronal excitability. In this paper we summarize recent evidence of the effects of Glu interactions with astrocytes, i.e., monoamine receptor-mediated regulation of Glu carriers, Glu receptor influences on different ion-channels, and astroglial cell volume.

Animals↗
PubMed1995

The changing urodynamic pattern in valve bladders during infancy.

Bladder dysfunction in boys with posterior urethral valves is well documented in studies of long-term followup. These reports suggest that dysfunctional bladders can be divided into 3 main types, including unstable, low compliant and over distended. To our knowledge urodynamic findings at presentation during infancy have not been described previously. We report on 16 male patients born between 1989 and 1993 who presented with symptoms of posterior urethral valves between birth and age 5 months, and who were followed with repeated urodynamic evaluations for a mean of 19 months. At presentation the bladder was hypercontractile with low capacity. During the first 3 years of life, the urodynamic pattern changed with vanishing hypercontractility and increasing bladder capacity, although instability remained unchanged with emptying difficulties. Thus, the 3 patterns of bladder dysfunction reported in older boys after resection of posterior urethral valves could not be found in infants and small children.

Humans↗
PubMed1995

Delmopinol interactions with cell walls of gram-negative and gram-positive oral bacteria.

The main purpose of the present study was to investigate the influence of delmopinol hydrochloride on the cell surface morphology of gram-negative and gram-positive bacterial cells by using transmission electron microscopy. A second purpose was to evaluate the extraction of cell wall material caused by delmopinol and the binding of radiolabelled delmopinol to the various strains. Fresh isolates and type strains of gram-negative rods associated with periodontal disease, Porphyromonas gingivalis, Prevotella intermedia, Actinobacillus actinomycetemcomitans, and strains of the gram-positive streptococci Streptococcus sanguis, Streptococcus mutans and Streptococcus salivarius, were exposed to 3.2 mM (0.1%) or 6.4 mM (0.2%) delmopinol hydrochloride from 1 to 90 min. For electron microscopy the cells were fixed and negatively contrast-stained. Treatment with 6.4 mM delmopinol for 1 min resulted in marked ultrastructural changes of cell wall components and the outer cell membrane of the 3 gram-negative species compared with control cells, whereas the gram-positive streptococci treated with delmopinol showed little or no morphologic alteration as compared with untreated cells. The result from the electron microscopy was confirmed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis of proteins released from bacterial cells treated as for electron microscopy. More material was extracted from the gram-negative rods than from the gram-positive cocci. Significantly more delmopinol bound to the gram-negative rods than to the streptococci. It appears that the amphiphilic properties of delmopinol make gram-negative rods more vulnerable to delmopinol than gram-positive streptococci.

Aggregatibacter actinomycetemcomitans↗
PubMed1995

Measurement of C-reactive protein and the erythrocyte sedimentation rate in general practice.

OBJECTIVE: To evaluate the NycoCard:::CRP test (Nycomed A/S, Oslo, Norway) in relation to ESR in consecutive patients in general practice. NycoCard:::CRP test was also compared with a reference method for CRP quantitation. DESIGN: C-reactive protein and ESR were simultaneously measured in 607 consecutive patients at four community health centres. SETTING: Four community health centres in southern Sweden. RESULTS: We obtained consistent results in 71% of the cases. In 20% CRP was increased more than ESR, while ESR was increased more than CRP in 9%. CRP was increased in 16% while ESR was below the upper reference limit for age and sex. On the other hand ESR was increased while CRP was below 10 mg/l in five % of the patients. In most of the cases where there was a discrepancy- for example, in infectious diseases-the CRP results were more clear-cut. Using the NycoCard test the CRP concentration can be measured directly in a whole blood sample with the result available within minutes. Comparison of the NycoCard:::CRP test with the reference method for CRP quantitation showed good agreement. CONCLUSION: In clinical situations with suspected inflammatory diseases, the CRP test appears often to yield more useful results than the ESR. The NycoCard:::CRP test is suitable for use in general practice.

Adolescent↗
PubMed1994

Metabotropic glutamate receptor activation induces astroglial swelling.

The activation of metabotropic glutamate receptors (mGluRs) by 1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) or ibotenate induced a rapid cell volume increase in primary cultures of type 1 astroglial cells from the cerebral cortex of a newborn rat. These relative volume changes and parallel Ca2+ transients in single cells were examined by microspectrofluorimetry after loading the cells with fura-2/AM and varying the excitation wavelengths between the isosbestic point of the probe and its ion-sensitive wavelength. L(+)-2-Amino-4-phosphonobutyric acid (L-AP4) evoked an astroglial swelling but few or no cytosolic Ca2+ transients. No rapid swelling was observed after stimulation of ionotropic Glu receptors. The Glu-induced volume increase was unaffected by gluconate or amiloride, partially blocked by Glu-carrier blockers, and totally blocked by ketamine. The Glu- or L-AP4-induced volume increases were blocked by BaCl2 or furosemide. Tetraethylammoniumchloride-1-hydrate blocked the Glu- and 1S,3R-ACPD-induced astroglial swelling but the voltage-dependent L-, N-, or T-type Ca2+ channels were not primarily involved in the Glu-, 1S,3R-ACPD-, or L-AP4-induced swelling. mGluRs induce inositol 1,4,5-trisphosphate synthesis, intracellular Ca2+ increase, and the opening of a delayed outward K+ rectifier, and along another route they activate a Gi protein and open an inward K+ rectifier. One Na(+)-K(+)-2Cl(-)-cotransporter and a Na(+)-K(+)-ATPase is activated and so also is an electrogenic Na(+)-dependent Glu carrier. Thus, Glu-induced astroglial swelling is not only the result of the above mechanisms, but requires another, until now unidentified mechanism, probably some ketamine-sensitive K+ outflux or Na+ influx.

Animals↗
PubMed1994

Mechanisms of glutamate induced swelling in astroglial cells.

Relative changes in volume were registered in single cells by using a microspectrofluorometric equipment and the fluorescent probe fura-2/AM, excited at its isosbestic point. At this wavelength the probe is ion-insensitive and the fluorescent signals emitted is dependent on variations in the concentration of the dye. Variations in cell volume thus lead to changes in fluorescence intensity as the probe concentration is changed in the lightened delimited zone selected for each cell. When changing the excitation wavelength Ca2+ transients can be recorded. Glutamate (Glu) induced swelling of type I astroglial cells in primary culture and a parallel intracellular Ca2+ increase was obtained. A Glu induced swelling was obtained even after blockade of the Glu ionotropic receptors with NBXQ, suggesting that activation of ionotropic receptors might not be necessary for swelling to occur. On the other hand, blockade of the Glu carrier, or of pertussis toxin sensitive G-proteins reduced the Glu induced swelling. Blockade of Ba2+ or TEA sensitive K+ channels completely blocked the Glu induced swelling as did also blockade with furosemide of the Na+/K+/Cl- co-transporter. Glu induced swelling occurred in parallel with intracellular Ca2+ transients but extracellular Ca2+ did not seem necessary for swelling to occur.

Amino Acid Transport System X-AG↗
PubMed1994

Resistance of rat CNS to brain stem infection with herpes simplex virus type 1.

Infection of the CNS by herpes simplex type 1 (HSV-1) via the trigeminal route to the brain stem was elucidated in a rat model. In contrast to the earlier described cortical and hippocampal infection after intracranial injection, the CNS showed a profound resistance to HSV-1 infection when the virus was administered by nose inoculation, as judged by histopathology and immunohistochemistry. In contrast, when the distribution of HSV-1 in the brain was investigated after nose inoculation by polymerase chain reaction, viral DNA was detected at all levels from the ganglia to the cortex. When replication of HSV-1 was assayed in primary cell cultures of rat astrocytes derived from brain stem, striatum, hippocampus and cerebral cortex, significantly lower virus yields were obtained in brain stem-derived astrocytes cultures as compared with in cortex-derived astrocytes. This finding was independent of whether HSV-1 strains used originated from brains of patients suffering from herpes simplex encephalitis or from patients with oral cutaneous lesions and lacking neurological symptoms. Also, by immunocytochemistry of cultures after HSV-1 infection, a lower number of plaques were seen in brain stem-derived astrocytes as compared with cortex-derived astrocytes. The observed relative resistance of brain stem-derived astrocytes to replicate HSV-1 might contribute to the ability of the brain stem to withstand infection during reactivation of this virus in the trigeminal neurons.

Animals↗
PubMed1994

Glutamate-induced swelling of single astroglial cells in primary culture.

Glutamate induced an increase in cell volume within one minute and evoked cytosolic Ca2+ transients in type 1 astroglial cells in primary culture obtained from the cerebral cortex of newborn rat. Even the metabotropic glutamate receptor agonists (1S,3R)-1-aminocyclopentane- 1,3-dicarboxylic acid (1S-3R-ACPD) and L(+)-2-amino-4 phosphonobutyric acid (L-AP4) induced a cell swelling with ACPD inducing a parallel Ca2+ transient while L-AP4 did not. A new method was used where rapid changes in relative cell volume could be followed at the single cell level. Relative volume changes in cultured single astroglial cells were examined by microspectrofluorimetry after loading the cells with the highly fluorescent intracellular probe fura-2/AM. At its isosbestic point, 358 nm, fura-2 is ion-insensitive and the fluorescent signals emitted are related only to the intracellular dye concentration. By varying the excitation wavelengths, changes in intracellular Ca2+ transients could be recorded simultaneously with the relative volume variations of the individual cells. Thus, as rapid changes in cell volume were followed, the results from this method could be of physiological significance. Glutamate-induced cell swelling was blocked by BaCl2 and by tetraethylammonium, suggesting that K+ channels are operative in glutamate-induced cell swelling. Furthermore, the glutamate-induced swelling was blocked by the Na+; K+, and 2Cl- co-transport inhibitor furosemide. The glutamate-induced swelling was partially blocked by pertussis toxin and partially blocked also by the glutamate carrier-blocker dihydroaspartate. When the ionotropic glutamate receptor alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid was blocked with the antagonist 2,3-dihydroxy-6-nitro-7- sulfamoyl-benzo(F)quinoxaline, glutamate still induced a swelling, suggesting that this receptor was not directly involved in the glutamate-induced volume increase. Even in situations of blocked or partially blocked swelling, intracellular Ca2+ transients could be obtained. Furthermore, the glutamate-induced swelling was evoked even in low extracellular Ca2+ concentrations. Our data suggest that glutamate-induced rapid swelling is a complex process at the molecular level. One hypothetical mechanism might be that glutamate interacts with metabotropic glutamate receptors and induces a release of Ca2+ from internal stores. Furthermore glutamate interacts with K+ channels, and probably at least one co-transporter and the sodium-dependent high-affinity uptake glutamate carrier, resulting in cell swelling.

Aminobutyrates↗
PubMed1994

Astroglial modulation of synaptic transmission.

Brain astrocytes appear as a class of cells with the capacity to produce integrated responses to multiple stimuli. The cells interact dynamically with neurons, sense and support synaptic transmission. The anatomy of the cells, their formation of an electrically coupled syncytium with long-distance, slow speed transfer of information within the syncytium together with their well-developed capacity for cell volume regulation, and thereby an indirect influence on extracellular volume, has made us put forward the possibility that this syncytium constitutes an extraneuronal system for excitability control.

Animals↗
PubMed1993

Receptor-mediated phospholipase D activity in primary astroglial cultures.

Phospholipase D, an enzyme involved in signal transduction cascades, catalyses the formation of phosphatidic acid and, when ethanol is present, the formation of phosphatidylethanol. In the present study we demonstrate that stimulation of muscarinic acetylcholine receptors as well as P2-purinergic receptors induces activation of phospholipase D in primary cultures of astroglial cells. Both the hydrolysis and the transphosphatidylation reactions were stimulated by receptor agonists. Carbachol and ATP induced a rapid increase in the amount of [3H]phosphatidic acid in astroglial cells prelabelled with [3H]oleic acid. When ethanol (150 mM) was present, phosphatidylethanol was formed. Furthermore, the receptor-mediated increase in the concentration of phosphatidic acid was inhibited by ethanol, indicating that the phosphatidic acid production was indeed mediated by phospholipase D. The formation of phosphatidylethanol was concentration dependent, with a half-maximal effective concentration of 5 x 10(-5) M for carbachol and 10(-5) M for ATP. The carbachol-induced response was almost completely inhibited by atropine, indicating activation of phospholipase D via muscarinic receptors. The purinergic response is most probably mediated via P2-receptors since ADP was almost as efficient as ATP in inducing phosphatidylethanol formation, whereas AMP was significantly less potent. We conclude that astroglial cells in primary culture display muscarinic and purinergic receptors coupled to phospholipase D. The relationship to cell function needs to be further investigated.

Adenosine Triphosphate↗
PubMed1993

GABA induces Ca2+ transients in astrocytes.

By using the Ca(2+)-sensitive indictor Fura-2/AM, the cytosolic Ca2+ levels [Ca2+]i were measured in type 1 astrocytes in rat cortical astroglial primary cultures, after stimulation with GABA, muscimol (GABAA agonist), or baclofen (GABAB agonist). We report the first evidence that stimulation of both GABAA and GABAB receptors evokes Ca2+ transients in type I astrocytes. Two types of Ca2+ responses were seen: the single-phase curve, which was the most common, and the biphasic, which consisted of an initial rise that persisted at the maximal or submaximal level. Both types of Ca2+ responses appeared with some latency. The responses were obtained in astrocytes grown for 12-16 days in culture and the response frequencies for all three agonists were 18% of the total number of examined cells. However, when the astrocytes were grown in a mixed astroglial/neuronal culture the response frequencies for all three agonists increased to 35% of the total number of examined cells. In some cells, the responses after GABA stimulation were blocked to baseline levels after exposure to bicuculline (GABAA antagonist). In other cells, bicuculline only slightly reduced the GABA-evoked responses, and the addition of phaclofen (GABAB antagonist) did not potentiate this partial inhibition. However, the muscimol-evoked rises in [Ca2+]i were completely inhibited after exposure to bicuculline, while the responses after baclofen could only be partly blocked by phaclofen. GABA evoked rises in [Ca2+]i which alternatively were inhibited (mostly) or persisted in Ca(2+)-free buffer. The rises in [Ca2+]i persisted, but were reduced, in Ca(2+)-free buffer after stimulation with muscimol, but were inhibited after baclofen stimulation. The GABA uptake blockers guvacine, 4,5,6,7-tetrahydroisoxazolo(4,5-c)pyridin-3-ol and nipecotic acid were also able to reduce the GABA-evoked rises in [Ca2+]i. However, the L-type Ca2+ channel antagonist nifedipine failed to influence on the GABA-evoked Ca2+ transients. The results suggest that type 1 astrocytes in primary culture express GABA receptors which can elevate [Ca2+]i directly or indirectly via Ca2+ channels and/or via release from internal Ca2+ stores. The results also suggest that GABA can have intracellular Ca(2+)-mobilizing sites since the GABA-evoked responses were reduced after incubation with GABA uptake blockers.

Animals↗
PubMed1993

Kappa-opioid receptors on astrocytes stimulate L-type Ca2+ channels.

Cultured astrocytes from the cerebral cortex of the rat respond to opioid kappa-receptor stimulation with a substantial elevation of the cytoplasmic free calcium, visualized through the use of the fluorescent calcium indicator Fura-2. The stimulation of kappa-receptors with U-50488H increases the level of calcium through a dose-related stimulatory effect on the transmembrane calcium influx. The kappa-receptor stimulation was completely blocked by the selective kappa-receptor blocker nor-binaltorphimine. Furthermore, the transmembrane calcium influx was completely blocked by nifedipine, indicating the involvement of L-type channels. The presence of L-type channels was verified by stimulation of L-type channels with Bay K8644. The effects of Bay K8644 were completely blocked by nifedipine. L-type channel-coupled kappa-receptors on astrocytes might represent a novel mechanism contributing to the depressant action of opioids on synaptic transmission via decreasing the availability of extracellular calcium necessary for presynaptic transmitter release.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗