| 1. |
- Broberg, Marita, 1973, et al.
(författare)
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Cell swelling precedes seizures induced by inhibition of astrocytic metabolism.
- 2008
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Ingår i: Epilepsy Res.. - : Elsevier BV. - 0920-1211. ; 80:2-3, s. 132-41
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Tidskriftsartikel (refereegranskat)abstract
- It is currently unknown what processes take place at the interface between non-ictal and ictal activity during seizure initiation. In this study, using paralysed awake rats, we focally inhibited astrocytic metabolism with fluorocitrate (FC), causing seizures. We measured changes in electroencephalogram (EEG) (0-300 Hz), and extracellular ion-concentrations during ictal onsets defining possible relationships with impedance-determined cell swelling. In animals showing ictal activity (69%) there were spike-wave discharges, spike-wave discharges followed by spreading depression and spreading depression without any discharges. In a high proportion of spike-wave discharges (>95%), just prior to the first spike-wave discharge, there was a decrease in the volume of the extracellular space. Following the initiation of cell swelling and prior to discharges, there were increases in high-frequency (150-300 Hz) EEG activity, increases in extracellular potassium- and decreases in extracellular calcium-concentrations. We suggest that EEG and ionic changes are not causative of cell swelling. Cell swelling due to metabolic failure in astrocytes at the injected site may release excitatory amino acids. At the same time, our results suggest ion homeostasis is not maintained and increased neuronal excitability and synchronisation occur. These could be the drivers changing normal brain activity into ictal activity.
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| 2. |
- Broberg, Marita, 1973
(författare)
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Platelet reactions in the non-self recognition of material surfaces
- 2001
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Every material introduced into the body in order to function in contact with a living tissue is defined as a biomaterial. Biomaterials are used throughout the world in an increasing rate to replace and augment organ functions. The insertion of an implant into the human body will initiate blood coagulation at the surface of the material.After water and electrolytes have adhered to the surface a protein film starts to form. Platelets appear at the surface after a few seconds and the contact between platelets and the protein film is one of the initial steps in the non-self recognition of a foreign material.The adhesion and reactions of platelets were investigated using both whole blood and isolated platelets. The platelets were isolated by a new method, where a reversible inhibition of platelet function was achieved by magnesium ions. The binding of platelets to the surface, their spreading, exposure of P-selectin, and release of granular contents were investigated.The results show that the initial platelet adhesion to both hydrophilic and hydrophobic surfaces is mediated by the fibrinogen receptor GPIIb/IIIa. The binding of von Willebrand factor and exposure of P-selectin on the platelet surface are thrombin dependent events, but the spreading of platelets is not. Different protein coatings were seen to generate different responses from platelets. IgG was seen to fragmentize adherent platelets, leaving surface bound micro particles, while von Willebrand factor was seen to induce exposure of P-selectin on the platelet surface. The exposure of P-selectin on the platelet surface is of importance for the subsequent signalling between platelets and neutrophils, as neutrophils are known to bind to P-selectin. The release of granules, both a- and dense, was highest for platelets adhering to IgG and thrombin coated surfaces. Neither of these proteins was seen to have the same effects when added in soluble form to fibrinogen adherent platelets.In conclusion, the initial platelet adhesion to surfaces in contact with blood is mediated by fibrinogen but the presence of other proteins in the film, as for example IgG and von Willebrand factor, generates very different platelet responses.
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| 3. |
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| 4. |
- Broberg, Marita, 1973, et al.
(författare)
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Spreading depression: Evidence of five electroencephalogram phases.
- 2014
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Ingår i: Journal of Neuroscience Research. - : Wiley. - 0360-4012 .- 1097-4547. ; 92:10, s. 1384-1394
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Tidskriftsartikel (refereegranskat)abstract
- Spreading depression (SD), a self-propagating wave of astroglial and neuronal depolarization, is an accompaniment of several neurological disorders including epilepsy. Its well-described features are initial depolarization, followed by EEG flattening. In this in vivo study in awake animals, the relationship of SDs to epileptiform activity was re-examined. We assessed SDs generated by mechanical stimulation and by metabolic inhibition with fluorocitrate. In addition to identifying prolonged EEG depression, we identified two periods, one prior to and another during depression, characterized by increases in power of specific frequencies that were sometimes associated with epileptiform discharges. The first period was characterized by ripple activity close to the induction site (88% of SDs with intracortical electrodes). The second period was characterized by localized low-frequency spikes (100% with dural screw electrodes, 65% with intracortical electrodes). By using fluorocitrate to induce SDs, the initial period was also characterized by runs of spikes (52%). Finally, with SDs induced by both methods, there was a period at the end of depression when additional, unprovoked SDs occurred (20%). Five stages of SD were defined by these phenomena, in the order: excitation, depression, excitation, depression, SD, with metabolic inhibition enhancing the expression of epileptiform spiking.
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| 5. |
- Olsson, Torsten, 1937, et al.
(författare)
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Cell Swelling, Seizures and Spreading Deprssion: An Impedance Study
- 2006
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Ingår i: Neuroscience. - : Elsevier BV. - 0306-4522. ; 140:2
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Tidskriftsartikel (refereegranskat)abstract
- The cellular processes that take place during the transition from pre-seizure state to seizure remain to be defined. In this study in awake, paralyzed rats, we used an electrical impedance measure of changes in extra-cellular intracranial volume to estimate changes in cell size in acute models of epilepsy. Animals were prepared with extradural electroencephalographic (EEG)/impedance electrodes and a venous catheter. On a subsequent day, animals were paralyzed, ventilated and treated with picrotoxin, kainic acid or fluorocitrate in doses that usually induce epileptiform discharges. We now report that increases in baseline impedance were induced by kainic acid and smaller increases by picrotoxin. We also demonstrated that epileptiform discharges were preceded by small, accelerated increases in impedance. Increases in baseline impedance were highly correlated with increases in power of non-ictal high frequency EEG activity. Seizures were accompanied by increases in impedance and all treatments induced transient, relatively large, increases in impedance often associated with unilateral reductions in low frequency EEG, likely periods of spreading depression. We conclude: cerebral cells swell in convulsant models of epilepsy, that there are pre-ictal accelerations in cell swelling, and that spreading depression-like events are frequently associated with seizures.
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