Interictal Discharges: Changes in Size of Extracellular Space in Relation to Changes in Extracellular K+ and Na+ Concentration

Author(s):  
A. Lehmenkühler ◽  
A. Richter
Author(s):  
Grace C.H. Yang

The size and organization of collagen fibrils in the extracellular matrix is an important determinant of tissue structure and function. The synthesis and deposition of collagen involves multiple steps which begin within the cell and continue in the extracellular space. High-voltage electron microscopic studies of the chick embryo cornea and tendon suggested that the extracellular space is compartmentalized by the fibroblasts for the regulation of collagen fibril, bundle, and tissue specific macroaggregate formation. The purpose of this study is to gather direct evidence regarding the association of the fibroblast cell surface with newly formed collagen fibrils, and to define the role of the fibroblast in the control and the precise positioning of collagen fibrils, bundles, and macroaggregates during chick tendon development.


2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Sara Baldini ◽  
Francesca Pittau ◽  
Gwenael Birot ◽  
Vincent Rochas ◽  
Miralena I Tomescu ◽  
...  

Abstract Monitoring epileptic activity in the absence of interictal discharges is a major need given the well-established lack of reliability of patients’ reports of their seizures. Up to now, there are no other tools than reviewing the seizure diary; however, seizures may not be remembered or dismissed voluntarily. In the present study, we set out to determine if EEG voltage maps of epileptogenic activity in individual patients can help to identify disease activity, even if their scalp EEG appears normal. Twenty-five patients with pharmacoresistant focal epilepsy were included. For each patient, 6 min of EEG with spikes (yes-spike) and without visually detectable epileptogenic discharges (no-spike) were selected from long-term monitoring recordings (EEG 31–37 channels). For each patient, we identified typical discharges, calculated their average and the corresponding scalp voltage map (‘spike-map’). We then fitted the spike-map for each patient on their (i) EEG epochs with visible spikes, (ii) epochs without any visible spike and (iii) EEGs of 48 controls. The global explained variance was used to estimate the presence of the spike-maps. The individual spike-map occurred more often in the spike-free EEGs of patients compared to EEGs of healthy controls (P = 0.001). Not surprisingly, this difference was higher if the EEGs contained spikes (P < 0.001). In patients, spike-maps were more frequent per second (P < 0.001) but with a shorter mean duration (P < 0.001) than in controls, for both no-spike and yes-spike EEGs. The amount of spike-maps was unrelated to clinical variables, like epilepsy severity, drug load or vigilance state. Voltage maps of spike activity are present very frequently in the scalp EEG of patients, even in presumably normal EEG. We conclude that spike-maps are a robust and potentially powerful marker to monitor subtle epileptogenic activity.


2000 ◽  
Vol 78 (5) ◽  
pp. 378-391 ◽  
Author(s):  
G V Obrocea ◽  
M E Morris

Ion-selective microelectrode recordings were made to assess a possible contribution of extracellular γ-aminobutyric acid (GABA) accumulation to early responses evoked in the brain by anoxia and ischemia. Changes evoked by GABA or N2 in [K+]o, [Cl-]o, [Na+]o, and [TMA+]o were recorded in the cell body and dendritic regions of the stratum pyramidale (SP) and stratum radiatum (SR), respectively, of pyramidal neurons in CA1 of guinea pig hippocampal slices. Bath application of GABA (1-10 mM) for approximately 5 min evoked changes in [K+]o and [Cl-]o with respective EC50 levels of 3.8 and 4.1 mM in SP, and 4.7 and 5.6 mM in SR. In SP 5 mM GABA reversibly increased [K+]o and [Cl-]o and decreased [Na+]o; replacement of 95% O2 -5% CO2 by 95% N2 -5% CO2 for a similar period of time evoked changes which were for each ion in the same direction as those with GABA. In SR both GABA and N2 caused increases in [K+]o and decreases in [Cl-]o and [Na+]o. The reduction of extracellular space, estimated from levels of [TMA+]o during exposures to GABA and N2, was 5-6% and insufficient to cause the observed changes in ion concentration. Ion changes induced by GABA and N2 were reversibly attenuated by the GABAA receptor antagonist bicuculline methiodide (BMI, 100 µM). GABA-evoked changes in [K+]o in SP and SR and [Cl-]o in SP were depressed by >=90%, and of [Cl-]o in SR by 50%; N2-evoked changes in [K+]o in SP and SR were decreased by 70% and those of [Cl-]o by 50%. BMI blocked Δ [Na+]o with both GABA and N2 by 20-30%. It is concluded that during early anoxia: (i) accumulation of GABA and activation of GABAA receptors may contribute to the ion changes and play a significant role, and (ii) responses in the dendritic (SR) regions are greater than and (or) differ from those in the somal (SP) layers. A large component of the [K+]o increase may involve a GABA-evoked Ca2+-activated gk, secondary to [Ca2+]i increase. A major part of [Cl-]o changes may arise from GABA-induced gCl and glial efflux, with strong stimulation of active outward transport and anion exchange at SP, and inward Na+/K+/2Cl- co-transport at SR. Na+ influx is attributable mainly to Na+-dependent transmitter uptake, with only a small amount related to GABAA receptor activation. Although the release and (or) accumulation of GABA during anoxia might be viewed as potentially protectant, the ultimate role may more likely be an important contribution to toxicity and delayed neuronal death. Key words: brain slices, ion-selective microelectrodes, stratum pyramidale, stratum radiatum, bicuculline methiodide, extracellular space shrinkage.


2006 ◽  
Vol 31 (11) ◽  
pp. 1297-1303 ◽  
Author(s):  
Stephanie Linke ◽  
Philipp Goertz ◽  
Stephan L. Baader ◽  
Volkmar Gieselmann ◽  
Mario Siebler ◽  
...  

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