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  • Cerebral cortex  (4)
  • Entorhinal cortex  (2)
  • 1
    ISSN: 1432-1106
    Keywords: Extracellular space ; Na+ and Cl− concentration ; Effects of metabolism on osmolarity ; Epilepsy ; Cerebral cortex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Extracellular Na+- and Cl−-concentrations ([Na+]o, [Cl−]o) were recorded with ion-selective microelectrodes during repetitive stimulation and stimulus-induced self-sustained neuronal afterdischarges (SAD) in the sensorimotor cortex of cats. In all cortical layers [Na+]o initially decreased by 4–7 mM. In depths of more than 600 μm below the cortical surface such decreases usually turned into increases of 2–6 mM during the course of the SADs, whereas in superficial layers [Na+]o never rose above its resting level. [Cl−]o always showed an increase in the course of the SADs often preceded by an initial small decrease. The average increase at a depth of 1,000 μm was about 7 mM. [Cl−]o reached peak values at about the end of the ictal period, whereas [Na+]o reached its maximum shortly after the end of the SAD, at times when [K+]o was still elevated above the baseline concentration. These data indicate that the extracellular osmolarity can increase during SAD by up to 30 mM. Such an increase in osmolarity can be explained by an increase in the number of intracellular particles, caused by cleavage of larger molecules during enhanced metabolism. This could lead to cell-swelling due to passive water influx from the extracellular space (ES). However, the resulting reduction of the size of the ES is calculated to be less than 10% for an increase in intracellular osmolarity by 30 mOsm. This value is too small as compared to previously measured ES-reductions under similar conditions (i.e., 30% reduction at 1,000 μm; Dietzel et al. 1980). Reductions of the size of the ES that accompany the observed changes in the ionic environment, are quantitatively explained on the basis of the extended glial buffering mechanism described in the preceding paper.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 40 (1980), S. 247-250 
    ISSN: 1432-1106
    Keywords: Extracellular Ca2+ activity ; Cerebral cortex ; Excitatory aminoacids ; Ca2+ antagonists ; GABA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Extracellular Ca2+ activity (aCa) changes were measured with Ca2+-sensitive microelectrodes in the cat cerebral cortex during iontophoretic administration of excitatory and inhibitory aminoacids. Glutamate, aspartate and DL homcysteate usually decreased aCa from a baseline of 1.3 mM to as low as 0.1 mM. The amplitude of the changes was largest at depths between 100 and 300 μm beneath the cortical surface. The aCa decreases could be deminished or blocked by Co2+, Mn2+ or La3+ as well as by GABA. These data suggest that large Ca2+ conductances that may be voltage-sensitive are present in apical dendrites of neocortical neurones.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 27 (1977), S. 237-243 
    ISSN: 1432-1106
    Keywords: Ca++ selective microelectrodes ; Ca++ activity ; K+ activity ; Seizure ; Cerebral cortex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Extracellular calcium and potassium activities (aCa and aK) as well as neuronal activity were simultaneously recorded with ion-sensitive electrodes in the somatosensory cortex of cats. Baseline aCa was 1.2–1.5 mM/1, baseline a k 2.7–3.2 mM/1. Transient decreases in aCa and simultaneous increases in aK were evoked by repetitive stimulation of the contralateral forepaw, the nucleus ventroposterolateralis thalami and the cortical surface. Considerable decreases in aCa (by up to 0.7 mM/1) were found during seizure activity. A fall in aCa preceded the onset of paroxysmal discharges and the rise in aK after injection of pentylene tetrazol. The decrease in aCa led also the rise in aK during cyclical spike driving in a penicillin focus. It is concluded that alterations of Ca++ dependent mechanisms participate in the generation of epileptic activity.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1106
    Keywords: Extracellular space ; K+ regulation ; Spatial K+ buffering ; Epilepsy ; Cerebral cortex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The time course of local changes of the extracellular space (ES) was investigated by measuring concentration changes of repeatedly injected tetramethylammonium (TMA+) and choline (Ch+) ions for which cell membranes are largely impermeable. After stimulus-induced extracellular [K+] elevations the δ[TMA+] and δ[Ch+] signals recorded with nominally K+-selective liquid ion-exchanger microelectrodes increased by up to 100%, thus indicating a reduction of the ES down to one half of its initial size. The shrinkage was maximal at sites where the K+ release into the ES was also largest. At very superficial and deep layers, however, considerable increases in extracellular K+ concentration were not accompanied by significant reductions in the ES. These findings can be explained as a consequence of K+ movement through spatially extended cell structures. Calculations based on a model combining the spatial buffer mechanism of Kuffler and Nicholls (1966) to osmolarity changes caused by selective K+ transport through primarily K+ permeable membranes support this concept. Following stimulation additional iontophoretically induced [K+]o rises were reduced in amplitude by up to 35%, even at sites where maximal decreases of the ES were observed. This emphasizes the importance of active uptake for K+ clearance out of the ES.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 87 (1991), S. 581-596 
    ISSN: 1432-1106
    Keywords: Temporal cortex ; Entorhinal cortex ; Hippocampus ; NMDA ; Low Mg2+ ; Epileptiform activity ; Status epilepticus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In order to study spatial interactions during low magnesium induced epileptiform activity, changes in extracellular potassium concentration ([K+]o) and associated slow field potentials (f.p.'s) were recorded in thin rat temporal cortex slices (400 μm) containing the neocortical temporal area 3 (Te3), the entorhinal cortex (EC) and the hippocampal formation with the dentate gyrus, area CA3 and CA1 and the subiculum (Sub). The epileptiform activity was characterized by short recurrent epileptiform discharges (40 to 80 ms, 20/min) in areas CA3 and CA1 and by interictal discharges and tonic and clonic seizure like events (SLE's) (13–88s) in the EC, Te3 and Sub. While interictal discharges occurred independent of each other in the different subfields, the three areas became synchronized during the course of a SLE. The EC, Te3 and Sub all could represent the “focus” for generation of the SLE's. This initiation site for SLE's sometimes changed from one area to another. The characteristics of the rises in [K+]o and subsequent undershoots were comparable to previous observations in in vivo preparations. Interestingly, rises in [K+]o could start before actual onset of seizure like activity in secondarily recruited areas. The epileptiform activity could change its characteristics to either a state of recurrent tonic discharge episodes or to a continuous clonic discharge state reminiscent of various forms of status epilepticus. We did not observe, in any of these states, active participation by area CA3 in the epileptiform activity of the EC in spite of clear projected activity to the dentate gyrus. Even after application of picrotoxin (20 μM), area CA3 did not actively participate in the SLE's generated in the entorhinal cortex. When baclofen (2 μM) was added to the picrotoxin containing medium, SLE's occurred both in the entorhinal cortex and in area CA3, suggesting that inhibition of inhibitory interneurons by baclofen could overcome the “filtering” of projected activity from the entorhinal cortex to the hippocampus.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-1912
    Keywords: Entorhinal cortex ; Isomers ; Low magnesium epilepsy ; Losigamone ; Maximal electroshock test ; Mice ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Losigamone (AO-33) is a recemate of a tetronic acid derivative. The effects of losigamone and its three isomers (AO-242, AO-294 and AO-23) were compared on maximal electroshock (MES) induced convulsions in mice and on different patterns of extracellularly recorded, low Mg 2+ induced epileptiform activity in slices of the rat temporal cortex. Lowering Mg 2+ induced recurrent short discharges in areas CA3 and CA1 while ictaform events that lasted for many seconds were induced in the entorhinal cortex. In the hippocampus the activity stayed stable over a number of hours. In contrast, the ictaform events in the entorhinal cortex changed their characteristics after one to two hours to recurrent discharges of 0.8 to 10 s. Afterdischarges and interictal events were absent. 50 μM AO-242 showed a similar efficacy to 50 μM AO-33 in reducing and blocking epileptiform discharges in areas CA1 and CA3 while 50 μM AO-294 and 50 μM AO-23 had weaker effects than 50 μM AO-33. Concentrations of 50 μM and 100 μM AO-242 showed a similar efficacy to AO-33 on ictaform events in the entorhinal cortex. Late recurrent discharges were also blocked by AO-33 and AO-242 although at higher concentrations (300 μM). The in vitro observations are with respect to order of efficacy in accordance with the in vivo data obtained in the maximal electroshock test in mice. The order of potency in the MES test was AO-242〉AO-33≫AO-294≫ AO-23. The results show that the erythro-isomer AO-23, although active, is much less potent than AO-33. Of the two optical isomers of losigamone the (+) isomer AO-242 is more active than the (−) form AO-294.
    Type of Medium: Electronic Resource
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