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  • Hippocampal slice  (3)
  • Epileptiform activity  (2)
  • Extracellular space  (2)
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  • 1
    Digitale Medien
    Digitale Medien
    Hippocampal slices of kindled rats reveal calcium involvement in epileptogenesis (1985)
    Springer
    Experimental brain research 57 (1985), S. 404-407 
    Details
    ISSN: 1432-1106
    Schlagwort(e): Epileptogenesis ; Kindling ; Hippocampal slice ; Extracellular calcium ; Extracellular potassium ; Rats
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Daily repeated tetanic electrical stimulation (kindling) of the brain may cause a long term enhancement of synaptic transmission and epileptiform activity of progressive severity and generalisation, eventually leading to spontaneous seizures. Evidence for a cellular mechanism underlying kindling has been obtained in vitro in slices from the hippocampus of kindled rats. A marked enhancement in extracellular calcium changes, induced by electrical stimulation or by iontophoresis of excitatory aminoacids was found in kindled tissue. This implies that changes in dendritic calcium conductances are involved in kindling epileptogenesis.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00236547
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  • 2
    Digitale Medien
    Digitale Medien
    Regional and time dependent variations of low Mg2+ induced epileptiform activity in rat temporal cortex slices (1991)
    Springer
    Experimental brain research 87 (1991), S. 581-596 
    Details
    ISSN: 1432-1106
    Schlagwort(e): Temporal cortex ; Entorhinal cortex ; Hippocampus ; NMDA ; Low Mg2+ ; Epileptiform activity ; Status epilepticus
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: 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.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00227083
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  • 3
    Digitale Medien
    Digitale Medien
    Spontaneous epileptiform activity of ca1 hippocampal neurons in low extracellular calcium solutions (1983)
    Springer
    Experimental brain research 51 (1983), S. 153-156 
    Details
    ISSN: 1432-1106
    Schlagwort(e): Hippocampal slice ; Epileptiform activity ; CA1 pyramidal cells ; Low calcium ; EGTA ; Rats
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Lowering extracellular [Ca2+] in rat hippocampal slices induces spontaneous epileptiform activity in area CA1, which is characterized by rhythmic burst firing of CA1 neurons and by prolonged negative potential shifts at the pyramidal cell body layer. This activity is accompanied by transient decreases of [Na+] and increases of [K+] in the extracellular space. In spite of the complete blockade of synaptic transmission, the wave of epileptiform activity propagates across area CA1. These findings suggest, that non-synaptic mechanisms may play a role in the generation and spread of epileptiform activity in the mammalian CNS.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00236813
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  • 4
    Digitale Medien
    Digitale Medien
    Stimulus-induced changes in extracellular Na+ and Cl− concentration in relation to changes in the size of the extracellular space (1982)
    Springer
    Experimental brain research 46 (1982), S. 73-84 
    Details
    ISSN: 1432-1106
    Schlagwort(e): Extracellular space ; Na+ and Cl− concentration ; Effects of metabolism on osmolarity ; Epilepsy ; Cerebral cortex
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: 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.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00238100
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  • 5
    Digitale Medien
    Digitale Medien
    Transient changes in the size of the extracellular space in the sensorimotor cortex of cats in relation to stimulus-induced changes in potassium concentration (1980)
    Springer
    Experimental brain research 40 (1980), S. 432-439 
    Details
    ISSN: 1432-1106
    Schlagwort(e): Extracellular space ; K+ regulation ; Spatial K+ buffering ; Epilepsy ; Cerebral cortex
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: 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.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00236151
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  • 6
    Digitale Medien
    Digitale Medien
    Effects of T-type, L-type, N-type, P-type, and Q-type calcium channel blockers on stimulus-induced pre-and postsynaptic calcium fluxes in rat hippocampal slices (1996)
    Springer
    Experimental brain research 109 (1996), S. 22-32 
    Details
    ISSN: 1432-1106
    Schlagwort(e): Calcium ; Hippocampal slice ; CA1 ; ω-Agatoxin IVA ; ω-Conotoxin GVIA ; ω-Conotoxin ; MVIIC ; Nimodipine ; Ethosuximide ; Trimethadion ; Rat
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract The contribution of T-, L-, N-, P-, and Q-type Ca2+ channels to pre-and postsynaptic Ca2+ entry during stimulus-induced high neuronal activity in area CA1 of rat hippocampal slices was investigated by measuring the effect of specific blockers on stimulus-induced decreases in extracellular Ca2+ concentration ([Ca2+]0). [Ca2+]0 was measured with ion-selective electrodes in stratum radiatum (SR) and stratum pyramidale (SP), while Ca2+ entry into neurons was induced with stimulus trains (20 Hz for 10 s) alternately delivered to SR and the alveus, respectively. The [Ca2+]0 decreases recorded in SR in response to SR stimulation represented mainly presynaptic Ca2+ entry (Capre), while [Ca2+]0 decreases recorded in SP in response to alvear stimulation were predominantly based on postsynaptic Ca2+ entry (Capost). Ethosuximide and trimethadione were ineffective m concentrations up to 1 mM. At 10 mM, they reduced Capost and, much less, also Capre Nimodipine (25 μM) reduced Capost and, to a minor extent, Capre. ω-Agatoxin IVA (0.4–1 μM) and ω-conotoxin MVIIC (1 μM) also reduced both Capre and Capost, but with a stronger action on Capre. ω-Conotoxin GVIA (3–8 μM) reduced Capost without effect on Capre. We conclude that during stimulus-induced, high-frequency neuronal activity Capost is carried by P/Q-, N-, and L-type channels and probably a further channel type different from these channels. Capre includes at least P/Q-and possibly L-type channels. N-type channels did not contribute to Capre in our experiments. Since ethosuximide and trimethadione were only effective in high concentrations, their action may be unspecific. Thus, T-type channels do not seem to play a major part in Ca2+ entry in this situation.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00228623
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