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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 51 (1983), S. 153-156 
    ISSN: 1432-1106
    Keywords: Hippocampal slice ; Epileptiform activity ; CA1 pyramidal cells ; Low calcium ; EGTA ; Rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: 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.
    Type of Medium: Electronic Resource
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  • 2
    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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