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  • 1
    ISSN: 1432-1106
    Schlagwort(e): Epilepsy ; Calcium antagonists ; Verapamil ; Flunarizine ; Neocortex
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Effects of the organic calcium antagonists verapamil and flunarizine on pentylenetetrazol induced paroxysmal depolarizations were tested in organotypic neocortical explants taken from neonatal rats. In these in vitro experiments the papaverin derivative verapamil depressed, and finally abolished, epileptic discharges in all cases. The piperazine derivative flunarizine, however, which is known to suppress epileptic discharges in hippocampal CA3 neurons (Bingmann and Speckmann 1986), showed no significant antiepileptic effects in the explanted neocortical neurons. Thus, the present findings may indicate that the suppressive action of flunarizine on the generation of paroxysmal depolarizations is restricted to distinct populations of neurons.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    ISSN: 1432-1106
    Schlagwort(e): Organic calcium antagonists ; Flunarizine ; Verapamil ; Epileptic discharges ; CA3 neurones in hippocampal slices
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Antiepileptic actions of the organic calcium antagonists flunarizine (cinnarizine derivate) and verapamil (papaverin derivat) on pentylenetetrazol-induced epileptic bioelectric activity were tested in CA3 neurones of hippocampal slices. In all experiments both calcium antagonists reduced the amplitudes and/or durations of paroxysmal depolarizations as well as their rate of occurrence, when the bath concentrations of flunarizine or verapamil exceeded 20 μmol/l. When they were added to the bath solution before pentylenetetrazol application, recordings of the resting membrane potential, of the membrane resistance, of action potentials and of spontaneous as well as of evoked excitatory and inhibitory postsynaptic potentials gave no indication that the antiepileptic effects of these drugs are due to unspecific depressive actions on neuronal excitability or spread of excitation.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 3
    Digitale Medien
    Digitale Medien
    Springer
    Experimental brain research 79 (1994), S. 376-384 
    ISSN: 1432-1106
    Schlagwort(e): Verapamil ; Calcium channel blockers Epilepsy ; Hippocampus ; Guinea pig
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract The aim of the present study was to test whether the organic calcium channel blocker verapamil acts not only on spontaneously occurring epileptiform field potentials (EFP) but also on EFP triggered by single electrical stimuli in the low-Mg2+ epilepsy model. The experiments were carried out on hippocampal slices of guinea pigs. EFP were elicited by omission of Mg2+ from the perfusate and recorded from stratum pyramidale and stratum radiatum in the CA1 subfield. Single electrical stimuli were applied to the Schaffer collateral pathway. Verapamil was added to the bath solution in concentrations of 40 and 60 μmol verapamil/1 at normal (4 mmol/l) and elevated (8 mmol/1) K+ levels. After omission of Mg2+ from the perfusate, spontaneously occurring EFP appeared in all trials. These spontaneously occurring EFP were suppressed dose-dependently upon addition of verapamil to the perfusate. At elevated K+ levels, the latencies to suppression were significantly reduced and the dose dependency was abolished for the two doses of verapamil used. Triggered EFP reappeared upon stimulation after spontaneously occurring EFP had been suppressed, except for trials with 60 /gmmol verapamil/1 bath solution with elevated K+ levels. The stimulus-evoked EFP were abolished with continuing perfusion of verapamil except for trials with 40 μmol/1 at normal extracellular K+ concentrations. This effect was again dose dependent and enhanced by elevating the K+ level. In all experiments, stimulus-evoked EFP reappeared upon wash-out of verapamil. A primary action of verapamil on pacemaker functions in epileptogenic tissue is assumed.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 4
    Digitale Medien
    Digitale Medien
    Springer
    Pflügers Archiv 319 (1970), S. 122-138 
    ISSN: 1432-2013
    Schlagwort(e): Spinal Neurones ; Membrane Potential ; Postsynaptic Potentials ; Asphyxia ; Gas Tensions ; Spinale Neurone ; Membranpotential ; postsynaptische Potentiale ; Asphyxie ; Gewebsgasdrucke
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Beschreibung / Inhaltsverzeichnis: Zusammenfassung An Albinoratten wurden die Veränderungen des Membranpotentials (MP), der postsynaptischen Potentiale (PSP) und der Entladungsfrequenz (EF) lumbaler Neurone bei Asphyxie untersucht und mit den Schwankungen despO2 undpCO2 korreliert. Die Versuche ergaben: 1. Im Beginn einer Asphyxie entwickelt sich an allen lumbalen Neuronen zunächst eine Depolarisation. Die Verminderung des MP ist in der Regel mit einer Zunahme excitatorischer PSP und mit einer Steigerung der EF gekoppelt. Dieser Effekt beruht auf der Senkung despO2. 2. Bei länger dauernden Atemstillständen und nach erfolgreicher Reventilation lassen sich zwei neuronale Reaktionstypen unterscheiden: a) Bei etwa 10% der lumbalen Einheiten, bei denen es sich ausschließlich um Interneurone handelt, nimmt die initiale Depolarisation weiter zu, bis der Spikegenerator versagt. In der postasphyktischen Phase steigt die EF sofort wieder an und zeigt dabei einen Überschuß. b) Bei etwa 90% der lumbalen Einheiten wird die initiale Depolarisation von einer intermediären Hyperpolarisation gefolgt, die erst nach einer Latenz von 3 bis 5 min in die terminale Depolarisation umschlägt. In der postasphyktischen Phase zeigen diese Neurone eine reaktive Hyperpolarisation, die mit einer längeren Hemmung der Spikeaktivität einhergeht, auch wenn derpO2 nach der Reventilation sofort wieder ansteigt. 3. Die beschriebenen Reaktionsunterschiede lumbaler Neurone lassen sich auf excitatorische und inhibitorische CO2-Wirkungen zurückführen. Bei der Interpretation der Befunde wird dementsprechend zwischen E- und I-Neuronen unterschieden.
    Notizen: Summary The action of asphyxiation on the membrane potential (MP), on postsynaptic potentials (PSP's) and on the discharge frequency (DF) of lumbar neurones was studied in rats. The bioelectric activity changes were related to the fluctuations of thepO2 andpCO2. The following results have been obtained: 1. At the onset of asphyxiation all lumbar neurones tend to depolarize. As a rule, the lowering of the MP is associated with an increase of excitatory PSP's and with a rise of DF. This initial effect can be attributed to oxygen deficiency. 2. With continued respiratory arrest and after reventilation two types of neuronal responses can be differentiated: a) In about 10% of lumbar units, all of which proved to be interneurones, the initial depolarization progresses until spike generation fails. In these units reventilation is followed by an increase of DF which passes an overshoot. b) About 90% of lumbar neurones develop an intermediate hyperpolarization interpersed among the initial and terminal depolarizations. In the postasphyxial phase these units show a reactive incease of MP accompanied by a suppression of excitatory PSP's and of spike discharges. This inhibitiory effect is demonstrable also with an immediate rise of tissuepO2 above normal level. 3. The diverging responses of lumbar neurones to asphyxiation can be attributed to excitatory and inhibitory actions of carbon dioxide on different cell types labelled as E- and I-neurones.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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