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W J Wadman

Publications and source records attributed to W J Wadman.

62 records · Page 4Linked to original sources
PubMed1986

Extracellular calcium and potassium concentration changes in chronic epileptic brain tissue.

Repetitive electrical stimulation and application of excitatory amino acids lead to decreases in extracellular Ca2+ concentration and to rises in extracellular K+ concentration [( Ca2+]o, [K+]o) with a typical laminar distribution in a given neo- or allocortical structure. These ionic changes result from transmembrane ion fluxes along their respective electrochemical gradients. Epileptogenic drugs that impair repolarizing K+ conductances or inhibitory synaptic transmission enhance such extracellular ionic changes, but they do not alter the laminar distribution of [K+]o and [Ca2+]o changes. Enhanced [Ca2+]o concentration changes are also observed in chronic epilepsies such as the chronic alumina cream and cobalt focus, the kindling epilepsy, and during photically induced seizures in the baboon Papio papio. In chronic epilepsies, the sites of maximal [Ca2+]o changes shift to other layers, suggesting changes in the distribution of ion channels over the surface of nerve cells that may be involved in epileptogenesis in chronic epilepsies. The K+ and Ca2+ concentration changes associated with seizure contribute to the generation and spread of epileptic activity. This is demonstrated by the fact that lowering of extracellular free calcium concentration can induce spreading epileptiform activity in the absence of chemical synaptic transmission, with [K+]o rises preceding epileptiform activity.

Aluminum Oxide↗
PubMed1985

Hippocampal slices of kindled rats reveal calcium involvement in epileptogenesis.

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.

Animals↗
PubMed1983

Two types of interictal transients of reversed polarity in rat hippocampus during kindling.

Two different types of spontaneous interictal transients (SITs) have been found in the course of the development of an epileptogenic focus by Schaffer collateral kindling in the CA1 region of rat hippocampus. The first type has peak amplitudes of 250 microV up to 1 mV, a duration of about 80 msec and the same polarity as field potentials recorded from the same sites evoked by Schaffer collateral stimulation. These SITs occur early during kindling, but are also observed at later stages. The second type, which is dominant in later stages of kindling, has peak amplitudes of 2-3 mV, a duration of about 20 msec and the opposite polarity; in a later stage it may also contain a clear population spike. Both types can be considered as being caused by equivalent dipoles situated across the pyramidal cell layer of CA1 but with inverted polarities.

Animals↗
PubMed1982

Common aspects of the development of a kindling epileptogenic focus in the prepyriform cortex of the dog and in the hippocampus of the rat: spontaneous interictal transients with changing polarities.

Long-term records of field potentials during kindling were analysed in 2 preparations: the prepyriform cortex (PPC) in dog and the CA1 subarea of the hippocampus in rat. Besides the occurrence of after-discharges directly following the kindling stimulus, short transients were found to occur spontaneously between seizures: spontaneous inter-ictal transients or SITs. In both the PPC and the hippocampus 2 different types of SITs were encountered. Both types corresponded to a dipole layer centred around the main local pyramidal neurones (PPC or hippocampus). One type occurred early in the course of kindling and had the same polarity as the local evoked potential (EP) produced by stimulation of the lateral olfactory tract in PPC or of the Schaffer collaterals in the hippocampus. The other type occurred at later stages and had a reversed polarity to the EP. These findings were interpreted as indicating that at the onset of kindling spontaneously occurring depolarizations corresponding to the early type of SITs are restricted to the level of the synapses to which the kindling stimulus is applied; at a later stage, when convulsions are likely to occur, large spontaneous depolarizations corresponding to the late type of SITs are generated at the level of the cell bodies.

Animals↗
PubMedDate not supplied

An experimental model of progressive epilepsy: the development of kindling of the hippocampus of the rat.

Kindling epileptogenesis was induced by periodic electrical stimulation of the Schaffer collateral/commissural pathway in the CA1 area of the rat hippocampus. The progressive nature of hippocampal kindling is demonstrated by a detailed description of the behavioral signs and the progressive increase of the after-discharge duration in the course of kindling acquisition. Furthermore, the evolution of the alterations in the paired-pulse local evoked field potentials and the modifications of the GABAA receptor binding and of the expression of mRNAs encoding for the subunits of the GABAA and glutamate receptors are considered. Evidence is presented that during kindling opposite changes occur in the CA1 and the fascia dentata in terms of the balance between excitation and inhibition due to contrasting changes in GABA-mediated inhibitory function.

Animals↗