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Epileptogenesis

If a subconvulsive stimulus is applied, generally in rats, at regular intervals, e.g. daily for some two weeks to a specific brain area, especially the amygdala or hippocampus, then eventually full localised (partial) or secondary generalised seizures develop. A similar effect can be obtained by the repeated localised injection of subconvulsive doses of some convulsants. The ability of a drug to reduce the kindled seizure itself may be indicative of value in partial seizure but if it slows the actual development of kindling that may indicate some ability to retard epileptogenesis. [Pg.328]

Figure 16.3 Changes in neuronal function required for the development of epileptic seizures. The factors that may control or induce the changes in neuronal function that turn a normal neuron into a focal one (A) recruit other neurons (focal epileptogenesis) to produce an interictal EEG spike (B) and ensure the spread of activity (general epileptogenesis) to full ictal activity (C) are discussed in the text. They include alterations to various ion channels, especially those for Na, a reduction in local inhibitory activity or an increase in local excitatory drive. The electrophysiological counterparts of some of the events involved are shown in Fig. 16.2... Figure 16.3 Changes in neuronal function required for the development of epileptic seizures. The factors that may control or induce the changes in neuronal function that turn a normal neuron into a focal one (A) recruit other neurons (focal epileptogenesis) to produce an interictal EEG spike (B) and ensure the spread of activity (general epileptogenesis) to full ictal activity (C) are discussed in the text. They include alterations to various ion channels, especially those for Na, a reduction in local inhibitory activity or an increase in local excitatory drive. The electrophysiological counterparts of some of the events involved are shown in Fig. 16.2...
NTs it is now appropriate to consider what evidence there is for a malfunction of NT activity in epilepsy, particularly in those responsible for primary excitation and inhibition, i.e. the amino acids. Before doing so the epileptogenesis of absence seizures (petit mal) justifies separate consideration. [Pg.335]

Avanzini, G (1992) Generalised epileptogenesis. In Epileptogenic and Excitotoxic Mechanisms (Eds Avanzini, G, Fariello, R, Heinemann, U and Mutani, R), John Libbey, London pp.29 0. [Pg.350]

Anticonvulsant action of the nucleoside transport inhibitor, soluflazine, on synaptic and non-synaptic epileptogenesis in the guinea-pig hippocampus. Epilepsy Res. 2 (2), 65-71. [Pg.353]

Cyclooxygenase-2 participates in aberrant synaptic plasticity during epileptogenesis 582... [Pg.575]

Cyclooxygenase-2 participates in aberrant synaptic plasticity during epileptogenesis. Neuronal COX-2 expression is also upregulated in experimental epileptogenesis, when aberrant synaptic plasticity is thought to... [Pg.582]

The exact mechanism by which COX-2 inhibition attenuates kindling epileptogenesis is not understood. Notwithstanding, COX-2 inhibition may diminish prostaglandin and/or PAF synthesis, lipid messengers that are both involved in synaptic facilitation [45]. Moreover, kindling epileptogenesis promotes selective neuronal COX-2... [Pg.583]

Epileptogenesis is the process by which a normal brain becomes epileptic 633... [Pg.629]

Identifying molecular mechanisms of epileptogenesis will provide new targets for developing small molecules to prevent epilepsy 633... [Pg.629]

Epileptogenesis is the process by which a normal brain becomes epileptic. The very complexity of understanding mechanisms underlying the hyperexcitability of the epileptic brain has contributed to enhanced emphasis in attempts to prevent development of epilepsy, i.e. epileptogenesis. [Pg.633]

DeLorey, T. M., and Olsen, R. W. (1999) GABA and epileptogenesis comparing gabrb3 gene-deficient mice with Angelman syndrome in man. Epilepsy Res. 36, 123-132. [Pg.110]

The cascade of histological/biochemical events that characterize epileptogenesis differs from those of ictogenesis. At the histological level, epileptogenesis involves cellular alterations (brain scarring, referred to as mesial temporal sclerosis) in a variety of... [Pg.431]

Neugebauer, V., Keele, N. B., Shinnick-Gallagher, P.. Epileptogenesis in vivo enhances the sensitivity of inhibitory presynaptic metabotropic glutamate receptors in basolateral amygdala neurons in vitro, J. Neurosci. 1997, 17, 983-995. [Pg.387]

Li T, Ren G, Lusardi T, Wilz A, Lan JQ, Iwasato T, Itohara S, Simon RP, Boison D (2008) Adenosine kinase is a target for the prediction and prevention of epileptogenesis in mice. J Clin Invest 118(2) 571-582... [Pg.185]

Bazan N. G., TuB., and Rodriguez de Turco E. B. (2002). What synaptic lipid signaling tells us about seizure-induced damage and epileptogenesis. In Sutula T. and Pitkanen A. (eds.), Do Seizures Damage the Brain. Perspectives in Analytical Philosophy Elsevier Science BV, Amsterdam, pp. 175-185. [Pg.190]


See other pages where Epileptogenesis is mentioned: [Pg.328]    [Pg.329]    [Pg.332]    [Pg.334]    [Pg.336]    [Pg.350]    [Pg.90]    [Pg.90]    [Pg.445]    [Pg.88]    [Pg.583]    [Pg.629]    [Pg.632]    [Pg.633]    [Pg.638]    [Pg.109]    [Pg.143]    [Pg.175]    [Pg.686]    [Pg.246]    [Pg.431]    [Pg.431]    [Pg.432]    [Pg.432]    [Pg.509]    [Pg.170]    [Pg.182]    [Pg.185]    [Pg.27]    [Pg.169]   
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See also in sourсe #XX -- [ Pg.431 ]

See also in sourсe #XX -- [ Pg.248 ]

See also in sourсe #XX -- [ Pg.85 , Pg.86 , Pg.114 , Pg.115 , Pg.116 ]




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Epilepsy epileptogenesis

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