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Showing papers on "Epileptogenesis published in 1988"


Journal ArticleDOI
04 Mar 1988-Science
TL;DR: In this paper, morphological evidence was provided that synchronous perforant path activation and kindling of limbic pathways induce axonal growth and synaptic reorganization in the hippocampus, in the absence of overt morphological damage.
Abstract: Abnormal functional activity induces long-lasting physiological alterations in neural pathways that may play a role in the development of epilepsy. The cellular mechanisms of these alterations are not well understood. One hypothesis is that abnormal activity causes structural reorganization of neural pathways and promotes epileptogenesis. This report provides morphological evidence that synchronous perforant path activation and kindling of limbic pathways induce axonal growth and synaptic reorganization in the hippocampus, in the absence of overt morphological damage. The results show a previously unrecognized anatomic plasticity associated with synchronous activity and development of epileptic seizures in neural pathways.

878 citations


Journal ArticleDOI
TL;DR: Frank Tortella reviews the proconvulsant/anticonvulsant pharmacology of opioid peptides, the evidence for their involvement in postictal mechanisms, and the possible existence in the CNS of an endogenous enticonVulsant substance with opioid peptide-like characteristics.

122 citations


Journal ArticleDOI
TL;DR: A novel model of focal, cortical epilepsy is described and a significant correlation was found between infusion time and duration of the excitability rebound, with the longer duration corresponding to the shorter infusion time.

72 citations



Book ChapterDOI
01 Jan 1988
TL;DR: Little attention has been directed at seizure propagation pathways beyond the level of the interneuron and there have been relatively few studies designed to identify the subcortical pathways which function as substrates of convulsant or anticonvulsant drug action.
Abstract: Rather than spreading randomly throughout the brain, convulsive seizure activity appears to be generated and propagated via specific anatomical routes. During the past fifty years, a broad range of experimental techniques have been applied to the study of cortical and subcortical circuitry involved in seizure development and spread. With respect to subcortical circuitry, substrates for seizure propagation were actively pursued during the 1950s but these investigations subsequently lost momentum, nearly disappearing until a few years ago. In the interim, technologies directed at molecular and cellular mechanisms of epileptogenesis have fostered a predominantly cortical perspective in epilepsy research (broadened today to include both neocortex and the archicortex of hippocampus). Along with this focus on cortical mechanisms has emerged an analysis of epileptiform activity using in vitro preparations of tissues isolated from the complex circuitry of the CNS in vivo. It has been in such isolated preparations that basic mechanisms of action of selective neuropharmacological agents have been best characterized. In contrast, little attention has been directed at seizure propagation pathways beyond the level of the interneuron and there have been relatively few studies designed to identify the subcortical pathways which function as substrates of convulsant or anticonvulsant drug action.

32 citations


Journal ArticleDOI
TL;DR: It is concluded that the deep prepyriform cortex kindles readily at a rate that is similar to that of surrounding basal forebrain tissue and that the integrity of the DPC is not necessary for basolateral amygdaloid kindling.

22 citations



Journal ArticleDOI
TL;DR: It is suggested that while kindling produces enduring increases in seizure susceptibility, it causes no persistent interictal changes in either basal activity or several measures of transmitter sensitivity of substantia nigra pars reticulata neurons.

12 citations


Journal ArticleDOI
TL;DR: The results suggest an inhibitory role of endogenous opioids and/or GABA in epileptogenesis in epilepsy, which is produced by repeated i.p. administration of naloxone chloride and sensory stimulation in freely moving cats.
Abstract: Epileptogenesis produced by repeated i.p. administration of naloxone chloride and sensory stimulation (photoacoustic stimulation at 1, 3, 10, and 15 Hz) every 15 min was studied in freely moving cats. The repeated administration of naloxone provoked some behavioral manifestations that resemble those produced by electrical amygdaloid kindling. Photoacoustic stimulation accentuated the manifestations. All the animals presented generalized behavioral seizures when total naloxone administration reached 80 mg/kg. None of the animals demonstrated postictal depression. These results suggest an inhibitory role of endogenous opioids and/or GABA in epileptogenesis.

7 citations


BookDOI
01 Jan 1988

4 citations


Book ChapterDOI
01 Jan 1988
TL;DR: It is reported that NE enhances both stimulus and NMDA induced Ca2+ influx into granule cells via α1 receptors, and elicits long-lasting depolarization requiring NMDA receptor activation to persist.
Abstract: Depleting brain norepinephrine (NE) impairs long-term potentiation (LTP) of perforant path (PP)-dentate gyrus (DG) synapses, promotes induction of kindled epilepsy, and NE elicits long-lasting potentiation of PP evoked potentials. We now report that NE enhances both stimulus and NMDA induced Ca2+ influx into granule cells via α1 receptors, and elicits long-lasting depolarization requiring NMDA receptor activation to persist. Furthermore, the induction of kindled epilepsy is associated with reduced sensitivity to NE, which may represent a neuronal “write-protect” mechanism and also contribute to epileptogenesis.