A permanent change in brain function resulting from daily electrical stimulation

Goddard, Graham V.; McIntyre, Dan C.; Leech, Curtis K.

doi:10.1016/0014-4886(69)90128-9

Cited by 2,887 publications

(982 citation statements)

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“…Kindling is a process whereby repeated electrical stimulation of certain brain areas, particularly the limbic system, with a fixed current strength and duration causes progressive and permanent intensification of epileptiform activity resulting in generalized seizures (Goddard, McIntyre, & Leech, 1969). Kindling in rodents has been well characterized both electrographically and behaviorally with progressive stages thought to mimic partial and secondary generalized human epilepsy (Racine, 1972).…”

Section: Introductionmentioning

confidence: 99%

Linking kindling to increased glutamate release in the dentate gyrus of the hippocampus through the STXBP5/tomosyn‐1 gene

et al. 2017

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IntroductionIn kindling, repeated electrical stimulation of certain brain areas causes progressive and permanent intensification of epileptiform activity resulting in generalized seizures. We focused on the role(s) of glutamate and a negative regulator of glutamate release, STXBP5/tomosyn‐1, in kindling.MethodsStimulating electrodes were implanted in the amygdala and progression to two successive Racine stage 5 seizures was measured in wild‐type and STXBP5/tomosyn‐1−/− (Tom−/−) animals. Glutamate release measurements were performed in distinct brain regions using a glutamate‐selective microelectrode array (MEA).ResultsNaïve Tom−/− mice had significant increases in KCl‐evoked glutamate release compared to naïve wild type as measured by MEA of presynaptic release in the hippocampal dentate gyrus (DG). Kindling progression was considerably accelerated in Tom−/− mice, requiring fewer stimuli to reach a fully kindled state. Following full kindling, MEA measurements of both kindled Tom+/+ and Tom−/− mice showed significant increases in KCl‐evoked and spontaneous glutamate release in the DG, indicating a correlation with the fully kindled state independent of genotype. Resting glutamate levels in all hippocampal subregions were significantly lower in the kindled Tom−/− mice, suggesting possible changes in basal control of glutamate circuitry in the kindled Tom−/− mice.ConclusionsOur studies demonstrate that increased glutamate release in the hippocampal DG correlates with acceleration of the kindling process. Although STXBP5/tomosyn‐1 loss increased evoked glutamate release in naïve animals contributing to their prokindling phenotype, the kindling process can override any attenuating effect of STXBP5/tomosyn‐1. Loss of this “braking” effect of STXBP5/tomosyn‐1 on kindling progression may set in motion an alternative but ultimately equally ineffective compensatory response, detected here as reduced basal glutamate release.

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Section: Introductionmentioning

confidence: 99%

Linking kindling to increased glutamate release in the dentate gyrus of the hippocampus through the STXBP5/tomosyn‐1 gene

et al. 2017

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“…In the kindling model of focal epilepsy, 15,30 daily repeated electrical stimulations (tetani, 2 s, 50 Hz) of limbic structures induce persistent enhancement of synaptic transmission and epileptiform activity. Ultimately, this leads to afterdischarges of increasing duration, severity and generalization.…”

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confidence: 99%

“…Ultimately, this leads to afterdischarges of increasing duration, severity and generalization. 15 In the CA1 area of the rat, 20-30 tetanic stimulations to the Schaffer collateral/commissural fibres are sufficient to evoke generalized tonic clonic seizures. 20 The enhanced excitability may last for months, even after termination of the stimulations.…”

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confidence: 99%

Calcium currents in pyramidal CA1 neurons in vitro after kindling epileptogenesis in the hippocampus of the rat

1996

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Calcium currents in pyramidal CA1 neurons in vitro after kindling epileptogenesis in the hippocampus of the rat Faas, G.C.; Vreugdenhil, M.; Wadman, W.J. Disclaimer/Complaints regulationsIf you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: http://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. Abstract--Calcium is an important second messenger which plays a role in the regulation of neuronal excitability and in many forms of synaptic plasticity. In kindling epileptogenesis, a model of focal epilepsy, calcium plays an important role. The in situ patch-clamp technique was used to record calcium currents in slices obtained from kindled rats and controls. We found that low-voltage-activated calcium currents, probably of dendritic origin, were larger after kindling (80%). The transient high-voltage-activated calcium currents were also enhanced after kindling (50% higher). The increase of the current is accompanied by a decrease in the time constant of inactivation. The change was still present six weeks after the kindling stimulations were stopped. These data demonstrate that low-voltage-activated calcium currents are involved in epileptogenesis. Their enhancement in the dendrites will boost synaptic depolarization and result in enhanced calcium influx, which is critically dependent on the specific activation pattern.

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“…Kindling epileptogenesis is effectuated by electrical tetanic stimulation, repeated at regular intervals, of a specific brain site [5]. In the course of kindling, the afterdischarges triggered by the stimulation become progressively longer and are accompanied by convulsive behaviour of increasing severity [25].…”

Section: Introductionmentioning

confidence: 99%

“…In the course of kindling, the afterdischarges triggered by the stimulation become progressively longer and are accompanied by convulsive behaviour of increasing severity [25]. The enhanced susceptibility for the generation and manifestation of epileptiform activity in the kindled animal is persistent for a long time [5].…”

Section: Introductionmentioning

confidence: 99%

Isozyme specific changes in the expression of protein kinase C isozyme (α-ζ) genes in the hippocampus of rats induced by kindling epileptogenesis

1995

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Isozyme specific changes in the expression of protein kinase C isozyme (alpha -) genes in the hippocampus of rats induced by kindling epileptogenesis Kamphuis, W.; Hendriksen, E.; Lopes da Silva, F.H. Disclaimer/Complaints regulationsIf you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: http://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. AbstractThe transcript levels of the protein kinase C (PKC) isoform genes during the development of a kindled epileptogenic focus, elicited by stimulation of Schaffer collateral/commissural fibres in the CA1 area of the rat hippocampus, were compared with the expression levels in control animals using a semi-quantitative in situ hybridization approach. In the hippocampus of control animals, the levels of PKC-o~-s r transcripts showed a gene-specific expression pattern and significant differences in expression level were observed between the neurons of CA1, CA3 and fascia dentata. In the early stages of kindling epileptogenesis, i.e. following 6 and 14 afterdischarges, specific changes in the expression levels of PKC-/3, -e, and -5 but not of PKC-a, -Y, and -6 were found. PKC-/3 expression was decreased in CA1, while the PKC-e and _r specific hybridization signals were increased in CAI, CA3 and fascia dentata. In fully kindled animals, that had experienced 10 generalized seizures, most expression levels tended to return to control values. One month after the last seizure no significant alterations were encountered. These results indicate an involvement of specific PKC-isoform gene expression in the induction of an epileptogenic focus, but not in the maintenance of the long-lasting kindled state.

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A permanent change in brain function resulting from daily electrical stimulation

Cited by 2,887 publications

References 10 publications

Linking kindling to increased glutamate release in the dentate gyrus of the hippocampus through the STXBP5/tomosyn‐1 gene

Linking kindling to increased glutamate release in the dentate gyrus of the hippocampus through the STXBP5/tomosyn‐1 gene

Calcium currents in pyramidal CA1 neurons in vitro after kindling epileptogenesis in the hippocampus of the rat

Isozyme specific changes in the expression of protein kinase C isozyme (α-ζ) genes in the hippocampus of rats induced by kindling epileptogenesis

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