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KA channels suppress cellular responses to fast ripple activity – implications for epilepsy
KTH, Skolan för datavetenskap och kommunikation (CSC), Beräkningsbiologi, CB.
KTH, Skolan för datavetenskap och kommunikation (CSC), Beräkningsbiologi, CB.ORCID-id: 0000-0003-0281-9450
2009 (engelsk)Inngår i: BMC neuroscience (Online), ISSN 1471-2202, E-ISSN 1471-2202, Vol. 10, nr Suppl 1, s. P226-Artikkel i tidsskrift (Fagfellevurdert) Published
sted, utgiver, år, opplag, sider
2009. Vol. 10, nr Suppl 1, s. P226-
HSV kategori
Identifikatorer
URN: urn:nbn:se:kth:diva-25916DOI: 10.1186/1471-2202-10-S1-P226OAI: oai:DiVA.org:kth-25916DiVA, id: diva2:360778
Merknad
QC 20101104. Eighteenth Annual Computational Neuroscience Meeting: CNS*2009 Berlin, Germany. 18–23 July 2009 Tilgjengelig fra: 2010-11-04 Laget: 2010-11-04 Sist oppdatert: 2018-01-12bibliografisk kontrollert
Inngår i avhandling
1. A-type Potassium Channels in Dendritic Integration: Role in Epileptogenesis
Åpne denne publikasjonen i ny fane eller vindu >>A-type Potassium Channels in Dendritic Integration: Role in Epileptogenesis
2009 (engelsk)Licentiatavhandling, med artikler (Annet vitenskapelig)
Abstract [en]

During cognitive tasks, synchronicity of neural activity varies and is correlated with performance. However, there may be an upper limit to normal synchronised activity – specifically, epileptogenic activity is characterized byexcess spiking at high synchronicity. An epileptic seizure has a complicated course of events and I therefore focused on the synchronised activity preceding a seizure (fast ripples). These high frequency oscillations (200–1000 Hz) have been identified as possible signature markers of epileptogenic activity and may be involved in generating seizures. Moreover, a range of ionic currents have been suggested to be involved in distinct aspects of epileptogenesis. Based on pharmacological and genetic studies, potassium currents have been implicated, in particular the transient A–type potassium channel (KA). Our first objective was to investigate if KA could suppress synchronized input while minimally affecting desynchronised input. The second objective was to investigate if KA could suppress fast ripple activity. To study this I use a detailed compartmental model of a hippocampal CA1 pyramidal cell. The ion channels were described by Hodgkin–Huxley dynamics.

The result showed that KA selectively could suppress highly synchronized input. I further used two models of fast ripple input and both models showed a strong reduction in the cellular spiking activity when KA was present. In an ongoing in vitro brain slice experiment our prediction from the simulations is being tested. Preliminary results show that the cellular response was reduced by 30 % for synchronised input, thus confirming our theoretical predictions. By suppressing fast ripples KA may prevent the highly synchronised spiking activity to spread and thereby preventing the seizure. Many antiepileptic drugs down regulate cell excitability by targeting sodium channels or GABA–receptors. These antiepileptic drugs affect the cell during normal brain activity thereby causing significant side effects. KA mainly suppresses the spiking activity when the cell is exposed to abnormally high synchronised input. An enhancement in the KA current might therefore be beneficial in reducing seizures while not affecting normal brain activity.

sted, utgiver, år, opplag, sider
Stockholm: KTH Royal Institute of Technology, 2009. s. x, 54
Serie
TRITA-CSC-A, ISSN 1653-5723 ; 2009:18
Emneord
epileptogenesis, fast ripples, synchronicity, dendritic potentials, transient A–type potassium current, KV 4.2
HSV kategori
Identifikatorer
urn:nbn:se:kth:diva-11291 (URN)978-91-7415-471-9 (ISBN)
Presentation
2009-11-04, RB35, Roslagstullsbacken 35, Stockholm, 10:00 (engelsk)
Opponent
Veileder
Tilgjengelig fra: 2009-10-16 Laget: 2009-10-14 Sist oppdatert: 2018-01-12bibliografisk kontrollert

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