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https://umu.diva-portal.org/smash/project.jsf?pid=project:1228
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Project
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Project grant
Title [sv]
Mekanismer bakom epilepsi och kronisk smärta: Kontroll av neuronal retbarhet via GABA- och glycin-aktiverade jonkanaler
Title [en]
Mechanisms underlying epilepsy and chronic pain: Control of neuronal excitability via GABA- and glycine-gated ion channels
Abstract [sv]
The project aims at identifying and elucidating the mechanisms that underlie increased neuronal excitability and thereby cause epilepsy and chronic pain. Recent research shows that a rise in the intracellular Cl- concentration, which makes the transmitters GABA and glycine excite neurons, is critical for the development of several types of epilepsy and chronic pain. The causes of the rise in Cl- concentration are not well understood. The present project will clarify the mechanisms behind altered Cl- concentration and raised neuronal excitability. We have shown that GABA- and glycine-controlled Cl- channels in the cell membrane may stay open longer than previously thought and thereby affect the Cl- concentration and the cellular excitability. We have also shown that outward transport of Cl- is very slow. On the basis of these findings, we have formulated, and will test, (i) a hypothesis specifying the conditions for the induction of increased excitability and (ii) a hypothesis that the increased excitability may be reversed to normal by appropriate stimulation! The studies of neuronal excitability are performed by electrophysiological and optical methods with measurements of neuronal impulse activity, ion currents and ion concentrations. The project, with clarification of cellular mechanisms behind epilepsy and chronic pain, is highly important for the possibilities to prevent such conditions and to treat them effectively.
Principal Investigator
Johansson, Staffan
Umeå University
Coordinating organisation
Umeå University
Funder
Vetenskapsrådet
Period
2013-01-01 - 2016-12-31
National Category
Neurosciences
Physiology
Cell and Molecular Biology
Identifiers
DiVA, id: project:1228
Project, id: 2012-01740_VR
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