dc.contributor.author
Angamo, Eskedar Ayele
dc.contributor.author
ul Haq, Rizwan
dc.contributor.author
Roesner, Joerg
dc.contributor.author
Gabriel, Siegrun
dc.contributor.author
Gerevich, Zoltan
dc.contributor.author
Heinemann, Uwe
dc.contributor.author
Kovacs, Richard
dc.date.accessioned
2018-06-08T10:57:34Z
dc.date.available
2017-11-20T09:22:38.066Z
dc.identifier.uri
https://refubium.fu-berlin.de/handle/fub188/21391
dc.identifier.uri
http://dx.doi.org/10.17169/refubium-24685
dc.description.abstract
Neuronal lactate uptake supports energy metabolism associated with synaptic
signaling and recovery of extracellular ion gradients following neuronal
activation. Altered expression of the monocarboxylate transporters (MCT) in
temporal lobe epilepsy (TLE) hampers lactate removal into the bloodstream. The
resulting increase in parenchymal lactate levels might exert both, anti- and
pro-ictogen effects, by causing acidosis and by supplementing energy
metabolism, respectively. Hence, we assessed the contribution of lactate to
the maintenance of transmembrane potassium gradients, synaptic signaling and
pathological network activity in chronic epileptic human tissue. Stimulus
induced and spontaneous field potentials and extracellular potassium
concentration changes (∆[K+]O) were recorded in parallel with tissue pO2 and
pH in slices from TLE patients while blocking MCTs by
α-cyano-4-hydroxycinnamic acid (4-CIN) or d-lactate. Intrinsic lactate
contributed to the oxidative energy metabolism in chronic epileptic tissue as
revealed by the changes in pO2 following blockade of lactate uptake. However,
unlike the results in rat hippocampus, ∆[K+]O recovery kinetics and field
potential amplitude did not depend on the presence of lactate. Remarkably,
inhibition of lactate uptake exerted pH-independent anti-seizure effects both
in healthy rat and chronic epileptic tissue and this effect was partly
mediated via adenosine 1 receptor activation following decreased oxidative
metabolism. View Full-Text
en
dc.rights.uri
http://creativecommons.org/licenses/by/4.0/
dc.subject
monocarboxylate transporter inhibitors
dc.subject
interictal activity
dc.subject
mesial temporal lobe epilepsy
dc.subject.ddc
600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit
dc.title
Contribution of Intrinsic Lactate to Maintenance of Seizure Activity in
Neocortical Slices from Patients with Temporal Lobe Epilepsy and in Rat
Entorhinal Cortex
dc.type
Wissenschaftlicher Artikel
dcterms.bibliographicCitation
Int. J. Mol. Sci. - 18 (2017), 9, S. 1835
dcterms.bibliographicCitation.doi
10.3390/ijms18091835
dcterms.bibliographicCitation.url
http://www.mdpi.com/1422-0067/18/9/1835
refubium.affiliation
Charité - Universitätsmedizin Berlin
de
refubium.mycore.fudocsId
FUDOCS_document_000000028502
refubium.note.author
Der Artikel wurde in einer reinen Open-Access-Zeitschrift publiziert.
refubium.resourceType.isindependentpub
no
refubium.mycore.derivateId
FUDOCS_derivate_000000009128
dcterms.accessRights.openaire
open access