Glial GABA Transporters as Modulators of Inhibitory Signalling in Epilepsy and Stroke
Research output: Chapter in Book/Report/Conference proceeding › Book chapter › Research › peer-review
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Glial GABA Transporters as Modulators of Inhibitory Signalling in Epilepsy and Stroke. / Lie, Maria E K; Al-Khawaja, Anas; Damgaard, Maria; Haugaard, Anne S; Schousboe, Arne; Clarkson, Andrew N; Wellendorph, Petrine.
Advances in Neurobiology. Vol. 16 2017. p. 137-167 (Advances in Neurobiology).Research output: Chapter in Book/Report/Conference proceeding › Book chapter › Research › peer-review
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TY - CHAP
T1 - Glial GABA Transporters as Modulators of Inhibitory Signalling in Epilepsy and Stroke
AU - Lie, Maria E K
AU - Al-Khawaja, Anas
AU - Damgaard, Maria
AU - Haugaard, Anne S
AU - Schousboe, Arne
AU - Clarkson, Andrew N
AU - Wellendorph, Petrine
PY - 2017
Y1 - 2017
N2 - Imbalances in GABA-mediated tonic inhibition are involved in several pathophysiological conditions. A classical way of controlling tonic inhibition is through pharmacological intervention with extrasynaptic GABAA receptors that sense ambient GABA and mediate a persistent GABAergic conductance. An increase in tonic inhibition may, however, also be obtained indirectly by inhibiting glial GABA transporters (GATs). These are sodium-coupled membrane transport proteins that normally act to terminate GABA neurotransmitter action by taking up GABA into surrounding astrocytes. The aim of the review is to provide an overview of glial GATs in regulating tonic inhibition, especially in epilepsy and stroke. This entails a comprehensive summary of changes known to occur in GAT expression levels and signalling following epileptic and ischemic insults. Further, we discuss the accumulating pharmacological evidence for targeting GATs in these diseases.
AB - Imbalances in GABA-mediated tonic inhibition are involved in several pathophysiological conditions. A classical way of controlling tonic inhibition is through pharmacological intervention with extrasynaptic GABAA receptors that sense ambient GABA and mediate a persistent GABAergic conductance. An increase in tonic inhibition may, however, also be obtained indirectly by inhibiting glial GABA transporters (GATs). These are sodium-coupled membrane transport proteins that normally act to terminate GABA neurotransmitter action by taking up GABA into surrounding astrocytes. The aim of the review is to provide an overview of glial GATs in regulating tonic inhibition, especially in epilepsy and stroke. This entails a comprehensive summary of changes known to occur in GAT expression levels and signalling following epileptic and ischemic insults. Further, we discuss the accumulating pharmacological evidence for targeting GATs in these diseases.
KW - Journal Article
U2 - 10.1007/978-3-319-55769-4_7
DO - 10.1007/978-3-319-55769-4_7
M3 - Book chapter
C2 - 28828609
VL - 16
T3 - Advances in Neurobiology
SP - 137
EP - 167
BT - Advances in Neurobiology
ER -
ID: 186088753