caa a22 4500 606201440 CHVBK 20210128100948.0 cr unu---uuuuu 210128e20150101xx s 000 0 eng 10.1007/s00429-013-0672-x doi (NATIONALLICENCE)springer-10.1007/s00429-013-0672-x Monocarboxylate transporters in temporal lobe epilepsy: roles of lactate and ketogenic diet [Elektronische Daten] [Fredrik Lauritzen, Tore Eid, Linda Bergersen] Epilepsy is a serious neurological disorder that affects approximately 1% of the general population, making it one of the most common disorders of the central nervous system. Furthermore, up to 40% of all patients with epilepsy cannot control their seizures with current medications. More efficacious treatments for medication refractory epilepsy are therefore needed. A better understanding of the mechanisms that cause this disorder is likely to facilitate the discovery of such treatments. Impairment in cerebral energy metabolism has been proposed as a possible causative factor in the pathogenesis of temporal lobe epilepsy (TLE), which is one of the most common types of medication-refractory epilepsies in adults. In this review, we will discuss some of the current hypotheses regarding the possible causal relationship between brain energy metabolism and TLE. Emphasis will be placed on the role of energy substrates (lactate and ketone bodies) and their transporter molecules, particularly monocarboxylate transporters 1 and 2 (MCT1 and MCT2). We recently reported that the cellular distribution of MCT1 and MCT2 is perturbed in the hippocampus in patients with TLE. The changes may be an adaptive response aimed at keeping high levels of lactate in the epileptic tissue, which may serve to counteract epileptic activity by downregulating cAMP levels through the lactate receptor GPR81, newly discovered in hippocampus. We propose that the perturbation of MCTs may be further involved in the pathophysiology of TLE by influencing brain energy homeostasis, mitochondrial function, GABA-ergic and glutamatergic neurotransmission, and flux of lactate through the brain. Springer-Verlag Berlin Heidelberg, 2013 Energy failure nationallicence Pathophysiology nationallicence Immunocytochemistry nationallicence Electronmicroscopy nationallicence Human nationallicence Rodent nationallicence Blood-brain barrier nationallicence Lauritzen Fredrik The Brain and Muscle Energy Group, Department of Anatomy and Department of Oral Biology, University of Oslo, Blindern, P.O. Box 1105, 0317, Oslo, Norway aut Eid Tore Department of Laboratory Medicine, Yale University School of Medicine, New Haven, CT, USA aut Bergersen Linda The Brain and Muscle Energy Group, Department of Anatomy and Department of Oral Biology, University of Oslo, Blindern, P.O. Box 1105, 0317, Oslo, Norway aut Brain Structure and Function Springer Berlin Heidelberg 220/1(2015-01-01), 1-12 1863-2653 220:1<1 2015 220 429 https://doi.org/10.1007/s00429-013-0672-x text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 review-article jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s00429-013-0672-x text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Lauritzen Fredrik The Brain and Muscle Energy Group, Department of Anatomy and Department of Oral Biology, University of Oslo, Blindern, P.O. Box 1105, 0317, Oslo, Norway aut NATIONALLICENCE 700 1- Eid Tore Department of Laboratory Medicine, Yale University School of Medicine, New Haven, CT, USA aut NATIONALLICENCE 700 1- Bergersen Linda The Brain and Muscle Energy Group, Department of Anatomy and Department of Oral Biology, University of Oslo, Blindern, P.O. Box 1105, 0317, Oslo, Norway aut NATIONALLICENCE 773 0- Brain Structure and Function Springer Berlin Heidelberg 220/1(2015-01-01), 1-12 1863-2653 220:1<1 2015 220 429