PMID- 27378558
OWN - NLM
STAT- MEDLINE
DCOM- 20170905
LR  - 20191210
IS  - 1873-7544 (Electronic)
IS  - 0306-4522 (Linking)
VI  - 332
DP  - 2016 Sep 22
TI  - Acetyl-l-carnitine restores synaptic transmission and enhances the inducibility 
      of stable LTP after oxygen-glucose deprivation.
PG  - 203-11
LID - S0306-4522(16)30285-8 [pii]
LID - 10.1016/j.neuroscience.2016.06.046 [doi]
AB  - Hypoxic circumstances result in functional and structural impairments of the 
      brain. Oxygen-glucose deprivation (OGD) on hippocampal slices is a technique 
      widely used to investigate the consequences of ischemic stroke and the potential 
      neuroprotective effects of different drugs. Acetyl-l-carnitine (ALC) is a 
      naturally occurring substance in the body, and it can therefore be administered 
      safely even in relatively high doses. In previous experiments, ALC pretreatment 
      proved to be effective against global hypoperfusion. In the present study, we 
      investigated whether ALC can be protective in an OGD model. We are not aware of 
      any earlier study in which the long-term potentiation (LTP) function on 
      hippocampal slices was measured after OGD. Therefore, we set out to determine 
      whether an effective ALC concentration has an effect on synaptic plasticity after 
      OGD in the hippocampal CA1 subfield of rats. A further aim was to investigate the 
      mechanism underlying the protective effect of this compound. The experiments 
      revealed that ALC is neuroprotective against OGD in a dose-dependent manner, 
      which is manifested not only in the regeneration of the impaired synaptic 
      transmission after the OGD, but also in the inducibility and stability of the 
      LTP. In the case of the most effective concentration of ALC (500muM), use of a 
      phosphoinositide 3-kinase (PI3K) inhibitor (LY294002) revealed that the PI3K/Akt 
      signaling pathway has a key role in the restoration of the synaptic transmission 
      and plasticity reached by ALC treatment.
CI  - Copyright (c) 2016 IBRO. Published by Elsevier Ltd. All rights reserved.
FAU - Kocsis, Kitti
AU  - Kocsis K
AD  - Department of Physiology, Anatomy and Neuroscience, University of Szeged, Kozep 
      fasor 52, H-6726 Szeged, Hungary; MTA-SZTE Neuroscience Research Group, 
      University of Szeged, Szeged, Hungary.
FAU - Frank, Rita
AU  - Frank R
AD  - Department of Physiology, Anatomy and Neuroscience, University of Szeged, Kozep 
      fasor 52, H-6726 Szeged, Hungary.
FAU - Szabo, Jozsef
AU  - Szabo J
AD  - Department of Physiology, Anatomy and Neuroscience, University of Szeged, Kozep 
      fasor 52, H-6726 Szeged, Hungary.
FAU - Knapp, Levente
AU  - Knapp L
AD  - Department of Physiology, Anatomy and Neuroscience, University of Szeged, Kozep 
      fasor 52, H-6726 Szeged, Hungary.
FAU - Kis, Zsolt
AU  - Kis Z
AD  - Department of Physiology, Anatomy and Neuroscience, University of Szeged, Kozep 
      fasor 52, H-6726 Szeged, Hungary.
FAU - Farkas, Tamas
AU  - Farkas T
AD  - Department of Physiology, Anatomy and Neuroscience, University of Szeged, Kozep 
      fasor 52, H-6726 Szeged, Hungary.
FAU - Vecsei, Laszlo
AU  - Vecsei L
AD  - Department of Neurology, Faculty of Medicine, University of Szeged, Semmelweis u. 
      6, H-6725 Szeged, Hungary; MTA-SZTE Neuroscience Research Group, University of 
      Szeged, Szeged, Hungary.
FAU - Toldi, Jozsef
AU  - Toldi J
AD  - Department of Physiology, Anatomy and Neuroscience, University of Szeged, Kozep 
      fasor 52, H-6726 Szeged, Hungary; MTA-SZTE Neuroscience Research Group, 
      University of Szeged, Szeged, Hungary. Electronic address: toldi@bio.u-szeged.hu.
LA  - eng
PT  - Journal Article
DEP - 20160701
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Chromones)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Morpholines)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Phosphoinositide-3 Kinase Inhibitors)
RN  - 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one)
RN  - 6DH1W9VH8Q (Acetylcarnitine)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Acetylcarnitine/*pharmacology
MH  - Animals
MH  - Brain Ischemia/*drug therapy/physiopathology
MH  - CA1 Region, Hippocampal/drug effects/physiopathology
MH  - Chromones/pharmacology
MH  - Dose-Response Relationship, Drug
MH  - Enzyme Inhibitors/pharmacology
MH  - Excitatory Postsynaptic Potentials/*drug effects/physiology
MH  - Glucose/*deficiency
MH  - Long-Term Potentiation/*drug effects/physiology
MH  - Male
MH  - Morpholines/pharmacology
MH  - Neuroprotective Agents/*pharmacology
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Phosphoinositide-3 Kinase Inhibitors
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Rats, Wistar
MH  - Signal Transduction/drug effects
MH  - Tissue Culture Techniques
OTO - NOTNLM
OT  - PI3K/Akt
OT  - acetyl-l-carnitine
OT  - ischemia
OT  - long-term potentiation
OT  - neuroprotection
OT  - oxygen-glucose deprivation
EDAT- 2016/07/06 06:00
MHDA- 2017/09/07 06:00
CRDT- 2016/07/06 06:00
PHST- 2016/04/04 00:00 [received]
PHST- 2016/06/09 00:00 [revised]
PHST- 2016/06/24 00:00 [accepted]
PHST- 2016/07/06 06:00 [entrez]
PHST- 2016/07/06 06:00 [pubmed]
PHST- 2017/09/07 06:00 [medline]
AID - S0306-4522(16)30285-8 [pii]
AID - 10.1016/j.neuroscience.2016.06.046 [doi]
PST - ppublish
SO  - Neuroscience. 2016 Sep 22;332:203-11. doi: 10.1016/j.neuroscience.2016.06.046. 
      Epub 2016 Jul 1.