title: Acetyl-L-carnitine and oxaloacetate in post-treatment against LTP impairment in a rat ischemia model. An in vitro electrophysiological study.
abstract: A high proportion of research relating to cerebral ischemia focuses on neuroprotection. The application of compounds normally present in the organism is popular, because they do not greatly influence the synaptic activity by receptor modulation, and can be administered without serious side effects. Oxaloacetate (OxAc) and acetyl-L-carnitine (ALC) are such favorable endogenous molecules. ALC can exert a protective effect by improving the energy state of the neurons under ischemic conditions. A promising neuroprotective strategy is glutamate scavenging, which can be achieved by the intravenous administration of OxAc. This study involved the possible protective effects of ALC and OxAc in different post-treatment protocols against long-term potentiation (LTP) impairment. Ischemia was induced in rats by 2-vessel occlusion, which led to a decreased LTP relative to the control group. High-dose (200 mg/kg) ALC or OxAc post-treatment resulted in a higher potentiation relative to the 2VO group, but it did not reach the control level, whereas low-dose ALC (100 mg/kg) in combination with OxAc completely restored the LTP function. Many previous studies have concluded that ALC can be protective only as pretreatment. The strategy described here reveals that ALC can also be neuroprotective when utilized as post-treatment against ischemia.
authors.affiliation: Department of Physiology, Anatomy and Neuroscience, University of Szeged, Közép fasor 52, 6726, Szeged, Hungary.
authors.forename: K
authors.initials: K
authors.lastname: Kocsis
authors.forename: L
authors.initials: L
authors.lastname: Knapp
authors.forename: J
authors.initials: J
authors.lastname: Mészáros
authors.forename: Z
authors.initials: Z
authors.lastname: Kis
authors.forename: T
authors.initials: T
authors.lastname: Farkas
authors.forename: L
authors.initials: L
authors.lastname: Vécsei
authors.forename: J
authors.initials: J
authors.lastname: Toldi
mesh_terms: D000108:Acetylcarnitine / Q000008:administration & dosage*; D000818:Animals; D002545:Brain Ischemia / Q000188:drug therapy* / Q000503:physiopathology; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004359:Drug Therapy, Combination; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D006624:Hippocampus / Q000187:drug effects* / Q000503:physiopathology; D017774:Long-Term Potentiation / Q000187:drug effects* / Q000502:physiology; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D018696:Neuroprotective Agents / Q000008:administration & dosage*; D062907:Oxaloacetic Acid / Q000008:administration & dosage*; D011897:Random Allocation; D017208:Rats, Wistar; D013997:Time Factors; D046509:Tissue Culture Techniques
chemical_list: D018696:Neuroprotective Agents; D062907:Oxaloacetic Acid; D000108:Acetylcarnitine