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Acetyl‐ l ‐carnitine reduces the infarct size and striatal glutamate outflow following focal cerebral ischemia in rats
Author(s) -
Jalal Fakhreya Yousuf,
Böhlke Mark,
Maher Timothy J.
Publication year - 2010
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2009.05351.x
Subject(s) - neuroprotection , glutamate receptor , ischemia , medicine , anesthesia , middle cerebral artery , pharmacology , receptor
Acetyl‐ l ‐carnitine (ALCAR), an endogenous water soluble molecule, is synthesized in the brain and is involved in many aspects of neuronal activity, including metabolism and neuronal membrane formation and integrity. To determine ALCAR's neuroprotective effects, focal cerebral ischemia was induced using four models of middle cerebral artery occlusion (MCAO) and treatment with 0–400 mg/kg ALCAR ( i.p. ) prior to MCAO. While acute doses were without effect, pretreatment with chronic ALCAR (400 mg/kg/day for five days) significantly reduced infarct size. Lower chronic ALCAR doses were not effective. Additionally, elevations in microdialysate glutamate post‐MCAO were attenuated by ALCAR treatment.