Acetyl-L-carnitine reduces the infarct size and striatal glutamate outflow following focal cerebral ischemia in rats.
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.
Jalal
Fakhreya Yousuf
FY
Department of Pharmaceutical Sciences, Massachusetts College of Pharmacy and Health Sciences, Boston, Massachusetts 02115, USA. fakhreya.jalal@my.mcphs.edu
Böhlke
Mark
M
Maher
Timothy J
TJ
D000108:Acetylcarnitine / Q000627:therapeutic use*; D000818:Animals; D002545:Brain Ischemia / Q000473:pathology / Q000517:prevention & control*; D020244:Infarction, Middle Cerebral Artery; D008297:Male; D017551:Microdialysis; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley
D018696:Neuroprotective Agents; D000108:Acetylcarnitine