The aim of the present study was to investigate the neuronal structure sthat mediate the Antiaging properties of acetyl-l-carnitine(ALCAR). The regional cerebral metabolic rates for Glucose (rCMRglc) have been determined with the quantitative autoradiographic [14C]2- Deoxyglucose procedure at different times after i.v. administration of saline or ALCAR 500mg/kg to naïve, non pretreated 3-, 12-and24-month-old rats and to24-month-old rats pretreated with ALCAR (100 mg/kg/day, for 3 months). rCMRglc increased maximally at 30 min after ALCAR in 3-, 12-and 24-month old rats (14, 15 and 15 areas affected, 19, 24 and 22% mean increments). Peak metabolic activations occorre with similar magnitude in motor, visual, limbic and talamic areas in all age rats and with large rmagnitude in hippocamp al and talami areas in aged rats. Cerebral metabolic activations subsided by 60 min after ALCAR in 3-month rats (3 brain regions affected, 4% decrease) and persisted by that time in12- and24-month-oldrats (14 and12 regions affected, 15 and 20% increases). Cerebral activations were enhanced in aged rats after chronic treatment with ALCAR (24 brain region saffected, 20% mean increase). Hence, duringaging, metabolic responsività to ALCAR is maintained in most brain areas and increate in limbic and thalamic regions. Increased responsivity to ALCAR may result from undetermined pharmacokinetic factors and/or from a higher sensitività and contribute to the aging reversal properties of ALCAR.
Cerebral metabolic effects of acetyl-L-carnitine in rats during aging
FREO, ULDERICO;ORI, CARLO
2009
Abstract
The aim of the present study was to investigate the neuronal structure sthat mediate the Antiaging properties of acetyl-l-carnitine(ALCAR). The regional cerebral metabolic rates for Glucose (rCMRglc) have been determined with the quantitative autoradiographic [14C]2- Deoxyglucose procedure at different times after i.v. administration of saline or ALCAR 500mg/kg to naïve, non pretreated 3-, 12-and24-month-old rats and to24-month-old rats pretreated with ALCAR (100 mg/kg/day, for 3 months). rCMRglc increased maximally at 30 min after ALCAR in 3-, 12-and 24-month old rats (14, 15 and 15 areas affected, 19, 24 and 22% mean increments). Peak metabolic activations occorre with similar magnitude in motor, visual, limbic and talamic areas in all age rats and with large rmagnitude in hippocamp al and talami areas in aged rats. Cerebral metabolic activations subsided by 60 min after ALCAR in 3-month rats (3 brain regions affected, 4% decrease) and persisted by that time in12- and24-month-oldrats (14 and12 regions affected, 15 and 20% increases). Cerebral activations were enhanced in aged rats after chronic treatment with ALCAR (24 brain region saffected, 20% mean increase). Hence, duringaging, metabolic responsività to ALCAR is maintained in most brain areas and increate in limbic and thalamic regions. Increased responsivity to ALCAR may result from undetermined pharmacokinetic factors and/or from a higher sensitività and contribute to the aging reversal properties of ALCAR.
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