TY - JOUR
T1 - Effect of acetyl-l-carnitine treatment on brain adenylate cyclase activity in young and aged rats
AU - Florio, Tullio
AU - Meucci, Olimpia
AU - Grimaldi, Maurizio
AU - Ventra, Carmelo
AU - Cocozza, Eleonora
AU - Avallone, Antonio
AU - Postiglione, Alfredo
AU - Marino, Adriano
AU - Schettini, Gennaro
PY - 1993
Y1 - 1993
N2 - The aim of the present study has been to evaluate the effect of acetyl-l-carnitine (ALCAR) on brain adenylate cyclase (AC) activity in adult and aged rats. In in vitro studies, ALCAR (1, 10 and 100 μM) did not exert any effect on frontal cortex basal AC activity. Acute and subchronic administrations of ALCAR were carried out in 4- and 25-month-old male Fisher rats and AC activity was determined in rat frontal cortex under both basal and stimulated conditions. The acute treatment of young rats with ALCAR (100 and 500 mg/kg s.c.) did not affect AC activity, whereas the subchronic administration of 250 mg/kg s.c. ALCAR enhanced the stimulation of AC by carbamylcholine (CCh), norepinephrine (NE) and dopamine (DA), without affecting the basal AC activity. Basal AC activity in old rats was lower than in young rats and was not modified by acute and subchronic ALCAR administration. Moreover, the response of the enzyme to CCh, NE and DA was potentiated by the subchronic administration of ALCAR. The concentration-response curve of CCh stimulation of AC activity in ALCAR-treated rats is shifted to the left in both young and aged rats. We conclude that ALCAR, subchronically administered, is able to enhance receptor-stimulated AC response in frontal cortex of both young and aged rats.
AB - The aim of the present study has been to evaluate the effect of acetyl-l-carnitine (ALCAR) on brain adenylate cyclase (AC) activity in adult and aged rats. In in vitro studies, ALCAR (1, 10 and 100 μM) did not exert any effect on frontal cortex basal AC activity. Acute and subchronic administrations of ALCAR were carried out in 4- and 25-month-old male Fisher rats and AC activity was determined in rat frontal cortex under both basal and stimulated conditions. The acute treatment of young rats with ALCAR (100 and 500 mg/kg s.c.) did not affect AC activity, whereas the subchronic administration of 250 mg/kg s.c. ALCAR enhanced the stimulation of AC by carbamylcholine (CCh), norepinephrine (NE) and dopamine (DA), without affecting the basal AC activity. Basal AC activity in old rats was lower than in young rats and was not modified by acute and subchronic ALCAR administration. Moreover, the response of the enzyme to CCh, NE and DA was potentiated by the subchronic administration of ALCAR. The concentration-response curve of CCh stimulation of AC activity in ALCAR-treated rats is shifted to the left in both young and aged rats. We conclude that ALCAR, subchronically administered, is able to enhance receptor-stimulated AC response in frontal cortex of both young and aged rats.
UR - http://www.scopus.com/inward/record.url?scp=0027882534&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0027882534&partnerID=8YFLogxK
U2 - 10.1016/0924-977X(93)90260-S
DO - 10.1016/0924-977X(93)90260-S
M3 - Article
C2 - 8364354
AN - SCOPUS:0027882534
VL - 3
SP - 95
EP - 101
JO - European Neuropsychopharmacology
JF - European Neuropsychopharmacology
SN - 0924-977X
IS - 2
ER -