Acetyl-L-carnitine (ALCAR) is the acetyl ester of carnitine that has been reported to be beneficial in depressive disorders and Alzheimer's disease. A 7-day administration of ALCAR in rats increased dopamine and serotonin output in the nucleus accumbens shell and it prevented the development of escape deficit produced by acute exposure to unavoidable stress. No tolerance developed to this protective effect, which appeared to be mediated by (1) the activation of 5-HT(1A) receptors, as it was antagonized by the administration of WAY100635 30 min before stress exposure; and (2) a process of neuronal plasticity dependent on NMDA receptor activity, as subcutaneous dizocilpine infusion during ALCAR treatment prevented the development of the protective effect on stress. Chronic stress exposure maintains an escape deficit condition that is reverted by a long-term treatment with antidepressants, but the same condition was not modified by long-term ALCAR administration. Thus, ALCAR cannot be defined as an antidepressant

Tolu, P., Masi, F., Leggio, B., Scheggi, S., Tagliamonte, A., DE MONTIS, M.G., et al. (2002). Effects of long-term acetyl-l-carnitine administration in rats: I. increased dopamine output in mesocorticolimbic areas and protection toward acute stress exposure. NEUROPSYCHOPHARMACOLOGY, 27(3), 410-420 [10.1016/S0893-133X(02)00306-8].

Effects of long-term acetyl-l-carnitine administration in rats: I. increased dopamine output in mesocorticolimbic areas and protection toward acute stress exposure

LEGGIO, BENEDETTA;SCHEGGI, SIMONA;TAGLIAMONTE, ALESSANDRO;DE MONTIS, MARIA GRAZIELLA;GAMBARANA, CARLA
2002-01-01

Abstract

Acetyl-L-carnitine (ALCAR) is the acetyl ester of carnitine that has been reported to be beneficial in depressive disorders and Alzheimer's disease. A 7-day administration of ALCAR in rats increased dopamine and serotonin output in the nucleus accumbens shell and it prevented the development of escape deficit produced by acute exposure to unavoidable stress. No tolerance developed to this protective effect, which appeared to be mediated by (1) the activation of 5-HT(1A) receptors, as it was antagonized by the administration of WAY100635 30 min before stress exposure; and (2) a process of neuronal plasticity dependent on NMDA receptor activity, as subcutaneous dizocilpine infusion during ALCAR treatment prevented the development of the protective effect on stress. Chronic stress exposure maintains an escape deficit condition that is reverted by a long-term treatment with antidepressants, but the same condition was not modified by long-term ALCAR administration. Thus, ALCAR cannot be defined as an antidepressant
2002
Tolu, P., Masi, F., Leggio, B., Scheggi, S., Tagliamonte, A., DE MONTIS, M.G., et al. (2002). Effects of long-term acetyl-l-carnitine administration in rats: I. increased dopamine output in mesocorticolimbic areas and protection toward acute stress exposure. NEUROPSYCHOPHARMACOLOGY, 27(3), 410-420 [10.1016/S0893-133X(02)00306-8].
File in questo prodotto:
File Dimensione Formato  
ALCAR 1.pdf

non disponibili

Tipologia: Post-print
Licenza: NON PUBBLICO - Accesso privato/ristretto
Dimensione 123.45 kB
Formato Adobe PDF
123.45 kB Adobe PDF   Visualizza/Apri   Richiedi una copia

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11365/21470
 Attenzione

Attenzione! I dati visualizzati non sono stati sottoposti a validazione da parte dell'ateneo