Effects of Long-term Acetyl-L-carnitine Administration in Rats I. Increased Dopamine Output in Mesocorticolimbic Areas and Protection toward Acute Stress Exposure

Tolu, Pierluigi

doi:10.1016/s0893-133x(02)00306-8

Cited by 45 publications

(36 citation statements)

References 72 publications

(77 reference statements)

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“…Tempesta et al (1985) showed that the ALCAR iontophoretic administration on single neurons of the rat medullary-pontine reticular formation leads to increased spontaneous and glutamate-evoked firing and potentiated both the cholinergic and the serotoninergic responses. Moreover, a 7-day administration of ALCAR in rats increased dopamine and serotonin output in the nucleus accumbens shell (Tolu et al 2002), whereas systemic acetyl Fig. 3 Ret phosphorylation in mouse brain areas.…”

Section: Discussionmentioning

confidence: 95%

Antidepressant-like effect of artemin in mice: a mechanism for acetyl-l-carnitine activity on depression

et al. 2011

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Section: Discussionmentioning

confidence: 95%

Antidepressant-like effect of artemin in mice: a mechanism for acetyl-l-carnitine activity on depression

et al. 2011

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“…Being a donor of acetyl groups, ALC is classically reported to enhance acetylcholine release (Imperato et al 1989) and to facilitate the neuronal response to acetylcholine (Tempesta et al 1985). Recently, a more specific action on neurotransmission has been proposed in rats, with ALC-induced increase of glucose utilization in the raphe, the locus coeruleus, and in limbic areas (Ori et al 2002), increased DA and 5-HT release from both nigrostriatal (Harsing et al 1992) and mesolimbic neurons (Tolu et al 2002), as well as facilitated neuronal response to 5-HT (Tempesta et al 1985). It is interesting to note that CC-lesioned rats are highly impulsive (Muir et al 1996).…”

Section: Discussionmentioning

confidence: 99%

Acetyl-l-carnitine reduces impulsive behaviour in adolescent rats

et al. 2004

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The attention deficit/hyperactivity disorder (ADHD) can affect human infants and adolescents. One important feature of this disorder is behavioural impulsivity. This study assessed the ability of chronic acetyl-L-carnitine (ALC, saline or 100 mg/kg SC, plus 50 mg/kg orally) to reduce impulsivity in a validated animal model for ADHD. Food-restricted rats were tested during adolescence (postnatal days, pnd, 30-45) in operant chambers with two nose-poking holes, one delivering one food pellet immediately, and the other five pellets after a delay. Delay length was increased over days (from 0 to 80 s). Individual differences in the preference-delay curve emerged, with the identification of two distinct subpopulations, i.e. one with a nearly horizontal curve and another with a very steep ("impulsive") slope. The impulsivity profile was slightly but consistently reduced by chronic ALC administration. Consistent results were also obtained with methylphenidate (MPH, saline or 3 mg/kg IP twice daily). Impulsive rats exhibited a lower metabolite/serotonin (5HIAA/5HT) ratio in the medial frontal cortex (MFC) and lower noradrenaline (NA) levels in the MFC and cingulate cortex (CC) when compared with the other subgroup. The ALC treatment increased NA levels in the CC and the 5HIAA/5HT ratio in both CC and MFC. Present data suggest that ALC, a drug devoid of psychostimulant properties, may have some beneficial effects in the treatment of ADHD children.

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“…Acetyl-L-carnitine (ALCAR), an acetyl ester of L-carnitine, is involved in fatty acids metabolism in mitochondria and has a potent anti-oxidative properties [15] Intra-striatal infusion [16] and long-term administration of ALCAR in a model of acute stress increased the dopamine efflux [17]. Moreover, ALCAR in combination with α-lipoic acid improved motor behaviour and ATP production and decreased lipid peroxidation in rotenone-induced rat model of PD-like phenotypes [18].…”

Section: Introductionmentioning

confidence: 99%

ALCAR Exerts Neuroprotective and Pro-Neurogenic Effects by Inhibition of Glial Activation and Oxidative Stress via Activation of the Wnt/β-Catenin Signaling in Parkinsonian Rats

2015

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Oxidative stress and neuroinflammation are known causative factors in progressive degeneration of dopaminergic (DAergic) neurons in Parkinson's disease (PD). Neural stem cells (NSCs) contribute in maintaining brain plasticity; therefore, survival of NSCs and neuroblasts during neurodegenerative process becomes important in replenishing the pool of mature neuronal population. Acetyl-L-carnitine (ALCAR), present in almost all body cells, increases endogenous antioxidants and regulates bioenergetics. Currently, no information is available about the putative mechanism and neuroprotective effects of ALCAR in 6-hydroxydopamine (6-OHDA)-induced rat model of PD-like phenotypes. Herein, we investigated the effect of ALCAR on death/survival of DAergic neurons, neuroblasts and NSCs and associates mechanism of neuroprotection in 6-OHDA-induced rat model of PD-like phenotypes. ALCAR (100 mg/kg/day, intraperitoneal (i.p.)) treatment started 3 days prior to 6-OHDA lesioning and continued for another 14 day post-lesioning. We found that ALCAR pretreatment in 6-OHDA-lesioned rats increased expression of neurogenic and the Wnt pathway genes in the striatum and substantia nigra pars compacta (SNpc) region. It suppressed the glial cell activation, improved antioxidant status, increased NSC/neuroblast population and rescued the DAergic neurons in nigrostriatal pathway. ALCAR pretreatment in 6-OHDA-lesioned rats decreased GSK-3β activation and increased nuclear translocation of β-catenin. Functional deficits were restored following ALCAR pretreatment in 6-OHDA-lesioned rats as demonstrated by improved motor coordination and rotational behaviour, confirming protection of DAergic innervations in lesioned striatum. These results indicate that ALCAR exerts neuroprotective effects through the activation of Wnt/β-catenin pathway, suggesting its therapeutic use to treat neurodegenerative diseases by enhancing regenerative capacity.

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Effects of Long-term Acetyl-L-carnitine Administration in Rats I. Increased Dopamine Output in Mesocorticolimbic Areas and Protection toward Acute Stress Exposure

Cited by 45 publications

References 72 publications

Antidepressant-like effect of artemin in mice: a mechanism for acetyl-l-carnitine activity on depression

Antidepressant-like effect of artemin in mice: a mechanism for acetyl-l-carnitine activity on depression

Acetyl-l-carnitine reduces impulsive behaviour in adolescent rats

ALCAR Exerts Neuroprotective and Pro-Neurogenic Effects by Inhibition of Glial Activation and Oxidative Stress via Activation of the Wnt/β-Catenin Signaling in Parkinsonian Rats

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