Acetyl-l-carnitine enhances acetylcholine release in the striatum and hippocampus of awake freely moving rats

Impérato, Assunta; Ramacci, M. T.; Angelucci, L.

doi:10.1016/0304-3940(89)90826-4

Cited by 88 publications

(51 citation statements)

References 13 publications

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“…Suh, and D. Heath, unpublished results). In other studies using lower ALCAR doses [0.5% (wt͞vol)], Liu et al (22) noted no ALCAR-induced changes in parameters of oxidative stress in rat brain, yet found that this dose significantly improved cognitive function in aged animals (9). Thus, smaller doses of ALCAR may effectively improve metabolic function without higher oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

“…We demonstrated that ALCAR supplementation reverses the age-associated decline in metabolic activity in rats, suggesting that ALCAR improves mitochondrial function and increases general metabolic activity (19,20). ALCAR-induced improvement in metabolic parameters appear to be responsible for improving short-term memory deficits and cognitive function in elderly subjects given ALCAR (21,22) and in old rats (9).…”

mentioning

confidence: 96%

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Feeding acetyl- l -carnitine and lipoic acid to old rats significantly improves metabolic function while decreasing oxidative stress

Hagen

Liu

Lykkesfeldt

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

287

162

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Mitochondrial-supported bioenergetics decline and oxidative stress increases during aging. To address whether the dietary addition of acetyl-L-carnitine [ALCAR, 1.5% (wt͞vol) in the drinking water] and͞or (R)-␣-lipoic acid [LA, 0.5% (wt͞wt) in the chow] improved these endpoints, young (2-4 mo) and old (24 -28 mo) F344 rats were supplemented for up to 1 mo before death and hepatocyte isolation. ALCAR؉LA partially reversed the age-related decline in average mitochondrial membrane potential and significantly increased (P ‫؍‬ 0.02) hepatocellular O 2 consumption, indicating that mitochondrial-supported cellular metabolism was markedly improved by this feeding regimen. ALCAR؉LA also increased ambulatory activity in both young and old rats; moreover, the improvement was significantly greater (P ‫؍‬ 0.03) in old versus young animals and also greater when compared with old rats fed ALCAR or LA alone. To determine whether ALCAR؉LA also affected indices of oxidative stress, ascorbic acid and markers of lipid peroxidation (malondialdehyde) were monitored. The hepatocellular ascorbate level markedly declined with age (P ‫؍‬ 0.003) but was restored to the level seen in young rats when ALCAR؉LA was given. The level of malondialdehyde, which was significantly higher (P ‫؍‬ 0.0001) in old versus young rats, also declined after ALCAR؉LA supplementation and was not significantly different from that of young unsupplemented rats. Feeding ALCAR in combination with LA increased metabolism and lowered oxidative stress more than either compound alone. H armon, Miguel, and others (1, 2) postulated that mitochondrial decay is a significant factor in aging, caused, in part, by the release of reactive oxygen species (ROS) as by-products of mitochondrial electron transport. Mitochondria are targets of their own oxidant by-products. The steady-state oxidative damage in mitochondria is high relative to other organelles, and the percentage of oxygen converted to superoxide increases with age (3-6). This leads to a vicious cycle of increasing mitochondrial damage, which adversely affects cell function (7), and results in a loss of ATP-generating capacity, especially in times of greater energy demand, thereby compromising vital ATP-dependent reactions. Cellular processes affected by mitochondrial decay include detoxification, repair systems, DNA replication, osmotic balance, and higher-order processes (7), such as cognitive function (7-9). Thus, preservation of mitochondrial function is important for maintaining overall health during aging (7). This theory is buttressed by the observation that caloric restriction, the only known regimen to increase mean life span in animals, maintains mitochondrial function and lowers oxidant production (7,8,(10)(11)(12). A spartan diet of calorie restriction appears to be too unappealing to be widely adopted in humans, and thus other alternative regimens to improve or maintain normal mitochondrial activities have been sought.Several dietary supplements, including the mitochondrial cofactor and antioxidant lipoi...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 96%

Feeding acetyl- l -carnitine and lipoic acid to old rats significantly improves metabolic function while decreasing oxidative stress

Hagen

Liu

Lykkesfeldt

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

287

162

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“…Aside from its role in fatty acid -oxidation, many other functions have been attributed to L-acetylcarnitine. It has been reported that L-acetylcarnitine modulates the activity of nerve growth factor (NGF) in the nervous system in rats [1,40,52], increases the activity of choline acetyltransferase, enhances the expression of NGF receptors in the striatum and hippocampus of rats during development [10] and modulates different neurotransmitter systems including the cholinergic and dopaminergic system [24,20]. Additionally L-acetylcarnitine functions as a donor of acetyl groups in oxidative glycolysis [4] and can also have important biological function due to its ability to contribute to acetylation of -OH or -NH 2 functional groups on amino acids and Nterminal groups in proteins and peptides [39].…”

Section: Biological Properties Of L-acetylcarni-tinementioning

confidence: 99%

L-Acetylcarnitine: A Proposed Therapeutic Agent for Painful Peripheral Neuropathies

Chiechio¹,

Copani²,

Nicoletti³

et al. 2006

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During the past two decades, many pharmacological strategies have been investigated for the management of painful neuropathies. However, neuropathic pain still remains a clinical challenge. A combination of therapies is often required, but unfortunately in most cases adequate pain relief is not achieved. Recently, attention has been focused on the physiological and pharmacological effects of L-acetylcarnitine in neurological disorders. There are a number of reports indicating that L-acetylcarnitine can be considered as a therapeutic agent in neuropathic disorders including painful peripheral neuropathies. In this review article, we will examine the antinociceptive and the neuroprotective effects of Lacetylcarnitine as tested in clinical studies and in animal models of nerve injury.

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“…85 ALCAR releases dopamine in rat corpus striatum by a calcium-dependent exocytotic process 86 and enhances acetylcholine release in the striatum and hippocampus of awake freely moving rats. 87 Sershen et al 88 demonstrated that ALCAR attenuates age-related changes in dopaminergic systems in rats and ALCAR, as well as carnitine, was reported to be a stereospecific neuroactive compound with cholinomimetic activity. 89 ALCAR given to rats for 4 days elevates substantia nigra levels of GABA but not striatal dopamine.…”

Section: Alcar's Modulation Of Synaptic Morphology and Transmissionmentioning

confidence: 99%

Acetyl-L-carnitine physical-chemical, metabolic, and therapeutic properties: relevance for its mode of action in Alzheimer's disease and geriatric depression

2000

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Acetyl-L-carnitine (ALCAR) contains carnitine and acetyl moieties, both of which have neurobiological properties. Carnitine is important in the ␤-oxidation of fatty acids and the acetyl moiety can be used to maintain acetyl-CoA levels. Other reported neurobiological effects of ALCAR include modulation of: (1) brain energy and phospholipid metabolism; (2) cellular macromolecules, including neurotrophic factors and neurohormones; (3) synaptic morphology; and (4) synaptic transmission of multiple neurotransmitters. Potential molecular mechanisms of ALCAR activity include: (1) acetylation of -NH 2 and -OH functional groups in amino acids and N terminal amino acids in peptides and proteins resulting in modification of their structure, dynamics, function and turnover; and (2) acting as a molecular chaperone to larger molecules resulting in a change in the structure, molecular dynamics, and function of the larger molecule. ALCAR is reported in double-blind controlled studies to have beneficial effects in major depressive disorders and Alzheimer's disease (AD), both of which are highly prevalent in the geriatric population. Molecular Psychiatry (2000) 5, 616-632.

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Acetyl-l-carnitine enhances acetylcholine release in the striatum and hippocampus of awake freely moving rats

Cited by 88 publications

References 13 publications

Feeding acetyl- l -carnitine and lipoic acid to old rats significantly improves metabolic function while decreasing oxidative stress

Feeding acetyl- l -carnitine and lipoic acid to old rats significantly improves metabolic function while decreasing oxidative stress

L-Acetylcarnitine: A Proposed Therapeutic Agent for Painful Peripheral Neuropathies

Acetyl-L-carnitine physical-chemical, metabolic, and therapeutic properties: relevance for its mode of action in Alzheimer's disease and geriatric depression

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