PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 1869064

Spatial-frequency-dependent changes in the human pattern electroretinogram after acute acetyl-L-carnitine administration.

B Falsini·V Porciatti·R Bolzani·A Marchionni
View original source ↗Export metadata ↓

Abstract

Acetyl-L-carnitine (LAC) is a neuroactive compound that is thought to be involved in cholinergic transmission. The effects of acute intravenous LAC administration (30 mg/kg) on pattern-evoked electroretinograms (P-ERGs) were evaluated in nine healthy volunteers ranging in age between 21 and 27 years. Nine age-matched, normal subjects treated with a placebo served as controls. Steady-state (8 Hz) P-ERGs recorded in response to counterphased sinusoidal gratings of variable spatial frequency (0.6-4.8 cycles/degree) were obtained before and at 20, 50 and 80 min after LAC or placebo administration. The amplitude and phase of the Fourier-analysed P-ERG second harmonic were measured. As compared with placebo-treated controls, LAC-treated subjects showed a selective P-ERG amplitude increase (Mann-Whitney rank test: P less than 0.05), which was found 80 min posttreatment at a spatial frequency of 4.8 cycles/degree. For the same stimulus a significant (P less than 0.05) P-ERG phase shortening (at 50 min after drug administration) was also found. The spatial frequencies of other stimuli did not show a significant difference between the LAC- and placebo-treated groups. These results indicate that acute LAC administration induces a spatial-frequency-dependent enhancement of the human P-ERG. This is compatible with a cholinergic excitatory effect and suggests a therapeutic role for this compound in retinal dysfunctions with selective vulnerability to medium-high spatial frequencies.

Explore related subjects

AcetylcarnitineAdultElectroretinographyFemaleFourier AnalysisHumansInjections, IntravenousMalePattern Recognition, VisualRetinaSpace PerceptionClinical TrialControlled Clinical TrialJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

B Falsini, V Porciatti, R Bolzani, A Marchionni. 1991. Spatial-frequency-dependent changes in the human pattern electroretinogram after acute acetyl-L-carnitine administration.. https://doi.org/10.1007/bf00167881

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2006

Is the human masticatory system devoid of recurrent inhibition?

The aim of the present study was to investigate the existence or otherwise of a functional recurrent inhibitory system (Renshaw cell system) in the motoneurons that innervate human masticatory muscles. In a previous study, L: -acetylcarnitine (L: -Ac), a substance known to potentiate recurrent inhibition in humans was found to alter, in a specific way, the discharge variability, and the synchronous activity of motor units depending on the presence or absence of recurrent inhibition in the corresponding motoneuron pool. Using a similar paradigm, we have recorded the tonic discharge activity of motor unit pairs from the masseter muscle during voluntary isometric contraction while subjects were undergoing continuous intravenous saline (SAL, NaCl 0.9%) perfusion. Following a brief baseline-recording period, the subjects were given a test injection of either L: -Ac or isotonic saline (SAL) in a double blind manner. The variability, synchronization, and coherence between the motor unit discharges were analysed during three successive periods: pre-injection, during injection, and post-injection, each lasting 2-3 min. Neither L: -Ac nor SAL injection induced a significant change in the inter-spike interval (ISI) or the coefficient of variation of the ISIs in the motor units tested. There were also no significant changes in the pattern of synchronous activity or in the coherence, which reflects the common frequency content of the unit discharges. Reminiscent of what had been observed previously with motoneurons without recurrent inhibition in the Abductor Digitorum Minimi muscle, the lack of effects of L: -Ac injection on the firing behaviour of masseter motoneurons may suggest that classical Renshaw cell inhibition is lacking in this motoneuron pool.

Acetylcarnitine↗
PubMed2006

Protective effect of acetyl-L-carnitine against oxidative stress induced by antiretroviral drugs.

Both HIV infection per se and antiretroviral drugs might contribute to oxidative stress and mitochondrial dysfunctions. In this study we assess zidovudine, stavudine and didanosine on U937 and CEM cell lines. All these drugs induced apoptosis and increased intracellular hydrogen peroxide but not superoxide anions. The addition of acetyl-l-carnitine (ALC) was able to prevent the pro-oxidant effect of the drugs tested. Supplementation with ALC, deficient in certain cohorts of HIV-infected individuals, especially on high active antiretroviral therapy regimen, has been associated with favourable effects. These data suggest that one of these effects could be a direct anti-oxidant action.

Acetylcarnitine↗
PubMed2006

Involvement of PI3K/PKG/ERK1/2 signaling pathways in cortical neurons to trigger protection by cotreatment of acetyl-L-carnitine and alpha-lipoic acid against HNE-mediated oxidative stress and neurotoxicity: implications for Alzheimer's disease.

Oxidative stress has been shown to underlie neuropathological aspects of Alzheimer's disease (AD). 4-Hydroxy-2-nonenal (HNE) is a highly reactive product of lipid peroxidation of unsaturated lipids. HNE-induced oxidative toxicity is a well-described model of oxidative stress-induced neurodegeneration. GSH plays a key role in antioxidant defense, and HNE exposure causes an initial depletion of GSH that leads to gradual toxic accumulation of reactive oxygen species. In the current study, we investigated whether pretreatment of cortical neurons with acetyl-L-carnitine (ALCAR) and alpha-lipoic acid (LA) plays a protective role in cortical neuronal cells against HNE-mediated oxidative stress and neurotoxicity. Decreased cell survival of neurons treated with HNE correlated with increased protein oxidation (protein carbonyl, 3-nitrotyrosine) and lipid peroxidation (HNE) accumulation. Pretreatment of primary cortical neuronal cultures with ALCAR and LA significantly attenuated HNE-induced cytotoxicity, protein oxidation, lipid peroxidation, and apoptosis in a dose-dependent manner. Additionally, pretreatment of ALCAR and LA also led to elevated cellular GSH and heat shock protein (HSP) levels compared to untreated control cells. We have also determined that pretreatment of neurons with ALCAR and LA leads to the activation of phosphoinositol-3 kinase (PI3K), PKG, and ERK1/2 pathways, which play essential roles in neuronal cell survival. Thus, this study demonstrates a cross talk among the PI3K, PKG, and ERK1/2 pathways in cortical neuronal cultures that contributes to ALCAR and LA-mediated prosurvival signaling mechanisms. This evidence supports the pharmacological potential of cotreatment of ALCAR and LA in the management of neurodegenerative disorders associated with HNE-induced oxidative stress and neurotoxicity, including AD.

Acetylcarnitine↗