The effects of aging on MAO activity and amino acid levels in rat brain

Benedetti, Μ. Strolin; Cini, M.; Fusi, R.; Marrari, P.; Dostert, P.

doi:10.1007/978-3-7091-9050-0_25

Cited by 16 publications

(17 citation statements)

References 34 publications

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“…The changes in concentrations of aspartic acid observed with age in the present study are in reasonable agreement with those noted in two previous studies where male Wistar rats of the same breeder were used (Strolin Benedetti et al, 1990aBenedetti et al, , 1991. In contrast, no age-related statistically significant decrease in glutamic acid concentrations was observed in the present work, in which rats were not injected with 3-mercaptopropionic acid prior to decapitation, as was done in the two previous studies where GABA levels had to be measured.…”

Section: Discussionsupporting

confidence: 93%

Effect of ageing on tissue levels of amino acids involved in the nitric oxide pathway in rat brain

Benedetti

Dostert

Marrari

et al. 1993

J. Neural Transmission

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Nitric oxide (NO) and citrulline are produced from L-arginine by the action of NO synthase after activation of excitatory amino acid receptors. In addition to its role in neurodegeneration, there is convincing evidence that NO is also involved in long-term potentiation, a cellular analog of learning and memory in the mammalian nervous system. In the present study, concentrations of L-arginine, citrulline, aspartic acid and glutamic acid were determined in various brain regions of young and old rats. The aim was to examine whether changes in brain concentrations of these amino acids might be indicative of a possible decrease in NO production with ageing, in relation with the well-established decline of cognitive function. Brain aspartic acid, citrulline and L-arginine concentrations were found to be lower in old rats compared to young animals, although the decrease did not always reach statistical significance. In contrast, no change in glutamic acid levels was found. In all brain structures of young and old rats, concentrations of L-arginine were higher than the concentration for NO synthase to function at maximum velocity in the rat brain. Therefore, the decrease in citrulline concentrations found in some brain regions of old rats might be seen, at least partly, as a reflection of a lower production of NO with ageing, although further work is clearly needed to ascertain a decrease in rat brain NO synthase activity with age.

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Section: Discussionsupporting

confidence: 93%

Effect of ageing on tissue levels of amino acids involved in the nitric oxide pathway in rat brain

Benedetti

Dostert

Marrari

et al. 1993

J. Neural Transmission

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“…In vivo and in vitro studies have failed to show any change in glutamate release, and an age-related decrease in glutamate content in the striatum, hippocampus and cortex is still a matter of debate (Price et al, 1981;BanaySchwartz et al, 1989;Strolin Benedetti et al, 1990;Zhang et al, 2009). The expression and function of glutamate receptors are strongly subject to age-dependent variation.…”

Section: Introductionmentioning

confidence: 99%

Reduction in glutamate uptake is associated with extrasynaptic NMDA and metabotropic glutamate receptor activation at the hippocampal CA1 synapse of aged rats

et al. 2010

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SummaryThis study aims to determine whether the regulation of extracellular glutamate is altered during aging and its possible consequences on synaptic transmission and plasticity. A decrease in the expression of the glial glutamate transporters GLAST and GLT-1 and reduced glutamate uptake occur in the aged (24-27 months) SpragueDawley rat hippocampus. Glutamatergic excitatory postsynaptic potentials recorded extracellularly in ex vivo hippocampal slices from adult (3-5 months) and aged rats are depressed by DL-TBOA, an inhibitor of glutamate transporter activity, in an N-Methyl-D-Aspartate (NMDA)-receptor-dependent manner. In aged but not in young rats, part of the depressing effect of DL-TBOA also involves metabotropic glutamate receptor (mGluRs) activation as it is significantly reduced by the specific mGluR antagonist d-methyl-4-carboxy-phenylglycine (MCPG). The paired-pulse facilitation ratio, a functional index of glutamate release, is reduced by MCPG in aged slices to a level comparable to that in young rats both under control conditions and after being enhanced by DL-TBOA. These results suggest that the age-associated glutamate uptake deficiency favors presynaptic mGluR activation that lowers glutamate release. In parallel, 2 Hz-induced long-term depression is significantly decreased in aged animals and is fully restored by MCPG. All these data indicate a facilitated activation of extrasynaptic NMDAR and mGluRs in aged rats, possibly because of an altered distribution of glutamate in the extrasynaptic space. This in turn affects synaptic transmission and plasticity within the aged hippocampal CA1 network.

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“…There are two MAO isoenzymes, A and B. The activity of MAO B, but not MAO A, appears to increase with age in various regions of the human and rat brain (Strolin et al 1990). This increase in MAO B is associated mainly with the proliferation of astrocytes that accompanies the neuronal loss that occurs in aging and AD (Riederer et al 1986).…”

Section: Discussionmentioning

confidence: 96%

Protective effects of Glycyrrhiza uralensis Fisch. on the cognitive deficits caused by β-amyloid peptide 25–35 in young mice

Ahn

Choi

et al. 2006

Biogerontology

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Amyloid beta protein (Abeta) may be involved in the progression of Alzheimer's disease (AD), by acting as a neurotoxin and eliciting oxidative stress. This study was designed to determine the effects of Glycyrrhiza uralensis Fisch. water extract (GWE) on the cognitive deficits and oxidative stress induced by the administration of Abeta(25-35) in mice. Mice in two of the four animal groups were fed an experimental diet containing either 0.5 or 1% GWE for the entire 6-week experimental period. Control mice and a further experimental group were fed a non-GWE diet. Abeta(25-35) was administered to the three experimental groups by intracerebroventricular (i.c.v.) injection (10 microg/10 microl/mouse) once per week in weeks 5 and 6 of the experimental period. Behavioral changes were assessed using both a passive avoidance (after the injection of Abeta(25-35) in week 5) and the Morris water-maze tests (after the injection of Abeta(25-35) in week 6). Control animals were administered vehicle alone. The prolonged consumption of a diet containing GWE ameliorated the cognitive deficits caused by the i.c.v. injections of Abeta(25-35). Treatment with Abeta(25-35) led to higher concentrations of thiobarbituric acid reactive substances in the brain, and GWE attenuated this response. There was a decrease in catalase activity in the group provided with 1% GWE. Acetylcholinesterase activity was significantly reduced in the brains of all GWE-treated animals compared to that in the non-GWE-fed experimental group. These results suggest that GWE exerts a protective effect against the cognitive impairments often observed in AD, and that in mice this effect is mediated by antioxidant actions against oxidative stress.

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The effects of aging on MAO activity and amino acid levels in rat brain

Cited by 16 publications

References 34 publications

Effect of ageing on tissue levels of amino acids involved in the nitric oxide pathway in rat brain

Effect of ageing on tissue levels of amino acids involved in the nitric oxide pathway in rat brain

Reduction in glutamate uptake is associated with extrasynaptic NMDA and metabotropic glutamate receptor activation at the hippocampal CA1 synapse of aged rats

Protective effects of Glycyrrhiza uralensis Fisch. on the cognitive deficits caused by β-amyloid peptide 25–35 in young mice

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