Marta Miquel

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Acetaldehyde, the first metabolite of ethanol, may mediate some ethanol-induced effects. Previous research in our laboratory has shown that D-penicillamine, an inactivation agent for acetaldehyde, is effective in decreasing locomotor stimulation and conditioned place preference induced by ethanol in mice. In the present study, the effects of D-penicillamine(More)
There is evidence to suggest that acetaldehyde is involved in the control of ethanol-seeking behavior and reward. d-penicillamine, a thiol amino acid, is a highly selective agent for the inactivation of acetaldehyde. Previous studies from our laboratory have demonstrated that d-penicillamine prevents both behavioral stimulation induced by ethanol and(More)
It has been suggested that some of the behavioral effects produced by ethanol are mediated by its first metabolite, acetaldehyde. The present research addressed the hypothesis that catalase-dependent metabolism of ethanol to acetaldehyde in the brain is an important step in the production of ethanol-related affective properties. Firstly, we investigated the(More)
OBJECTIVE The present experiments analyze the effects of the brain catalase inhibitor 3-amino-1,2,4-triazole (AT) on the locomotor activity induced by ethanol. METHOD In the first experiment, mice received injections of either AT (0.5 g/kg) or saline (S) 5 hours prior to an ethanol injection (0, 0.8, 1.6, 2.4, 3.2 or 4 g/kg). In the second experiment,(More)
BACKGROUND D-Penicillamine, a sulfhydryl amino acid derived from penicillin, is a highly selective agent for sequestering in vivo acetaldehyde, the first metabolic product of ethanol. A substantial amount of research supports the idea that brain acetaldehyde, produced by central ethanol metabolism, plays a key role in determining some of the behavioral(More)
Lesions of the arcuate nucleus by monosodium glutamate, goldthioglucose and oestradiol valerate treatments are known to prevent the acute stimulating effect of ethanol in mice. On the basis of these results, the current study analysed whether a lesion of the arcuate nucleus by monosodium glutamate was able to block ethanol-induced locomotor sensitization.(More)
The antioxidant enzyme catalase by reacting with H(2)O(2), forms the compound known as compound I (catalase-H(2)O(2)). This compound is able to oxidise ethanol to acetaldehyde in the CNS. It has been demonstrated that 3-nitropropionic acid (3-NPA) induces the activity of the brain catalase-H(2)O(2) system. In this study, we tested the effect of 3-NPA on(More)
The involvement of catalase in ethanol-induced locomotion has been clearly proven. However, studies addressing the role of this enzyme in the effects that ethanol exerts on memory are lacking. In the present study, the social recognition test (SRT) was used to evaluate ethanol effects on memory. In this test, the reduction in investigation time of a(More)
Previous studies have demonstrated that there is a bidirectional modulation of ethanol-induced locomotion produced by drugs that regulate brain catalase activity. In the present study we have assessed the effect in rats of intraperitoneal, intraventricular or intracraneal administration of the catalase inhibitor sodium azide in the locomotor changes(More)
It has been proposed that brain catalase plays a role in the modulation of some psychopharmacological effects of ethanol. The acute administration of lead acetate has demonstrated a transient increase in several antioxidant cell mechanisms, including catalase. In the present study, we investigated the effects of acute lead acetate administration on(More)