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Effect of Acetaldehyde on Behavioral and Neurochemical Changes Induced by MK‐801 in Rats
Author(s) -
Padillade la Torre Mónica,
FrancoPérez Javier,
Santamaría Abel,
Galvan Sonia,
González Edith,
Paz Carlos
Publication year - 2008
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1432.038
Subject(s) - neurochemical , dopamine , dizocilpine , dopaminergic , chemistry , striatum , neurotransmitter , medicine , endocrinology , glutamate receptor , nmda receptor , 3,4 dihydroxyphenylacetic acid , pharmacology , central nervous system , receptor , homovanillic acid , biochemistry , serotonin
Alterations in motor activity related to dopamine changes in some brain regions have been described as consequences of the modifications produced by systemic administration of MK‐801 (a noncompetitive NMDA receptor antagonist) in rats. Acetaldehyde (ACH), the main metabolite of ethanol, has been implicated in different alterations in the central nervous system after ethanol ingestion. ACH might exert some control on dopaminergic transmission through the formation of other compounds with dopamine, which eventually may modify dopamine content and its metabolism. In order to evaluate such a hypothesis, we used Wistar rats in the present study to evaluate the effect of ACH on locomotor alterations and dopamine metabolism changes induced by MK‐801. Our results show that the MK‐801‐treated group had a significant increase in locomotor activity. In contrast, we did not find significant differences in locomotion tests after ACH administration. However, the group to which both drugs were administered showed a significant decrease in locomotor activity compared with those given MK‐801 alone. Neurochemical analysis showed an increase in dopamine content in the striatum and frontal cortex after MK‐801 administration, however; the increase was reversed by giving 200 mg/kg of ACH. These results indicate that ACH can produce an antagonic‐like effect on locomotor alterations and dopamine content changes induced by MK‐801, thus modulating the MK‐801‐induced hyperlocomotion by interfering with dopamine metabolism.