NDLI: Long-Term Methionine Exposure Induces Memory Impairment on Inhibitory Avoidance Task and Alters Acetylcholinesterase Activity and Expression in Zebrafish (Danio rerio)

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Long-Term Methionine Exposure Induces Memory Impairment on Inhibitory Avoidance Task and Alters Acetylcholinesterase Activity and Expression in Zebrafish (Danio rerio)

Content Provider	Springer Nature Link
Author	Vuaden, Fernanda Cenci Savio, Luiz Eduardo B. Piato, Angelo L. Pereira, Talita C. Vianna, Mônica R. Bogo, Maurício R. Bonan, Carla D. Wyse, Angela T. S.
Copyright Year	2012
Abstract	Hypermethioninemic patients exhibit a variable degree of neurological dysfunction. However, the mechanisms involved in these alterations have not been completely clarified. Cholinergic system has been implicated in many physiological processes, including cognitive performances, as learning, and memory. Parameters of cholinergic signaling have already been characterized in zebrafish brain. Since zebrafish is a small freshwater teleost which is a vertebrate model for modeling behavioral and functional parameters related to human pathogenesis and for clinical treatment screenings, in the present study we investigated the effects of short- and long-term methionine exposure on cognitive impairment, AChE activity and gene expression in zebrafish. For the studies, animals were exposed at two methionine concentrations (1.5 and 3.0 mM) during 1 h or 7 days (short- or long-term treatments, respectively). We observed a significant increase in AChE activity of zebrafish brain membranes after long-term methionine exposure at 3.0 mM. However, AChE gene expression decreased significantly in both concentrations tested after 7 days of treatment, suggesting that post-translational events are involved in the enhancement of AChE activity. Methionine treatment induces memory deficit in zebrafish after long-term exposure to this amino acid, which could be related, at least in part, with cognitive impairment observed in hypermethioninemia. Therefore, the results here presented raise a new perspective to use the zebrafish as a complementary vertebrate model for studying inborn errors of metabolism, which may help to better understand the pathophysiology of this disease.
Starting Page	1545
Ending Page	1553
Page Count	9
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	37
Issue Number	7
e-ISSN	15736903
Language	English
Publisher	Springer US
Publisher Date	2012-03-22
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Acetylcholinesterase Hypermethioninemia Memory Zebrafish Neurology Neurosciences Cell Biology Biochemistry Neurochemistry
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

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