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MANGANESE‐INDUCED BEHAVIORAL DYSFUNCTION AND ITS NEUROCHEMICAL MECHANISM IN GROWING MICE
Author(s) -
Chandra Satya V.,
Shukla Girja S.,
Saxena D. K.
Publication year - 1979
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1979.tb05267.x
Subject(s) - neurochemical , manganese , weaning , homovanillic acid , offspring , dopamine , endocrinology , medicine , striatum , motor activity , norepinephrine , chemistry , physiology , pregnancy , biology , serotonin , receptor , genetics , organic chemistry
— Suckling mice were exposed to manganese from birth indirectly through their mothers and then directly through drinking water after weaning. The growth and development of these mice and their age‐matched controls were almost identical. Motor activity of offspring measured at 30‐day intervals showed a significant increase at 60 and 90 days in manganese‐treated mice compared to controls. Increased motor activity was associated with significant elevation in the levels of dopamine and norepinephrine in the corpus striatum of treated mice. The levels of striatal tyrosine, homovanillic acid and manganese were also significantly increased in mice after manganese exposure. Thus an animal model of early manganese poisoning has been developed with a possible role of striatal amines in the production of behavioral dysfunction in the treated mice. Implications of these findings are discussed in relation to the manifestations of the psychiatric phase of early manganese poisoning in man.