Functional Deficits and Anatomical Sparing after Prenatal Brain Damage in the Rat
One important aspect of plasticity is the extent to which animals can develop normal behaviour despite interference with the structural development of the brain. A teratogen derived from the glucoside cycasin, called methylazoxymethanol acetate (MAMa), selectively destroys dividing cells. When administered to a pregnant rat MAMa will inhibit the development of structures forming in the foetus at that time. Treatment with MAMa on embryonic day 15 produces offspring whose brain is the only organ revealing gross malformation. The brain is microencephalic, a phenomenon first described by Spatz and Laqueur (1968). This reduction in brain size in MAMa treated rats is mainly due to a failure of neocortical development (see Fig. 1).
KeywordsPyramidal Cell Caudal Region Brightness Discrimination Shock Level Brightness Vision
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