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Functional Deficits and Anatomical Sparing after Prenatal Brain Damage in the Rat

  • Sandra C. Pereira
  • Charles R. Legg
  • Ian Steele Russell
  • Mitchell Glickstein
Part of the Advances in Behavioral Biology book series (ABBI, volume 28)

Abstract

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).

Keywords

Pyramidal Cell Caudal Region Brightness Discrimination Shock Level Brightness Vision 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Press, New York 1985

Authors and Affiliations

  • Sandra C. Pereira
    • 1
  • Charles R. Legg
    • 2
  • Ian Steele Russell
    • 1
  • Mitchell Glickstein
    • 1
  1. 1.MRC Unit on Neural Mechanisms of Behaviour, Department of Anatomy & EmbryologyUniversity College LondonLondonEngland
  2. 2.The Psychology Unit, Department of Social Science and HumanitiesThe City UniversityLondonEngland

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