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Related Experiment Videos

Abnormal retinal projections alter GAP-43 patterns in the diencephalon.

K L Moya1, L I Benowitz, G E Schneider

  • 1Department of Brain and Cognitive Sciences, Whitaker College, Massachusetts Institute of Technology, Cambridge.

Brain Research
|September 17, 1990
PubMed
Summary
This summary is machine-generated.

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Abnormally routed optic fibers in hamsters show reduced growth-associated protein (GAP-43) in the lateral posterior nucleus. These fibers also displace normal GAP-43 positive terminals, which originate from local interneurons.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Cell Biology

Background:

  • Mature retinal terminals have low levels of growth-associated protein (GAP-43).
  • The lateral posterior nucleus (LP) of the thalamus normally has high GAP-43 levels.
  • Damage to the superior colliculus in neonatal hamsters causes aberrant retinal projections to the LP.

Purpose of the Study:

  • To investigate the expression of GAP-43 in abnormally routed optic fibers in the hamster LP.
  • To determine the source of normal GAP-43-positive terminals within the LP.
  • To understand the interaction between aberrant retinal fibers and the thalamic target zone.

Main Methods:

  • Immunohistochemistry using GAP-43 antibodies.
  • Surgical removal of major extrinsic afferents to the LP (superior colliculus and posterior cortex).

Related Experiment Videos

  • Chemical elimination of local interneurons in the LP using ibotenic acid.

    • Main Results:

    • Abnormal retinal projections to the LP exhibited very low levels of GAP-43.
    • Retinal fibers excluded GAP-43 from normal territories, creating negatively-stained islands.
    • Destruction of local interneurons significantly reduced GAP-43 levels in the LP.
    • Removal of SC or posterior cortex projections did not affect LP GAP-43 immunoreactivity.

    Conclusions:

    • Retinal terminals in anomalous target areas undergo normal developmental decline in GAP-43.
    • Aberrant retinal projections displace endogenous GAP-43-rich terminals originating from local interneurons in the LP.