Premium
Terminal degeneration in the mediodorsal cerebral cortex of the lizard Agama agama : Light and electron microscopy
Author(s) -
Wouterlood F. G.,
Alones V. E.,
Elprana D.,
Lohman A. H. M.
Publication year - 1982
Publication title -
journal of morphology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.652
H-Index - 74
eISSN - 1097-4687
pISSN - 0362-2525
DOI - 10.1002/jmor.1051720105
Subject(s) - biology , degeneration (medical) , electron microscope , axon , lizard , anatomy , cortex (anatomy) , dendritic spine , pathology , ultrastructure , cerebral cortex , hippocampal formation , neuroscience , medicine , physics , optics , zoology
Abstract The degeneration of axon terminals in the small‐celled part of the mediodorsal cortex (sMDC) of the lizard Agama agama has been studied after lesions in the dorsal cortex at various survival periods. The Fink‐Heimer stain was used to map and demonstrate terminal degeneration with the light and electron microscope. Electron microscopy was used to identify and describe degenerating boutons ultrastructurally. One sham‐operated and three unoperated animals served as controls. Between 6 and 21 days postsurgically, degenerating terminals can be seen through 80% of the superficial plexiform layer, the zone adjacent to the cellular layer remaining free of degeneration. Swelling of dendrites in the outer part of the superficial plexiform layer and increased numbers of vacuolar invaginations, both present at short (24 hr–6 days; peak at 48–54 hr) survival periods, can be regarded as reaction to the surgical trauma. Degeneration of axon terminals takes three forms, all of the electron‐dense type: gray boutons, degenerating bouton‐dendritic spine complexes surrounded or engulfed by glia, and degeneration debris inside glial processes. Several forms of terminal degeneration occur concomitantly at any short (3–12 days) survival time. At longer survival times (15–21 days) only debris is present. From 6 days on, considerable numbers of degenerating structures are present, but the majority of degenerating boutons and debris are associated with reactive glia rather than with dendrites. From these observations it is concluded that in this lizard application of the combined degeneration‐Golgi‐EM technique would probably lead to little success. Electron microscopy of Fink‐Heimer‐stained sections suggests that degenerating bouton‐dendritic spine complexes and degeneration debris accumulate silver particles, whereas gray boutons do not.