Thalamo-cortical tracts as a neocortical structure organizer?

Vincent A Mazzarella vamg6792 at uxa.cso.uiuc.edu
Fri May 17 09:37:06 EST 1991


The following is a one page synopsis of a recent one-hour seminar.
The impressions are my own and do not reflect accuracy of the facts
contained in the presentation. Corrections and discussion are welcomed.

Brain size roughly correlates with body size, but for any given
body size, there may be as much as a 10x variation of brain size
for different species. As brain size increases, so does cortical
size, in an orderly fashion. Furthermore, the "birth dates" or
development of different areas of the brain, progress in similar
sequences and at proportionate rates in different species. What
types of mechanisms might maintain such orderly development? 
    The size of a brain area depends in part on how long its cells
remain in the mitotic cycle. Motoneurons are "born" (cease mitotic
division) early; their number is few. Neocortex and retinal cells
are born late; they initailly have large numbers of cells. Thus,
control of mitosis is an one intrinsic mechanism of area size and
development. 
    Cell death further modulates the size of an area. In a D7
(post-natal day 7) hamster, an area of cingulate medial cortex may
have a large degree of pyknotic cell death, but a neighboring area
of the visual cortex may show none. 
    What processes may modulate both boundaries of a brain region
and the amount of cell death within that region? Obviously, either
or both intra-regional cellular interactions or interactions with
neighboring regions may influence such processes.
    Dr. Finlay's hypothesis is that the thalamo-cortical projection
may be an example of a neighboring region input that influences
structure and cell number in another region, the visual neocortex.
When a large lesion of the thalamus encompassing the LGN and VB
nuclei is made, an increase in the number of degenerating cells in
the area that the LGN normally projects to is seen, with a decrease
in the size of the layer to which such afferents would normally
innervate (i.e. layer IV granule cells), as seen by Nissl stain. 
    That the thalamo-cortical projections have a unique
organizational role is contrasted to the lack of effect on cortical
cell degeneration or layer diminution when corpus callosal fibers
(to layers II, III, V, VI of areas 17-18a, 3, and 6) or superior
colliculus (whose fibers would project to layer V) lesions are
made.
      Using the flurorescent Dye I for retrograde labelling at
different days of embryonal development, it was determined that the
thalamo-cortical projections were the first to reach the visual
cortex. Cortico-fugal efferent tracts then appear later. Further-
more, these thalamo-cortical afferents were directed to a very
well-defined area of the cortex. If the thalamus is lesioned and
these connections are not made, then other areas of the thalamus
will not form alternate connections. Thus, some specific, inherent
recognition signal seems to be needed to direct these pioneering
thalamo-cortical fibers to the right area of cortex. 
      Could these thalamo-cortical fibers, once laid down, act as
some sort of framework for other fiber tract development into or
out of the cortex?  Double labelling of other tracts show no
physical connection between cortico-fugal tracts developing shortly
after the thalamo-cortical tracts are in place, questioning such a
hypothesis. Furthermore, there are few thalamic projections to
association cortex, so for this large part of the neocortex, there
would be no such thalamo-cortical framework available.



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