vamg6792@uxa.cso.uiuc.edu (Vincent A Mazzarella) (05/17/91)
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. From a one hour lecture at Univ. of Illinois in Spring 1991: Plasticity & Constraint in Neocortical Organization & Evolution -- Barbara Finlay, Cornell U. -- Vincent Mazzarella College of Medicine, Neuroscience Program University of Illinois, Urbana-Champaign e-mail: mazz@vmd.cso.uiuc.edu