scholarly journals Restricted Migration of Transplanted Oligodendrocytes or their Progenitors, Revealed by Transgenic Marker MβP

1993 ◽  
Vol 4 (2) ◽  
pp. 139-146 ◽  
Author(s):  
Victor L. Friedrich, Jr. ◽  
Robert A. Lazzarini

Transgenic mice of line MβP3 express bacterial β-galactosidase in oligodendrocytes but not other cells of the CNS. The marker enzyme, demonstrated histochemically or by immunostaining in oligodendrocyte cell bodies and along myelin internodes, appears at the time of myelination and persists thereafter; in transplantation experiments, the marker may serve to indicate both the source of particular cells and their state of differentiation. The subventricular zone of the lateral ventricle, grafted from transgenic to wild-type perinatal recipient mice, yields histochemically labeled oligodendrocytes in surrounding host tissue. When grafts are placed in cerebral cortex near callosal radiations, graft-derived oligodendrocytes are found in cerebral cortex and subcortical white matter as far as 1.5 mm from the site of implant but not in nearby caudoputamen. This study is the first to document differentiation of transplant-derived oligodendrocytes in normal developing CNS. Our results are consistent with the well- established notion that oligodendrocyte progenitors migrate during normal development and suggest that such migration might be guided or restricted by mechanisms yet to be identified.

1971 ◽  
Vol 19 (1) ◽  
pp. 43-45
Author(s):  
Y. TAKAHASHI ◽  
Y. SUZUKI

Acid ribonuclease activity of the cortical layer and the subcortical white matter of area parietalis of rabbit brain was measured microchemically and the distribution of enzyme activity was related to the histologic composition. The cytoarchitectonic distribution pattern of acid ribonuclease showed it to be higher in layers III, IV, V and VI than in layers I and II, and especially high in layer V. The activity in white matter was the lowest among all examined layers.


2018 ◽  
Vol 115 (22) ◽  
pp. E5183-E5192 ◽  
Author(s):  
Chad J. Donahue ◽  
Matthew F. Glasser ◽  
Todd M. Preuss ◽  
James K. Rilling ◽  
David C. Van Essen

Humans have the largest cerebral cortex among primates. The question of whether association cortex, particularly prefrontal cortex (PFC), is disproportionately larger in humans compared with nonhuman primates is controversial: Some studies report that human PFC is relatively larger, whereas others report a more uniform PFC scaling. We address this controversy using MRI-derived cortical surfaces of many individual humans, chimpanzees, and macaques. We present two parcellation-based PFC delineations based on cytoarchitecture and function and show that a previously used morphological surrogate (cortex anterior to the genu of the corpus callosum) substantially underestimates PFC extent, especially in humans. We find that the proportion of cortical gray matter occupied by PFC in humans is up to 1.9-fold greater than in macaques and 1.2-fold greater than in chimpanzees. The disparity is even more prominent for the proportion of subcortical white matter underlying the PFC, which is 2.4-fold greater in humans than in macaques and 1.7-fold greater than in chimpanzees.


1938 ◽  
Vol 57 ◽  
pp. 385-399 ◽  
Author(s):  
Flora Cochrane

It is generally accepted that the function of the mutant genes which affect eye colour in Drosophila is to produce either quantitative or qualitative changes in the normal development of eye pigment. Wright (1932) believes that these genes act by interfering with some part of a chain of reactions which give rise to eye-colour characteristic of the wild type. Mainx (1935) suggested that recessive eye-colour genes (with the exception of sepia) reduce the total amount of pigment, and that the degree of reduction is characteristic for each gene. Transplantation experiments of Beadle and Ephrussi (1935, 1936, 1937 a and b) have led them to the view that certain eye-colour mutants lack specific substances which are necessary for the development of additional pigment present in wild type eye colour. Johannson (1924) and Schultz (1935) studied the histology of the adult eye of D. melanogaster and classified the mutant eye colours according to the distribution of granules in their pigment cells. Schultz (1932) had previously noted the time of pigment deposition and subsequent changes in wild type and some mutants of D. melanogaster. In an earlier paper the author (1936) described in detail similar colour changes in the eyes of developing pupæ of D. pseudo-obscura. Previous work in this laboratory (1932, 1934, 1935) by Crew and Lamy make it appear that each mutant eye colour is the expression of a gene which acts to suppress normal development during a certain period of time, allowing the rest of the development to proceed as in wild type.


Sign in / Sign up

Export Citation Format

Share Document