scholarly journals INTRALAMINAR DISTRIBUTION OF ACID RIBONUCLEASE IN RABBIT CEREBRAL CORTEX

1971 ◽  
Vol 19 (1) ◽  
pp. 43-45
Author(s):  
Y. TAKAHASHI ◽  
Y. SUZUKI
Keyword(s):  
Enzyme Activity ◽  
Cerebral Cortex ◽  
White Matter ◽  
Distribution Pattern ◽  
Subcortical White Matter ◽  
Cortical Layer ◽  
Ribonuclease Activity ◽  
Rabbit Brain ◽  
Rabbit Cerebral Cortex ◽  
Layer V

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.

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
Keyword(s):  
Cerebral Cortex ◽  
White Matter ◽  
Transgenic Mice ◽  
Subventricular Zone ◽  
Normal Development ◽  
Subcortical White Matter ◽  
Host Tissue ◽  
Marker Enzyme ◽  
Wild Type ◽  
Transplantation Experiments

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.

scholarly journals Quantitative assessment of prefrontal cortex in humans relative to nonhuman primates

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
Keyword(s):  
Cerebral Cortex ◽  
Prefrontal Cortex ◽  
White Matter ◽  
Corpus Callosum ◽  
Quantitative Assessment ◽  
Nonhuman Primates ◽  
Subcortical White Matter ◽  
Association Cortex ◽  
Cortical Gray Matter ◽  
And Function

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.

Oligodendrocytes in Developing Hameter Cerebral Cortex

1976 ◽  
Vol 34 ◽  
pp. 126-127
Author(s):  
MB. Tank Buschmann
Keyword(s):  
Cerebral Cortex ◽  
Optic Nerve ◽  
Frontal Cortex ◽  
Osmium Tetroxide ◽  
Sodium Cacodylate Buffer ◽  
Sodium Cacodylate ◽  
Tissue Samples ◽  
Cacodylate Buffer ◽  
Layer V ◽  
Adult Hamster

Development of oligodendrocytes in rat corpus callosum was described as a sequential change in cytoplasmic density which progressed from light to medium to dark (1). In rat optic nerve, changes in cytoplasmic density were not observed, but significant changes in morphology occurred just prior to and during myelination (2). In our study, the ultrastructural development of oligodendrocytes was studied in newborn, 5-, 10-, 15-, 20-day and adult frontal cortex of the golden hamster (Mesocricetus auratus).Young and adult hamster brains were perfused with paraformaldehyde-glutaraldehyde in sodium cacodylate buffer at pH 7.3 according to the method of Peters (3). Tissue samples of layer V of the frontal cortex were post-fixed in 2% osmium tetroxide, dehydrated in acetone and embedded in Epon-Araldite resin.

Cognitive dysfunctions associated with white matter damage due to cardiovascular burden – determinants and interpretations

2014 ◽  
Vol 45 (3) ◽  
pp. 334-345 ◽  
Author(s):  
Paweł Krukow
Keyword(s):  
Cerebral Cortex ◽  
White Matter ◽  
Cardiovascular Diseases ◽  
Cognitive Disorder ◽  
Theoretical Background ◽  
Dynamic Aspect ◽  
Pathological Changes ◽  
White Matter Damage ◽  
Neuropsychological Disorders ◽  
Considerable Research

AbstractAlthough considerable research has been devoted to cognitive functions deteriorating due to diseases of cardiovascular system, rather less attention has been paid to their theoretical background. Progressive vascular disorders as hypertension, atherosclerosis and carotid artery stenosis generate most of all pathological changes in the white matter, that cause specific cognitive disorder: disconnection syndromes, and disturbances in the dynamic aspect of information processing. These features made neuropsychological disorders secondary to cardiovascular diseases different than the effects of cerebral cortex damage, which may be interpreted modularly.

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