The mesencephalic dopamine (DA) cell system was examined in mice homozygous and heterozygous for the weaver (wv) gene and in wild-type controls to estimate the extent of cell losses associated with the genetically determined central DA deficiency observed in weaver homozygotes. Animals of the three genotypes (+/+, wv/+, wv/wv) were studied at postnatal day (P)20 and P90. Serial coronal sections were obtained through the brainstem. Half of the sections were immunolabeled with antiserum to tyrosine hydroxylase (TH). Cell counts were obtained in areas A8 (retrorubral nucleus, RRN), A9 (substantia nigra, SN), and A10 (ventral tegmental area, VTA). The counts were analyzed with repeated measures analysis of variance followed by individual comparisons among group means. In A8, weaver homozygotes did not differ significantly from wild-type controls at P20, whereas there was a significant difference of 56% at P90. In A9, weaver homozygotes differed significantly from wild-type mice by 42% at P20 and by 69% at P90. The decrease in cell number between P20 and P90 in weaver homozygotes was 54%. In A10, weaver homozygotes did not differ significantly from wild-type controls at P20, whereas there was a significant difference of 26% at P90. Cell numbers in all three areas of heterozygotes did not differ significantly from wild-type control values at either age point. These findings demonstrate that by three months of age homozygous weaver mutants exhibit nerve cell losses in all three areas of the mesencephalic DA cell system. Such losses account for the DA deficiency seen in striatal, limbic and cortical projection fields.
The monumental Atlas of Cytoarchitectonics of the Adult Human Cerebral Cortex of Economo and Koskinas represents a gigantic intellectual and technical effort, never sufficiently recognized. One reason might have been the limited number of copies produced; another, the complex (albeit logical and precise) symbol notation, which comprises a Roman capital (from the initial of the respective lobe), a calligraphic capital (the sequence of a gyrus within a lobe), and a Latin or Greek subscript (for microscopic features). Economo and Koskinas defined 107 cortical areas, as opposed to Brodmann’s 44 areas for the human brain. Their cytoarchitectonic criteria confer the advantage of a more detailed parcellation scheme, despite the traditional familiarity of neuroscientists with Brodmann numbers. The system of 107 areas of Economo and Koskinas may be especially useful for modern studies on functional localization.
The genetically-determined loss of Purkinje cells (PCs) in 'Purkinje cell degeneration' (pcd) mutant mice results in the loss of presynaptic afferents to the deep cerebellar nuclei (DCN). This deafferentation takes place between postnatal day (P)17 and P45, i.e. after the maturation of cerebellar circuitry. We examined the DCN of normal and pcd mutant mice by quantitative light microscopic methods to determine whether neuronal atrophy or loss in the DCN take place during and after the loss of their input from the PCs. Neuronal diameters in control mice were 16.4 +/- 0.72 microns (mean +/- S.D.) at P23 and 15.6 +/- 0.64 microns at P300. The respective values in pcd mutant mice were 15.7 +/- 0.58 microns and 13.5 +/- 0.24 microns. Diameters in 300-day-old mutants were significantly smaller than those in both age-matched controls and 23-day-old mutants (P less than 0.001). Neuronal populations in the DCN of control mice were 10,167 +/- 949 at P23 and 10,429 +/- 728 at P300. The respective values in mutants were 9,436 +/- 1,366 and 7,424 +/- 1,324. There was a significant difference of 29% [95% confidence limits: 9-45%] between 300-day-old mutants and age-matched controls (P less than 0.01), and a significant loss of 21% [95% confidence limits: 4-36%] in 300-day-old mutants with respect to 23-day-old mutants (P less than 0.05). The total volume of the DCN was 22% less in 300-day-old mutants in relation to 23-day-old mutants (P less than 0.05). These findings support the idea that the stability of DCN neurons in the mature cerebellum depends in part on the synaptic input from PCs.
The genetically determined loss of cerebellar Purkinje cells (PCs) in "Purkinje cell degeneration" (pcd) mutant mice deprives inferior olivary (IO) neurons of their major postsynaptic target. The degeneration of PCs starts on postnatal day (P) 17 and loss of these neurons is virtually complete by P45. We examined the inferior olivary complex (IOC) of normal and pcd mutant mice by quantitative light microscopy to determine whether the degeneration of PCs is associated with atrophy and loss of their presynaptic neurons in the IOC. The number of IO neurons in 17-day-old mutants did not differ significantly from controls (P greater than .1). IO neurons in 23-day-old mutants were 23% (95% confidence limits: 12-34%) fewer than in age-matched controls, and in 300-day-old mutants they were 48% (95% confidence limits: 37-58%) fewer than in their controls (P less than .001 in both cases). The decline of the number of IO neurons in pcd mice between days 17 and 300 was 49% (P less than .0001; 95% confidence limits: 38-57%). The medial accessory olive (MAO) appeared less affected than the principal (PO) and the dorsal accessory olive (DAO). The mean neuronal diameter in control mice was 11.6 micron at 23 days and 10.8 micron at 300 days of age. The respective values in pcd mutants were 11.5 micron and 8.7 micron. Diameters in old mutants were significantly smaller than those in both age-matched controls and young mutants (P less than .001). These findings suggest that in the mature olivocerebellar system the stability of IO neurons depends on the state of their postsynaptic PCs.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.