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Rostrocaudal expression of antibody HNK‐1‐reactive glycolipids in mouse cerebellum: Relationship to developmental compartments and leaner mutation
Author(s) -
Nair Sukumaran M.,
Prasadarao Nemani,
Tobet Stuart A.,
Jungalwala Firoze B.
Publication year - 1993
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.903320303
Subject(s) - cerebellum , purkinje cell , biology , glycolipid , granule cell , epitope , granular layer , microbiology and biotechnology , cerebellar cortex , immunocytochemistry , neuroscience , central nervous system , antibody , biochemistry , endocrinology , immunology , dentate gyrus
Sulfoglucuronylglycolipids (SGGLs) and glycoproteins, reacting with monoclonal antibody HNK‐1, are developmentally and spatially regulated in the mammalian cortex and cerebellum. It has been proposed that the HNK‐1 carbohydrate epitope is involved in intercellular adhesion and cell‐cell interactions. Biochemical analysis and immunocytochemical localization of SGGLs and other neolacto series glycolipids were studied in the leaner mutant mouse cerebellum, where a slow and progressive rostral to caudal degeneration occurs with a gradual loss of both granule cells and Purkinje cells. Biochemical analyses showed that SGGLs and other neolacto series of glycolipids were significantly decreased in the adult leaner cerebellum; however, HNK‐1‐reactive glycoproteins were not affected. By an immunocytochemical method which selectively localizes the lipid antigens, it is shown that SGGLs are primarily associated with Purkinje cell bodies and their dendrites in the molecular layer and in cerebellar nuclei where Purkinje cell axons terminate. At postnatal day 30 (P30), SGGL immunoreactivity (rSGGL‐ir) in the leaner cerebellum was reduced moderately compared to normal littermates, which correlated with the minimal degree of Purkinje cell degeneration at this age in leaner and with the biochemical data. At P67 and P90, the SGGL‐ir was significantly more reduced in the leaner as Purkinje cell degeneration proceeded. There was a direct correlation between loss of Purkinje cells and SGGL‐ir in the cerebellar molecular layer. In both normal and young leaner cerebella, the SGGL‐ir in different lobules was not uniform; there were distinct rostrocaudal and mediolateral differences. SGGL‐ir was markedly more intense in rostral than in caudal lobules in the vermis, the dividing line being the region immediately caudal to the primary fissure and rostral to the declival sulcus. In the lateral cerebellum, the SGGL‐ir was less intense than in the vermis and the rostrocaudal difference was not as pronounced. There was also nonuniformity in the intensity of staining in different folia. The rostrocaudal as well as mediolateral differences in the intensity of SGGL‐ir were confirmed independently by biochemical analysis. The differential phenotypic expression of SGGLs and the selective susceptibility to Purkinje cell death in leaner mutant are discussed in relation to the known embryologic and ontogenetic compartmentation of cerebellum. © 1993 Wiley‐Liss, Inc.