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Regional brain variations of cytochrome oxidase activity in Reln rl‐orl mutant mice
Author(s) -
Strazielle C.,
Hayzoun K.,
Derer M.,
Mariani J.,
Lalonde R.
Publication year - 2006
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.20772
Subject(s) - reeler , neocortex , reelin , cytochrome c oxidase , biology , ventral tegmental area , cerebellum , hippocampus , neuroscience , deep cerebellar nuclei , tegmentum , hippocampal formation , microbiology and biotechnology , dopaminergic , central nervous system , dopamine , midbrain , mitochondrion , cerebellar cortex , extracellular matrix
Cell malpositioning has been described in laminated structures of the spontaneous mutation, reeler , including the cerebellum, the hippocampus, and the neocortex. Despite the ectopic positions of different neuronal populations, the specificity of synaptic connections is maintained. The metabolic consequences of this form of neuropathology were examined in Reln rl mutant mice by quantitative measures of cytochrome oxidase (CO) activity, a mitochondrial enzyme essential for oxidative metabolism in neurons. Despite severe tissue disorganization but in line with the intact synaptic organization, the reeler mutation did not affect global metabolic activity of the laminated structures of the brain. CO activity, however, was altered in specific subregions of the cerebellum, hippocampus, and neocortex, as well as in septum and various brainstem (medial pontine, paramedial reticular, paragigantocellular reticular) regions anatomically related to these structures, attesting to large functional alterations in Reln rl‐orl brain. Metabolic activity variations were also detected in the ventral tegmental area and ventral neostriatum of the mesolimbic dopaminergic pathway. The results are discussed and compared to the regional CO variations found in other ataxic mice, in regard to the structural defects, the integrity of the connections, and the mutation‐specific effects. © 2006 Wiley‐Liss, Inc.