Inhibition of peroxisomal beta‐oxidation and brain development in rats

Christiane Van Den Branden; Georges Dacremont; Robert Hooghe; Frank Roels

doi:10.1002/glia.440020407

Inhibition of peroxisomal beta‐oxidation and brain development in rats

Christiane Van Den Branden, Georges Dacremont, Robert Hooghe, Frank Roels

Research output › peer-review

Abstract

Thioridazine, an inhibitor of peroxisomal beta‐oxidation, was administered orally to nursing rats during the period of maximal myelination in the pups (8–21 days postnatally). Under the experimental conditions, thioridazine causes accumulation of C24 and C26 fatty acids in pup brain lipids, an effect we consider to be a typical consequence of inhibited peroxisomal beta‐oxidation. In the corpus callosum of treated pups, the relationship between axon diameter and myelin sheath thickness is altered compared with matched controls. Thioridazine also induces undernourishment effects in 21 day‐old rats. Body and brain weight are severely reduced. Liver peroxisomes show a starvation‐type metabolism. Undernourishment is known to influence myelination in developing rat brain. However, known consequences of undernourishment, such as decreased myelin concentration in whole brain, decreased percentage of myelinated fibers, and decreased granule‐to‐Purkinje cell ratio are not present.

Original language	English
Pages (from-to)	260-265
Number of pages	6
Journal	Glia
Volume	2
Issue number	4
DOIs	https://doi.org/10.1002/glia.440020407
State	Published - 1989

ASJC Scopus subject areas

Neurology
Cellular and Molecular Neuroscience

Access to Document

10.1002/glia.440020407

Cite this

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title = "Inhibition of peroxisomal beta‐oxidation and brain development in rats",

abstract = "Thioridazine, an inhibitor of peroxisomal beta‐oxidation, was administered orally to nursing rats during the period of maximal myelination in the pups (8–21 days postnatally). Under the experimental conditions, thioridazine causes accumulation of C24 and C26 fatty acids in pup brain lipids, an effect we consider to be a typical consequence of inhibited peroxisomal beta‐oxidation. In the corpus callosum of treated pups, the relationship between axon diameter and myelin sheath thickness is altered compared with matched controls. Thioridazine also induces undernourishment effects in 21 day‐old rats. Body and brain weight are severely reduced. Liver peroxisomes show a starvation‐type metabolism. Undernourishment is known to influence myelination in developing rat brain. However, known consequences of undernourishment, such as decreased myelin concentration in whole brain, decreased percentage of myelinated fibers, and decreased granule‐to‐Purkinje cell ratio are not present.",

keywords = "Corpus callosum, Metabolic disease, Myelin, Thioridazine, Undernourishment",

author = "{Van Den Branden}, Christiane and Georges Dacremont and Robert Hooghe and Frank Roels",

year = "1989",

doi = "10.1002/glia.440020407",

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TY - JOUR

T1 - Inhibition of peroxisomal beta‐oxidation and brain development in rats

AU - Van Den Branden, Christiane

AU - Dacremont, Georges

AU - Hooghe, Robert

AU - Roels, Frank

PY - 1989

Y1 - 1989

N2 - Thioridazine, an inhibitor of peroxisomal beta‐oxidation, was administered orally to nursing rats during the period of maximal myelination in the pups (8–21 days postnatally). Under the experimental conditions, thioridazine causes accumulation of C24 and C26 fatty acids in pup brain lipids, an effect we consider to be a typical consequence of inhibited peroxisomal beta‐oxidation. In the corpus callosum of treated pups, the relationship between axon diameter and myelin sheath thickness is altered compared with matched controls. Thioridazine also induces undernourishment effects in 21 day‐old rats. Body and brain weight are severely reduced. Liver peroxisomes show a starvation‐type metabolism. Undernourishment is known to influence myelination in developing rat brain. However, known consequences of undernourishment, such as decreased myelin concentration in whole brain, decreased percentage of myelinated fibers, and decreased granule‐to‐Purkinje cell ratio are not present.

AB - Thioridazine, an inhibitor of peroxisomal beta‐oxidation, was administered orally to nursing rats during the period of maximal myelination in the pups (8–21 days postnatally). Under the experimental conditions, thioridazine causes accumulation of C24 and C26 fatty acids in pup brain lipids, an effect we consider to be a typical consequence of inhibited peroxisomal beta‐oxidation. In the corpus callosum of treated pups, the relationship between axon diameter and myelin sheath thickness is altered compared with matched controls. Thioridazine also induces undernourishment effects in 21 day‐old rats. Body and brain weight are severely reduced. Liver peroxisomes show a starvation‐type metabolism. Undernourishment is known to influence myelination in developing rat brain. However, known consequences of undernourishment, such as decreased myelin concentration in whole brain, decreased percentage of myelinated fibers, and decreased granule‐to‐Purkinje cell ratio are not present.

KW - Corpus callosum

KW - Metabolic disease

KW - Myelin

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