The ventricular system in hydrocephalic rat brains produced by a deficiency of vitamin B₁₂ or of folic acid in the maternal diet

Abstract

TWENTY-SEVEN PIQURES IKTRODUCTIONRichardson and Hogan ('46) observed that about 2% of the infant rats produced by darns fed a synthetic type ration were hydrocephalic and showed that the abnormality could be prevented by including a liver extract in the diet. O'Dcll, Whitley a i d Hogan ( '48) found that hydrocephalus among tho offspring was largely prevented when folic acid was added to the diet. Later, O'Dell, Tl'hitley and Hogan ('51) showed that a much higher incidence of hydrocephalus, approximately 20% of the offspring, occurred when the dams consumed an all vegetable diet deficient in vitamin B12. The addition of vitamin B,, to the diet completely prevented the occurrence of hydrocephalus. More recent evidence (unpublished) has shown that an incidence of hydrocephalus of the order of 207. may be induced in the offspring of dams fed a folic acid antagonist (0.05% of crude methylfolic acid) even though vitamin B,, is present in adequate amounts. Nelson, Asling and Evans ('52) have used this same antagonist at a level

Reduced subcommissural organ glycoprotein immunoreactivity precedes aqueduct closure and ventricular dilatation in H-Tx rat hydrocephalus

“…Although not proven, it is conceivable that in fetal life when the SCO cells appear to be active but before the formation of the insoluble Reissner's fiber, the SCO secretes soluble glycoproteins that are important for normal brain ontogeny. This idea was first presented by Overholzer as a hypothesis to explain hydrocephalus induced in fetal rats (Overholzer et al 1954). Over the years, evidence has accumulated to support this suggestion.…”

“…Overholzer proposed that secretory material from the SCO in the fetus prevents aqueduct closure and maintains a patent pathway for CSF circulation (Overholzer et al 1954). His hypothesis was based on histological observations in fetuses and pups born to rats with vitamin B 12 or folic acid deficiency.…”

Development of Hydrocephalus in Mice Expressing the Gi-Coupled GPCR Ro1 RASSL Receptor in Astrocytes

“…Although SCO secretory function could not be determined from our histological examination of Ro1 brains, the observation that the SCO is disorganized in Ro1 mice is significant. The presence of a normal SCO appears to be necessary for the development and maintenance of the aqueduct, because impaired SCO formation and/or function are found in multiple animal hydrocephalus models and in human infantile hydrocephalus (Overholser et al, 1954;Newberne, 1962;Takeuchi and Takeuchi, 1986;Jones et al, 1987;Jones and Bucknall, 1988;Takahashi et al, 1997;Perez-Figares et al, 1998;Takahashi et al, 1998;Louvi and Wassef, 2000;Estivill-Torrus et al, 2001;Sakakibara et al, 2002;Fernandez-Llebrez et al, 2004). The SCO secretes negatively charged glycoproteins, such as SCO-spondin and RF-Gly I, that appear to be critical for maintaining an open aqueduct by their physical presence.…”

Acute Encephalitis and Hydrocephalus in Dogs Caused by Canine Parainfluenza Virus

“…None of our hydrocephalic beagles showed comparable conformation deficits. Deficiency of any nutrient in the diet as cause for hydrocephalus [37] can be excluded, because other gnotobiotic dogs raised in this laboratory have not developed hydrocephalus. Furthermore, many dogs received canine distemper virus viral inocula intracerebrally [32, 331 without subsequent development of hydrocephalus, indicating that mechanical factors associated with the inoculation procedure cannot account for development of hydrocephalus.…”