Periventricular localization of a toxic encephalopathy induced by a mechanism involving choroid plexus.
An aliphatic triamine has been reported to cause lesions in rats in the vicinity of the area postrema and the median eminence of the hypothalamus, sites known to lack a blood-brain barrier. The present study revealed that some of the rats developed lesions in the cerebellum as well. The cerebellar lesions were related topographically to the choroid plexus in the underlying fourth ventricle. This periventricular distribution could be due to passage of the triamine from blood to choroid plexus and cerebrospinal fluid and then to parenchyma. In further experiments, the permeability of the plexus was increased by inducing choroid plexitis with cyclophosphamide. Subsequent administration of the triamine induced periventricular cerebellar lesions in higher incidence and at lower dose levels than in normal rats. Thus, the induction of choroid plexitis supported the aforementioned hypothesis and also suggested that it might be a useful model for periventricular localization of other types of lesions or diseases.
D000818:Animals; D001921:Brain / Q000187:drug effects / Q000473:pathology*; D002531:Cerebellum / Q000187:drug effects / Q000473:pathology / Q000648:ultrastructure; D002552:Cerebral Ventricles / Q000473:pathology; D002831:Choroid Plexus / Q000473:pathology*; D003520:Cyclophosphamide / Q000494:pharmacology; D005260:Female; D008297:Male; D008854:Microscopy, Electron; D011073:Polyamines / Q000633:toxicity*; D051381:Rats; D011917:Rats, Inbred Lew
D011073:Polyamines; C033506:3,3'-methyliminobis(N-methylpropylamine); D003520:Cyclophosphamide