Humans and guinea pigs are unable to produce vitamin C, with deficiency resulting in a well-known disorder of collagen synthesis. Pial basement membrane structure preservation is essential in the proper migration of neurons. In our study, intrauterine deprivation of vitamin C in guinea pig fetuses led to a collagen synthesis disorder, weakness, and finally a breach of pial basement membrane. We found excessive migration of the external germinal layer cells into the subarachnoid space of the cerebellum through defects in the pial basement membrane. The changes ranged from focal rupture of pial basement membranes to their complete disintegration. The loss of proper folia formation resulted in macroscopically visible flattening of the cerebellar surface. Different grades of dysplastic changes in the folia of the cerebellar cortex were observed in 2 experimental groups assigned different limits to mark the time of commencement and duration of vitamin C deprivation. The most severe form of dysplastic changes was characterized by marked irregularity of the cerebellar cortex similar to that in lissencephaly type II. Thus, prenatal vitamin C deficiency represents a novel animal model to study the effects of collagen synthesis on development of breaches in the pial basement membrane, disordered migration of neurons, dysplasia of cerebellar cortex, and the pathogenesis of lissencephaly.Keywords scurvy, cerebellum, guinea pigs, vitamin c deficiency, lissencephaly, animal model Lissencephaly type II is a disease caused by alteration to the pial basement membrane (PBM) proteins, which causes it to weaken and become porous. This causes a deficiency of the glia limitans superficialis and radial glial cell connectivity. As a result, migrating neural cells pass through the pial gaps to form cell ectopia near the brain surface. This leads to loss of gyri and sulci, forming irregularities on the brain surface and a so-called cobbled formation, which is why lissencephaly type II is also sometimes called cobblestone lissencephaly. 9,34Based on the fact that the structural integrity of the PBM is necessary for proper migration of the neurons, 2 main approaches have been established for experimental modeling of lissencephaly type II. First, animal models with targeted inactivation of genes involved in membrane protein synthesis have been studied. The lack of these proteins, such as collagen, laminin, and others, causes the PBM to weaken and finally rupture. 13,16,17,25,43 The second approach uses chemical destruction of meningeal cells over the developing cerebellum through exposure to 6-hydroxydopamine (6-OHDA). The loss of glio-pial membrane allows for overmigration of neurons through the pial breaches into the subarachnoid space. 1,29,30 Collagen is one of the key structural units of the basement membrane, and its synthesis is dependent on vitamin C. Humans, monkeys, and guinea pigs are unable to synthesize vitamin C because of a lack of L-gulono-g-lactone oxidase. 27It is well known that a deficiency of vitamin C in guinea...