Miguel Perez-Pouchoulen1,2, Marta Miquel3, Paul Saft1,2, Brenda Brug1,2, Rebeca Toledo1**, Ma. Elena Hernandez1**, Jorge Manzo1*
Centro de Investigaciones Cerebrales, Universidad Veracruzana, Xalapa, Ver., México.1 Doctorado en Neuroetología, Universidad Veracruzana, Xalapa, Ver., México.2 Area de Psicobiología, Universitat Jaume I, Castellón, España.3 Cuerpo Académico de Neurociencias.* Cuerpo Académico de Neuroquímica.**
Abstract
Autism is considered as a neurodevelopmental disorder which affects boys more than girls, in a proportion 4:1 respectively. Autism presents neuroanatomical abnormalities located in the frontal cortex, the amygdala and the cerebellum. Autistic cerebellar postmortem studies have revealed a reduced number of Purkinje cells as well as a reduced Purkinje cell size when compared with non-autistic subjects. These anatomical alterations compromise the role of the cerebellum in cognitive, motor, emotional, learning and memory neural processes resulting in a different interpretation of the world, and therefore a different way to respond and behave. There are both biological and environmental insults causing the behavioral and neuroanatomical autistic phenotype. Valproic acid, an antiepileptic drug, has been related to some autistic cases after mothers were under medication with this drug during the first trimester of gestation and given birth autistic children. Therefore, in this brief review we analyzed the most recent advances of autism research in humans, with a primary focus on the use of valproic acid as a teratogen that mimics in rats some of the neuroanatomical alterations seen in autistic humans. In addition to the peculiar cerebellar pathology, all of this to shed light on a better understating of this disorder.
Key words: Autism, Purkinje neuron, Valproic acid, Teratogenicity.
Corresponding Author: M. en C. Miguel Pérez-Pouchoulén Centro de Investigaciones Cerebrales, Universidad Veracruzana Av. Dr. Luis Castelazo s/n, Col. Industrial Las Animas Xalapa, Ver. C.P. 91190 Teléfono: (228) 8418900 Ext. 13609 Fax: (228) 8418900 Ext. 13611 Correo electrónico: miguel8329@gmail.com