La Dra. Annie Andrieux del INSERM de Paris disertará en el Ciclo de Conferencias organizado por el CIQUIBIC
El próximo miércoles 6 de mayo, a las 11 horas, en el Auditorio del Centro Científico Tecnológico CONICET (CCT-Córdoba) dará continuación el Ciclo de Conferencias de Investigadores Externos “CIQUIBIC de Puertas Abiertas”.
En esta oportunidad, la conferencia estará a cargo de la Dra. Annie Andrieux, Jefa del laboratorio de Patofisiología del Citoesqueleto en el INSERM de París y de la Comissariat à l’EnergieAtomique (CEA) (Francia).
“MAP6 proteins: from microtubules stabilization to integrated brain functions”
MAP6 proteins have been initially identified as the factor responsible for the stabilization of mammalian microtubules. MAP6 null mice exhibited synaptic defects, associated with severe behavioural defects including increased locomotor activity with purposeless and disorganized activity; severe social withdrawal; deficits in prepulse inhibition and spatial and social learning impairments. MAP6 null mice also exhibit hyper-reactivity of dopamine release associated with a hypoglutamatergic phenotype, in accordance with the dopamine/glutamate neurotransmission imbalance hypothesis in schizophrenia. Importantly, conventional and non-conventional neuroleptics alleviate behavioural and synaptic defects in STOP-null mice although differently.
MAP6 deletion leads to reduction of brain volume, mainly affecting white matter, spine density defects, and disrupts brain connectivity, with a notable absence of post-commissural fornix fibers. MAP6 contributes to fornix development by regulating axonal elongation induced by the guidance molecule Semaphorin (Sema) 3E through the binding to the Sema3E receptor complex and acts downstream receptor activation through a mechanism that requires a proline-rich domain. We show that MAP6 directly binds to SH3 domain proteins known to be involved in neurite extension and semaphorin function. Finally, epothilone D, a microtubule stabilizing drug, alleviates behavioural and synaptic defects of STOP-null mice providing experimental evidence for a role of microtubule regulation as a target of future antipsychotic agents.
Diseño: Jeremías Di Pietro / Diseño Gráfico CCT CONICET CÓRDOBA