Nuclear organization and 3D chromatin architecture in cognition and neuropsychiatric disorders.
The current view of neuroplasticity depicts the changes in the strength and number of synaptic connections as the main physical substrate for behavioral adaptation to new experiences in a changing environment. Although transcriptional regulation is known to play a role in these synaptic changes, the specific contribution of activity-induced changes to both the structure of the nucleus and the organization of the genome remains insufficiently characterized. Increasing evidence indicates that plasticity-related genes may work in coordination and share architectural and transcriptional machinery within discrete genomic foci. Here we review the molecular and cellular mechanisms through which neuronal nuclei structurally adapt to stimuli and discuss how the perturbation of these mechanisms can trigger behavioral malfunction.
Instituto de Neurociencias (Universidad Miguel Hernández-Consejo Superior de Investigaciones Científicas), Av. Santiago Ramón y Cajal s/n. Sant Joan d'Alacant, 03550, Alicante, Spain.
Alejandro
A
Medrano-Fernández
Instituto de Neurociencias (Universidad Miguel Hernández-Consejo Superior de Investigaciones Científicas), Av. Santiago Ramón y Cajal s/n. Sant Joan d'Alacant, 03550, Alicante, Spain. abarco@umh.es.
Angel
0000-0002-0653-3751
A
Barco
D000818:Animals; D002843:Chromatin / Q000378:metabolism*; D003071:Cognition; D016678:Genome; D006801:Humans; D001523:Mental Disorders / Q000378:metabolism*; D008954:Models, Biological; D009474:Neurons / Q000378:metabolism
D002843:Chromatin
Chromatin; Chromosomal interactions; Epigenetics; Neuronal plasticity; Neuropsychiatric disorders; Nuclear structure