Selective Lis1 inactivation disrupts migration and positioning of cortical somatostatin interneurons

One subtype of interneurons, classified by their neurochemical properties, are somatostatin-positive (SST+) interneurons, which express somatostatin along with GABA and form synapses with both pyramidal neurons and other interneurons. SST+ interneurons originate in the medial ganglionic eminence and...

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Detalles Bibliográficos
Autores: Pombero, Ana, García López, Raquel, Geijo-Barrientos, Emilio, Martínez, Salvador
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2026
País:España
Institución:Consejo Superior de Investigaciones Científicas (CSIC)
Repositorio:DIGITAL.CSIC. Repositorio Institucional del CSIC
OAI Identifier:oai:dnet:digitalcsic_::75eb04174b5002c80d7bf4ae682884e7
Acceso en línea:http://hdl.handle.net/10261/426430
https://api.elsevier.com/content/abstract/scopus_id/105030567172
Access Level:acceso abierto
Palabra clave:Cingulate cortex
Lis1
Somatostatin
Descripción
Sumario:One subtype of interneurons, classified by their neurochemical properties, are somatostatin-positive (SST+) interneurons, which express somatostatin along with GABA and form synapses with both pyramidal neurons and other interneurons. SST+ interneurons originate in the medial ganglionic eminence and migrate tangentially to the cortex, making them potentially vulnerable to gene mutations linked to neuronal migration disorders. The Lis1 gene (Pafah1b1) regulates dynein-mediated motility, mitosis, and microtubule organization. Mutations in Lis1 are associated with lissencephaly and cortical disorganization. To investigate its role, we developed a mouse model with Lis1 deletion specifically in SST+ interneurons. We studied the anatomical and developmental effects of this deletion, focusing on tangential migration during embryonic and early postnatal stages. We analyzed SST+ interneuron numbers in the cingulate cortex (anterior and retrosplenial regions) of young mutant mice (P30). Our findings show a reduction in SST+ interneurons in mutants compared to controls, indicating impaired migration and/or maturation. Further research is needed to uncover the mechanisms behind this reduction and to determine its functional implications.