Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 1 de 1
Filter
Add more filters










Database
Language
Publication year range
1.
Development ; 147(2)2020 01 17.
Article in English | MEDLINE | ID: mdl-31915148

ABSTRACT

The precise migration of cortical interneurons is essential for the formation and function of cortical circuits, and disruptions to this key developmental process are implicated in the etiology of complex neurodevelopmental disorders, including schizophrenia, autism and epilepsy. We have recently identified the Jun N-terminal kinase (JNK) pathway as an important mediator of cortical interneuron migration in mice, regulating the proper timing of interneuron arrival into the cortical rudiment. In the current study, we demonstrate a vital role for JNK signaling at later stages of corticogenesis, when interneurons transition from tangential to radial modes of migration. Pharmacological inhibition of JNK signaling in ex vivo slice cultures caused cortical interneurons to rapidly depart from migratory streams and prematurely enter the cortical plate. Similarly, genetic loss of JNK function led to precocious stream departure ex vivo, and stream disruption, morphological changes and abnormal allocation of cortical interneurons in vivo These data suggest that JNK signaling facilitates the tangential migration and laminar deposition of cortical interneurons, and further implicates the JNK pathway as an important regulator of cortical development.


Subject(s)
Cell Movement , Cerebral Cortex/cytology , Interneurons/cytology , MAP Kinase Signaling System , Animals , Animals, Newborn , Cell Movement/drug effects , Cell Shape/drug effects , Interneurons/drug effects , MAP Kinase Signaling System/drug effects , Mice, Inbred C57BL , Mice, Knockout , Protein Kinase Inhibitors/pharmacology
SELECTION OF CITATIONS
SEARCH DETAIL
...