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The N-terminal region of reelin regulates postnatal dendritic maturation of cortical pyramidal neurons.


ABSTRACT: Cajal-Retzius cells, located in layer I of the cortex, synthesize and secrete the glycoprotein reelin, which plays a pivotal role in neuronal migration during embryonic development. Cajal-Retzius cells persist after birth, but their postnatal role is unknown. Here we show that Cajal-Retzius cells receive a major excitatory synaptic input via serotonin 5-HT(3) receptors. Blocking this input using pharmacological tools or neutralization of reelin signaling results in hypercomplexity of apical, but not basal, dendrites of cortical layer II/III pyramidal neurons. A similar hypercomplexity is observed in the cortex of the 5-HT(3A) receptor knockout mouse. The increased dendritic complexity can be rescued by application of recombinant full-length reelin or its N-terminal fragment, but not by the central fragment of reelin, and involves a signal transduction pathway independent of the activation of the canonical reelin receptors. Taken together, our results reveal a novel role of serotonin, Cajal-Retzius cells, and reelin in the postnatal maturation of the cortex.

SUBMITTER: Chameau P 

PROVIDER: S-EPMC2678467 | biostudies-literature | 2009 Apr

REPOSITORIES: biostudies-literature

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The N-terminal region of reelin regulates postnatal dendritic maturation of cortical pyramidal neurons.

Chameau Pascal P   Inta Dragos D   Vitalis Tania T   Monyer Hannah H   Wadman Wytse J WJ   van Hooft Johannes A JA  

Proceedings of the National Academy of Sciences of the United States of America 20090406 17


Cajal-Retzius cells, located in layer I of the cortex, synthesize and secrete the glycoprotein reelin, which plays a pivotal role in neuronal migration during embryonic development. Cajal-Retzius cells persist after birth, but their postnatal role is unknown. Here we show that Cajal-Retzius cells receive a major excitatory synaptic input via serotonin 5-HT(3) receptors. Blocking this input using pharmacological tools or neutralization of reelin signaling results in hypercomplexity of apical, but  ...[more]

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