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Serotonin 1A receptor functions during development to refine the dendritic arbor of principal hippocampal neurons
Mice lacking the serotonin receptor 1A (Htr1a) display increased anxiety behavior, a phenotype that depends on the expression of the receptor in the forebrain during the third through fifth postnatal weeks. Within the forebrain, Htr1a is prominently expressed in the soma and dendrites of CA1 pyramidal neurons of the hippocampus that during this period undergo rapid synapse formation and dendritic growth. Consistent with a possible role of Htr1a in synaptic maturation, CA1 pyramidal neurons in the Htr1a knockout mice show increased ramification of oblique dendrites and increased excitability to Schaffer collateral inputs. These findings suggest that Htr1a may shape hippocampal circuits by directly modulating dendritic growth. The experiments here described show that in vivo pharmacological blockade of the receptor during the third through fifth postnatal weeks is sufficient to reproduce the increased branching of oblique dendrites seen in Htr1a knockout mice. Using dissociated hippocampal cultures we demonstrate that serotonin functions through Htr1a to attenuate the motility of dendritic growth cones and reduce their content of filamentous actin. All together, these findings suggest that serotonin modulates actin cytoskeletal dynamics in hippocampal neurons during a limited developmental period to restrict dendritic growth and achieve a long-term adjustment of synaptic inputs.
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570 Biowissenschaften, Biologie
570 Life sciences