Journal article

Axonal Growth of Midbrain Dopamine Neurons is Modulated by the Cell Adhesion Molecule ALCAM Through Trans-Heterophilic Interactions with L1cam, Chl1, and Semaphorins

Christopher R Bye, Valeria Rytova, Walaa F Alsanie, Clare L Parish, Lachlan H Thompson

The Journal of Neuroscience | SOC NEUROSCIENCE | Published : 2019

Abstract

The growth of axons corresponding to different neuronal subtypes is governed by unique expression profiles of molecules on the growth cone. These molecules respond to extracellular cues either locally though cell adhesion interactions, or over long distance through diffusible gradients. Here we report that that the cell adhesion molecule ALCAM (CD166) can act as an extracellular substrate to selectively promote the growth of murine midbrain dopamine (mDA) neuron axons through a trans-heterophilic interaction with mDA-bound adhesion molecules. In mixed-sex primary midbrain cultures the growth promoting effect of ALCAM was abolished by neutralising antibodies for components of the Semaphorin r..

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Grants

Awarded by National Health and Medical Research Council (NHMRC)


Funding Acknowledgements

This work was supported by the National Health and Medical Research Council (NHMRC Grants 1042584 and 1022637). The Florey Institute of Neuroscience and Mental Health acknowledges the strong support from the Victorian Government and in particular the funding from an Operational Infrastructure Support Grant. C.R.B. is supported by an NHMRC Peter Doherty training fellowship, C.L.P. is an NHMRC Senior Research Fellow. We thank Jason Howitt for technical assistance with PLA Assays, Mong Tien and Jessica Kauhausen for assistance with tissue processing and histology, and Richard Anderson and John Hemperly for provision of the 6096 L1 blocking antibody.