Receptor guanylyl cyclase B-mediated cGMP signalling controls axon bifurcation of cranial sensory ganglion neurons at the embryonic hindbrain
© Ter-Avetisyan et al; licensee BioMed Central Ltd. 2013
Published: 29 August 2013
Axonal branching is a key principle for the establishment of neuronal circuitry that allows an individual neuron to innervate several target areas thus providing a physical framework for parallel processing of information. Our previous search for molecular determinants of axonal branching unravelled a cGMP signalling pathway in embryonic dorsal root ganglion (DRG) neurons composed of the ligand C-type natriuretic peptide (CNP), the receptor guanylyl cyclase B (GC-B, also termed Npr2), and the cGMP-dependent protein kinase Iα (cGKIα) that is essential for the bifurcation of sensory axons at the dorsal root entry zone of the spinal cord. Absence of any of these components causes a complete loss of bifurcation where sensory axons only turn in either a rostral or a caudal direction (Figure 1A). Consequently mutant mice reveal a reduced synaptic input onto second-order neurons in the dorsal horn of the spinal cord.
To examine whether the cGMP signalling system that underlies axon bifurcation in DRG neurons may also extend to other neuronal subpopulations we generated a GC-B-lacZ reporter mouse line for a detailed analysis of the GC-B expression pattern during embryonic development. A strong expression of GC-B that correlated with the localization of cGKIα was detected in neurons of all cranial sensory ganglia (CSG) at early embryonic stages when their central afferents enter the brainstem. Furthermore, a complimentary distribution of the ligand CNP at the entry zones of these axons in the hindbrain was observed.
Our data demonstrate that neurons of CSG - similar to DRG neurons - use GC-B-mediated cGMP signalling to trigger axonal bifurcation.
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