Migration of sympathetic preganglionic neurons in the spinal cord of a C3G-deficient mouse suggests that C3G acts in the reelin signaling pathway.

Proper positioning of sympathetic preganglionic neurons(SPNs) in the spinal cord is regulated by reelin signaling. SPNs in reeler (which lacks reelin), and in mice deficient in components of the reelin signaling pathway (reelin receptors VldlR and ApoER2, the cytoplasmic adaptor protein Dab1, Src and Fyn of the Src-family of non-receptor protein tyrosine kinases, and CrkL) are located adjacent to the central canal instead of in the intermediolateral column (IML) of the spinal cord. Events downstream of CrkL in control of SPN migration are unclear.

Reelin inhibits migration of sympathetic preganglionic neurons in the spinal cord of the chick.

The present study examined the effects of Reelin in the migration of sympathetic preganglionic neurons (SPN) in the spinal cord of the chick. SPN in the chick first migrate from the neuroepithelium to the ventrolateral spinal cord. They then undergo a secondary migration to cluster adjacent to the central canal, forming the column of Terni (CT).

Ectopic expression of reelin alters migration of sympathetic preganglionic neurons in the spinal cord.

Reelin, an extracellular matrix molecule, regulates neuronal positioning in the brain, brainstem, and spinal cord. Although Reelin was identified more than a decade ago, its function on neuronal migration is still poorly understood. Using a transgenic mouse that expressed reelin under the nestin promoter, we examined here the function of Reelin in control of sympathetic preganglionic neurons (SPN) migration in the spinal cord.

Cdk5 selectively affects the migration of different populations of neurons in the developing spinal cord.

It has been shown that cyclin-dependent kinase 5 (Cdk5) is crucial for neuronal migration and survival in the brain. However, the role of Cdk5 in neuronal migration in the spinal cord has never been investigated. The present study is the first to show that Cdk5 affects the migration of different populations of neurons in the developing spinal cord.

Migration of sympathetic preganglionic neurons in the spinal cord is regulated by Reelin-dependent Dab1 tyrosine phosphorylation and CrkL.

The actions of Reelin in neuronal positioning in the developing cortex and cerebellum are relayed by Src-family kinase (SFK)-mediated phosphorylation of Dab1. Biochemical studies show that after phosphorylation Dab1 binds to an adaptor protein, CrkL. Whether CrkL is important for Reelin signaling in vivo is unknown, because crkl(-/-) embryos die before cortical development is complete.

Location of preganglionic neurons is independent of birthdate but is correlated to reelin-producing cells in the spinal cord.

Many studies suggest that during neuronal development the birthdate of a neuron appears to have significant consequences for its ultimate location and identity. Our past study shows that sympathetic preganglionic neurons (SPN) in mice lacking the reelin gene settle in abnormal positions in the spinal cord. In the present study we determined that birthdate is not a factor contributing to the abnormal position of SPN in reeler.

Components of the reelin signaling pathway are expressed in the spinal cord.

The Reelin signaling pathway in the brain involves the binding of Reelin to very-low-density lipoprotein receptors (VLDLR) and apolipoprotein E receptor 2 (ApoER2). After Reelin binds the lipoprotein receptors on migrating neurons, the intracellular adaptor protein Disabled-1 (Dab1) becomes phosphorylated, ultimately resulting in the proper positioning of cortical neurons. Previous work showed that Reelin also affects the positioning of sympathetic preganglionic neurons (SPN) in the spinal cord (Yip et al.

Migratory pathway of sympathetic preganglionic neurons in normal and reeler mutant mice.

Our previous study showed that the migration of sympathetic preganglionic neurons (SPN) in the spinal cord is affected in the reeler mutant. The present study, using morphometric analysis to describe and compare the location of SPN at progressive developmental stages, provides detailed information on how SPN migrate in the presence or absence of the reelin gene. We found that the initial migration (prior to E11.