Here, we show that scgn is expressed earlier than CB, CR or PV in pioneer neurons exiting the pallidal differentiation zone by E11 in mouse. Histochemically noticeable scgn expression is restricted to postmitotic neurons because scgn+ cells lack the expression of RC2 and nestin, radial glia and neural stem/progenitor cell markers (Carleton et al., 2003),
respectively. The majority of scgn+ cells we identified migrated towards the prospective EA, and selectively inhabited its subpallial domain by forming a continuum of scgn+ neurons extending from the anterior tip of the VP towards the CA and MA. The lack selleck of Brn-1, a POU homeodomain protein specifying neocortical pyramidal cells (Sugitani et al.,
2002), supports the idea that scgn+ cell contingents are destined towards subpallial territories. Scgn+ neurons commute in at least two major migratory streams along the palliosubpallial boundary and clearly avoid venturing into neocortical territories during forebrain development. Scgn+ neurons populating the OB travel in the anterior direction and upon reaching the olfactory granular layer frequently (> 20%) acquire GAD67+/GABA+ phenotypes. In contrast, scgn+ neurons travelling caudally to colonize the EA exhibit a substantially lower percentage (7–9%) of co-localization with GAD67 en route to their final positions. The diversity of neuronal contingents destined to the EA is first demonstrated by the bifurcation of Wortmannin chemical structure their migratory stream at the level of the IPAC: small- to-medium-sized scgn+ neurons, many of which are GABAergic (Fig. 5), invade the CA and MA. Whilst we show that scgn can developmentally co-exist with GAD, our prior (Mulder et al., 2009b) and present analysis in adult
mouse and primate forebrain reveal a limited likelihood of co-expression of scgn with the other known neuron-specific CBPs, particularly CR and CB. Alternatively, Niclosamide scgn+ neurons can co-express ChAT, a ubiquitous cholinergic marker (Riedel et al., 2002), upon populating the SI. Intracellular Ca2+signalling underpins the responsiveness of developing neurons to extracellular guidance cues. We unexpectedly found that scgn is already plentiful in subsets of neurons engaged in long-distance migration with histochemically-detectable levels of this CBP maintained throughout neuronal morphogenesis. This notion may pinpoint that the scgn-mediated control of intracellular Ca2+signalling can play a role in generating adequate cellular responses to microenvironmental stimuli that are specifically present at the palliosubpallial boundary. Otherwise, scgn may be one of the early molecular determinants required for amygdala neurons to integrate into neuronal networks and to acquire specialized functions therein.