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In adult lizards, new neurons are generated from neural stem cells in the ventricular zone of the lateral ventricles. These new neurons migrate and integrate into the main telencephalic subdivisions. In this work we have studied adult neurogenesis in the lizard Podarcis liolepis (formerly Podarcis hispanica) by administering [3H]-thymidine and bromodeoxyuridine as proliferation markers and euthanizing the animals at different survival times to determine the identity of progenitor cells and to study their lineage derivatives. After short survival times, only type B cells are labeled, suggesting that they are neural stem cells. Three days after administration, some type A cells are labeled, corresponding to recently formed neuroblasts. Type A cells migrate to their final destinations, where they differentiate into mature neurons and integrate into functional circuits. Our results after long survival periods suggest that, in addition to actively dividing type B cells, there is also a type B subpopulation with low proliferative activity. We also found that new neurons incorporated into the olfactory bulb are generated both in situ, in the walls of the anterior extension of the lateral ventricle of the olfactory bulbs, but also at more caudal levels, most likely in anterior levels of the sulcus ventralis/terminalis. These cells follow a tangential migration toward the olfactory bulbs where they integrate. We hypothesized that at least part of the newly generated neurons would undergo a specialization process over time. In support of this prediction, we found two neuronal populations in the cellular layer of the medial cortex, which we named type I and II neurons. At intermediate survival times (1 month) only type II neurons were labeled with [3H]-thymidine, while at longer survival times (3, 6, or 12 months) both type I and type II neurons were labeled. This study sheds light on the ultrastructural characteristics of the ventricular zone of P. liolepis as a neurogenic niche, and adds to our knowledge of the processes whereby newly generated neurons in the adult brain migrate and integrate into their final destinations. [ABSTRACT FROM AUTHOR]

The neocortex (NCx) generates at the dorsal region of the pallium in the forebrain. Several adjacent structures also contribute with neurons to NCx. Ventral pallium (VP) is considered to generate several populations of neurons that arrive through tangential migration to the NCx. Amongst them are the Cajal-Retzius cells and some transient pyramidal neurons. However, the specific site and timing of generation, trajectory of migration and actual contribution to the pyramidal population remains elusive. Here, we investigate the spatio-temporal origin of neuronal populations from VP in an in vivo model, using a transposase mediated in utero electroporation method in embryonic mouse. From E11 to E14 cells born at the lateral corner of the neocortical neuroepithelium including the VP migrated ventro-laterally to settle all areas of the ventral telencephalon. Specifically, neurons migrated into amygdala (Ag), olfactory cortices, and claustrum (Cl). However, we found no evidence for any neurons migrating tangentially toward the NCx, regardless the antero-posterior level and developmental time of the electroporation. Our results challenge the described ventral-pallial origin of the transient pyramidal neuron population. In order to find the exact origin of cortical neurons that were previously Dbx1-fate mapped we used the promoter region of the murine Dbx1 locus to selectively target Dbx1-expressing progenitors and label their lineage. We found these progenitors in low numbers in all pallial areas, and not only in the ventral pallial ventricular zone. Our findings on the local cortical origin of the Dbx1-derived pyramidal neurons reconcile the observation of Dbx1-derived neurons in the cortex without evidence of dorsal tangential migration from VP and provide a new framework for the origin of the transient Dbx1-derived pyramidal neuron population. We conclude that these neurons are born locally within the dorsal pallial neuroepithelium.