Lesion induced new neuron incorporation in the adult hypothalamus of the avian brain.

Cell loss in most adult vertebrate brain regions is thought to be irreversible. Here, we explore the effects of electrolytic lesions on the induction of cell proliferation and newborn neurons in the ventromedial nuclei (VMN) of the hypothalamus in young and adult ring doves. The hypothalamus does not normally recruit new neurons. Bromodeoxyuridine (BrdU) and tritiated thymidine ([3H]Thy) were used to identify cells born before and after bilateral electrolytic lesions. Hu and NeuN were used to identify neurons. TUNEL test for apoptosis and 3A7 antibodies were used to identify morphological changes of pre-existing cells. Lesions produced significantly more newborn cells in the subventricular zone (SVZ). The rate of cell proliferation peaked at 7-14 days postlesion. A fraction of these newborn cells were neuronal precursor and began to migrate away along the radial glial fibers 2 weeks after lesion. During this period, the outer area of the lesion site was marked with massive apoptosis and re-expression of radial glial-like fibers. In birds that survived 5 months, we found newly differentiated neurons in the outer area of the lesion site. We conclude that electrolytic lesion can invoke neuronal recruitment in the adult hypothalamus. We further suggest that lesion-induced apoptosis and re-expression of developmental mechanisms might be involved in the recruitment process.