Natural and lesion-induced apoptosis in the dorsal lateral geniculate nucleus during development.

We investigated natural and lesion-induced apoptosis in the developing rat dorsal lateral geniculate nucleus (dLGN). These lesions involved: i) monocular enucleation, and ii) unilateral ablation of the visual cortex at different postnatal ages before eye opening. We identified dying cells as apoptotic with light and electron microscopy, using terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL), and immunohistochemistry for active caspase-3. In the dLGN of normal animals, TUNEL+cells were detected during the first postnatal week, with a peak at postnatal day (P) 1. Following enucleation at birth or at P7, the frequency of apoptotic cells in the contralateral dLGN increased significantly at postlesion day (PLD) 1 and returned to normal values by PLD7. In contrast to early lesions, enucleation at P14 did not induce significant changes in apoptosis in the dLGN. Cortical lesions performed at P0, P7 or at P14 induced the death of the overwhelming majority of cells in the ipsilateral dLGN, which led to a severe reduction in size of the nucleus by PLD7 and its complete elimination by adulthood. Double labeling with TUNEL and immunofluorescence for neuronal nuclear protein (NeuN) showed that in both normal and lesioned animals, apoptotic cells were mainly neurons. We suggest that: i) apoptosis in the dLGN occurs during the precritical period of neuronal maturation; ii) developing neurons in the dLGN are more dependent on the integrity of their connections with the visual cortex than with the retina for survival; and iii) lesion-induced apoptosis in the dLGN during development depends on the type and extent of the connectivity affected.