Control of neuronal survival by anomalous targets in the developing brain.
Described here is an aberrant parabigeminothalamic projection that follows neonatal lesions of the superior colliculus in rats, with evidence that this anomalous projection may sustain a normal number of neurons in the parabigeminal nucleus after early removal of the latter's tectal target. The aberrant projection was traced radioautographically to the tectorecipient zone of the lateral posterior nucleus after an injection of tritiated amino acid in the parabigeminal nucleus. Histochemical staining for cholinesterase revealed an anomalous patch of high enzyme activity in register with both the aberrant parabigeminothalamic projection and an abnormal retinal projection that also follows tectal lesions. Histochemical staining after either binocular enucleation or a tegmental lesion made simultaneous with the tectal ablation showed that the anomalous enzyme patch is a reliable marker of the aberrant parabigeminothalamic projection. It was also shown that the retinal projection is not needed for the formation of the anomalous parabigeminothalamic pathway. Ablation of the superior colliculus at birth failed to produce a net cell loss in the contralateral middle division of the parabigeminal nucleus after the period of natural neuronal death. Lesions extending toward the anomalous terminal field in the lateral posterior nucleus, however, prevented the survival of a normal number of neurons in the parabigeminal nucleus. When the unilateral tectal ablation was made together with a lesion of the ipsilateral posterior neocortex that produced cell loss in the thalamus, the number of neurons remaining in the middle division of the contralateral parabigeminal were linearly related to the cell content of the lateral posterior nucleus. We conclude that the anomalous target in the tectorecipient zone of the lateral posterior nucleus effectively replaces the normal projection field in the superior colliculus, with regard to the trophic requirements for neuronal survival during development of the parabigeminal nucleus.
Linden
R
R
Instituto de Biofisica da UFRJ, Rio de Janeiro, Brazil.
D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D008636:Mesencephalon / Q000254:growth & development / Q000378:metabolism / Q000502:physiology*; D009473:Neuronal Plasticity; D051381:Rats; D013477:Superior Colliculi / Q000502:physiology; D013788:Thalamus / Q000254:growth & development / Q000378:metabolism / Q000502:physiology*; D014795:Visual Pathways / Q000502:physiology*
D000110:Acetylcholinesterase