Molecular mechanisms of neuronal death in the dorsal lateral geniculate nucleus following visual cortical lesions
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Updated: Sep 26, 2026

Optic Nerve Transection: A Model of Adult Neuron Apoptosis in the Central Nervous System
Published on: May 12, 2011
M Repici1, C Atzori, A Migheli
1Department of Anatomy, Pharmacology and Forensic Medicine, University of Torino Medical School, Corso M. d'Azeglio 52, 10126, Torino, Italy. mariaelena.repici@unito.it
Abstract:
We investigated the molecular mechanisms of cell death in the dorsal lateral geniculate nucleus of the rat, following suction lesion of the visual cortex at birth or in the third postnatal week, using terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) technique and immunohistochemistry for caspase-3, -7, -8, and cleaved poly(ADP-ribose) polymerase. Following lesion at birth, TUNEL-positive neurons were found in the dorsal lateral geniculate nucleus between 24 h and 3 days after lesion, with a peak on the second day. Shorter survival times (12-18 h) resulted in labeling of very few neurons in dorsal lateral geniculate nucleus and of several neurons in the perilesional cortex. Activated caspase-3 was expressed from the first to the third days after lesion, whereas cleaved poly(ADP-ribose) polymerase and activated caspase-8 were expressed on the second and third day. Activated caspase-7 was expressed mainly in pretectal nuclei. Caspase-3 activation coincided with the appearance of TUNEL-positive profiles, but decreased earlier than TUNEL. In the ipsi- and contralateral cerebral cortex, all parameters were unchanged. In animals lesioned in the third week, rare apoptotic thalamic neurons were detected as TUNEL- and activated caspase-3-positive profiles 2 days after cortical ablation, and were still present 1 week after lesion.Thus, early target ablation has dramatic effects on neonatal thalamic neurons, which die following activation of caspases 3 and 8. In contrast, cortical neurons are relatively unaffected by target deprivation. Compared with early lesions, late lesions induce a limited thalamic cell death, that persists over time.
Insights
Early visual cortex lesions trigger thalamic neuron death via caspase activation in rats. Later lesions cause less cell death, showing target deprivation impacts developing neurons significantly.
Area of Science:
- Neuroscience
- Developmental Biology
- Cell Biology
Background:
- The dorsal lateral geniculate nucleus (dLGN) is a key relay for visual information.
- Understanding how neuronal cell death occurs after injury is crucial for developmental neuroscience.
Purpose of the Study:
- To investigate the molecular mechanisms of cell death in the rat dLGN following visual cortex lesions at different developmental stages.
- To determine the role of caspases in programmed cell death after target ablation.
Main Methods:
- Suction lesion of the visual cortex in rats at birth or postnatal week 3.
- Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) for DNA fragmentation.
- Immunohistochemistry for activated caspases (caspase-3, -7, -8) and cleaved poly(ADP-ribose) polymerase (PARP).
Main Results:
- Neonatal lesions induced significant TUNEL-positive neurons and caspase activation (caspase-3, -8) in the dLGN, peaking around day 2.
- Caspase-3 activation correlated with TUNEL labeling but subsided earlier.
- Later lesions (postnatal week 3) resulted in fewer apoptotic thalamic neurons, with cell death persisting longer.
Conclusions:
- Early visual cortex ablation triggers significant thalamic neuron apoptosis through caspase-3 and -8 activation.
- Neonatal thalamic neurons are highly vulnerable to target deprivation, unlike cortical neurons.
- The timing of target ablation critically influences the extent and persistence of neuronal cell death in the developing visual system.
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