Apoptotic cell death induced by optic nerve lesion in the neonatal rat
| Autor: | Rabacchi Sylvia A, Luca Bonfanti, Lamberto Maffei, XH Liu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 1994 |
| Předmět: |
Retinal Ganglion Cells
Pathology medicine.medical_specialty Programmed cell death Necrosis Cell Survival medicine.medical_treatment Apoptosis Cycloheximide Biology Retinal ganglion chemistry.chemical_compound medicine Animals General Neuroscience Optic Nerve Articles Denervation Axons Ganglion Rats medicine.anatomical_structure chemistry Animals Newborn Nerve Degeneration Optic nerve Dactinomycin Axotomy medicine.symptom Animals Inbred Strains DNA Damage |
| Popis: | Cell death can be ascribed to one of two distinct modes of degeneration: apoptosis (programmed or active cell death) or necrosis (passive degeneration). While apoptosis is generally assumed to occur in physiological conditions such as normal development or tissue turnover, necrotic cell degeneration is induced in pathological situations. Here we report that also in a pathological situation, such as after axotomy in the CNS, apoptotic type of cell death comes into play: following intracranial transection of the optic nerve in the neonatal rat in vivo, retinal ganglion cells undergo an active, apoptotic cell death. In fact, the administration of protein synthesis inhibitors (actinomycin D and cycloheximide) prevents the appearance of pyknotic nuclei as well as of fragmented DNA of ganglion cells at 24 hr postlesion. Correspondingly, the number of surviving cells after actinomycin D and cycloheximide treatment is comparable to normal, unlesioned retinas. In addition, cycloheximide decreases the number of pyknotic ganglion cells during spontaneous cell death. |
| Databáze: | OpenAIRE |
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