Reciprocal changes in the expression of Bcl-2 and Bax in hypoglossal nucleus after axotomy in adult rats: possible involvement in the induction of neuronal cell death

• Published in: Brain research Vol. 827; no. 1; pp. 122 - 129
• Main Authors: Baba, Nobuyuki, Koji, Takehiko, Itoh, Michiichiro, Mizuno, Akio
• Format: Journal Article
• Language: English
• Published: London Elsevier B.V 08.05.1999; Amsterdam Elsevier; New York, NY
• Subjects: Adult rat; Age Factors; Ageing, cell death; Animals; Apoptosis; Apoptosis - physiology; Axotomy; Bax; Bcl-2; bcl-2-Associated X Protein; Biological and medical sciences; Cell physiology; Fundamental and applied biological sciences. Psychology; Hypoglossal nerve; Hypoglossal Nerve - cytology; Hypoglossal Nerve - metabolism; Hypoglossal Nerve - surgery; In Situ Nick-End Labeling; Molecular and cellular biology; Neuronal cell death; Neurons - chemistry; Neurons - cytology; Neurons - metabolism; Proliferating Cell Nuclear Antigen - analysis; Proto-Oncogene Proteins - analysis; Proto-Oncogene Proteins - biosynthesis; Proto-Oncogene Proteins c-bcl-2 - analysis; Proto-Oncogene Proteins c-bcl-2 - biosynthesis; Rats; Rats, Wistar; Bcl-2; Axotomy; Adult rat; Hypoglossal nerve; Neuronal cell death; Bax; Apoptosis; Vertebrata; Mammalia; Rat; Cell death; Rodentia; Central nervous system; Gene expression; Hypoglossal nucleus; Brain (vertebrata)
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(99)01315-3

Numerous studies of neonatal neuronal development in mammals have revealed that neuronal cell death following axotomy is apoptotic in nature. In adult animals, however, neuronal cell death following axonal injury may or may not exhibit features of apoptosis. Bcl-2 and Bax have been identified as inhibitor and promoter proteins, respectively, of apoptosis. To investigate the relationship between these proteins and neuronal cell death following axotomy in adult animals, we performed axotomy of the right hypoglossal nerve in adult male Wistar rats, and sacrificed the rats at various intervals after axotomy. We analyzed the expression of Bcl-2 and Bax immunohistochemically in the hypoglossal nuclei of the adult rats following axotomy. Our analysis showed an increase in the percentage of Bax-positive motoneurons relative to the total number of motoneurons in the hypoglossal nucleus on the axotomy side at three days after axotomy. In contrast, a low percentage of Bcl-2-positive motoneurons to the total number of motoneurons was noted at the same time interval after axotomy. Quantitative analysis of the signal intensity for Bcl-2 and Bax in individual neurons showed that Bax immunostaining significantly increased 7 days after axotomy, while the intensity of Bcl-2 immunostaining decreased in most of Bcl-2-positive neurons. Our results confirmed the occurrence of motoneuron cell death in adult rats after axotomy, and that a close temporal relationship exists between the reciprocal changes in Bcl-2/Bax expression and the loss of motoneurons. These results indicate the possible involvement of the Bcl-2/Bax system in the induction of neuronal cell apoptosis after axotomy in adult rats.