1. ¹Department of Neuronatomy & Embryology, Fukushima Medical University School of Medicine, 1-Hikarigaoka, Fukushima 960-1295, Japan
2. ²Department of Neurobiology & Anatomy, and Neuroscience Program, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA

Correspondence: N Sato, Department of Anatomy, Fukushima Medical University School of Medicine, 1-Hikarigaoka, Fukushima 960-1295, Japan. Tel: +81 24 547 1116; Fax: +81 24 549 8811; E-mail: nsato@fmu.ac.jp

Received 14 December 2004; Revised 19 July 2005; Accepted 29 July 2005; Published online 9 September 2005.

Abstract

Bax is a proapoptotic protein that is required for programmed cell death (PCD) of many neuronal populations. Here we show that, during an early period of retinal PCD and in naturally occurring sensory and motor neuron (MN) death in the spinal cord, Bax delivery results in enhanced death of these neural populations. In contrast, Bax overexpression fails to enhance an early phase of MN death that occurs in the cervical spinal cord, although overexpressed Bax appears to be activated in dying MNs. Bax overexpression does not also affect the survival of immature neurons prior to the PCD period. Taken together, these data provide the first in vivo evidence suggesting that Bax appears to act selectively as an executioner only in neurons undergoing PCD. Furthermore, although Bax appears to mediate the execution pathway for PCD, the effect of Bax overexpression on susceptibility to death differs between different neuronal populations.