G(0) protein-dependent survival of primary accessory olfactory neurons

Citation
M. Tanaka et al., G(0) protein-dependent survival of primary accessory olfactory neurons, P NAS US, 96(24), 1999, pp. 14106-14111
Citations number
32
Categorie Soggetti
Multidisciplinary
Journal title
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
ISSN journal
00278424 → ACNP
Volume
96
Issue
24
Year of publication
1999
Pages
14106 - 14111
Database
ISI
SICI code
0027-8424(19991123)96:24<14106:GPSOPA>2.0.ZU;2-O
Abstract
Extensive G protein-coupled receptor families in both the main and accessor y olfactory systems have been implicated in axonal targeting, sensory funct ion, and cell survival. Although sensory function seems to be mediated by G proteins, axonal guidance and cell survival may be G protein-independent p rocesses. in the accessory olfactory system, the G(o)-containing neurons in the basal vomeronasal organ (VNO) project to the posterior accessory olfac tory bulb (AOB), whereas more apically located VNO neurons contain G(12) an d project to the anterior AOB. Herein, we investigate the organization of t he accessory olfactory system in mice with a targeted deletion in the G(o)a lpha gene. The accessory alpha-factory system seems normal at birth; howeve r, postnatally, the number of G(o)-receptor-containing VNO neurons decrease s by half, and apoptotic neurons are detected. The axons of VNO neurons rem ain restricted to the posterior AOB. The posterior AOB is reduced in size b ut contains a synaptophysin-positive layer with the normal number of glomer uli. The posterior AOB has reduced mitral cell c-Fos immunoreactivity, cons istent with decreased sensory activation of G(o) protein-coupled VNO recept or neurons. Thus, in the accessory olfactory system, receptor-coupled G pro teins are required for cell survival.