AI Article Synopsis

  • The study investigates how deleting the pro-apoptotic gene Bax affects spinal motoneurons and sensory neurons in the dorsal root ganglion (DRG) during development, particularly their survival from programmed cell death (PCD).
  • In Bax-deficient mice, researchers found an increase in certain DRG neurons marked by specific markers (TrkA, CGRP, TRPV1, TrkC), alongside visible cell atrophy and heightened sensitivity to mechanical stimuli.
  • While deletion of Bax protects all DRG neuron types from PCD, the study highlights that the resulting excess cell populations exhibit different functional consequences based on the sensory type of the neurons.

Article Abstract

During development, the rescue of spinal motoneurons as well as sensory neurons in the dorsal root ganglion (DRG) from programmed cell death (PCD) depends on the integrity of peripheral target innervation. Following deletion of the pro-apoptotic gene Bax, both motoneurons and DRG neurons are rescued from PCD. In the present paper, we asked whether different cell types in the DRG exhibit distinct responses to Bax deletion. In 1-month-old Bax-deficient (Bax-/-) mice, distinct subsets of DRG neurons that were immunopositive for TrkA, CGRP, TRPV1 or TrkC, were all increased in number and exhibited cell atrophy compared to wild type DRG neurons. In addition there was hyperinnervation of the epidermis by CGRP immunopositive processes and a correlated functional hypersensitivity of mechanical nociception in Bax-/- mice. By contrast, the functional properties of populations of rescued thermoreceptor and mechanoreceptor DRG neurons were unchanged. These data indicate that although Bax deletion rescues all of the DRG cell types examined here from PCD, the functional consequences of having excess cells differ between sensory phenotypes.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2994063PMC
http://dx.doi.org/10.1016/j.brainres.2010.09.027DOI Listing

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