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Whole-mount Imaging of Mouse Embryo Sensory Axon Projections
Published on: December 9, 2014
Characterization of sensory neurons in the dorsal root ganglia of Bax-deficient mice
Hiromichi Suzuki1, Youhei Aoyama, Kouji Senzaki
1Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan.
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.
Insights
Deleting the Bax gene rescues dorsal root ganglion (DRG) neurons from cell death, but excess CGRP-positive neurons cause hypersensitivity. Other DRG neuron types show no functional changes, indicating varied consequences of cell rescue.
Area of Science:
- Neuroscience
- Developmental Biology
- Genetics
Background:
- Spinal motoneurons and dorsal root ganglion (DRG) neurons undergo programmed cell death (PCD) during development, contingent on peripheral target innervation.
- The pro-apoptotic gene Bax plays a critical role in PCD, and its deletion rescues these neurons.
- The differential impact of Bax deletion on distinct DRG neuron subtypes remains unclear.
Purpose of the Study:
- To investigate the distinct cellular and functional responses of various dorsal root ganglion (DRG) neuron subsets following the deletion of the Bax gene.
- To determine if Bax deletion leads to differential cell numbers and morphology across different sensory neuron populations in the DRG.
Main Methods:
- Utilized Bax-deficient (Bax-/-) mice and wild-type littermates for comparative analysis.
- Employed immunohistochemistry to identify and quantify DRG neuron subsets expressing TrkA, CGRP, TRPV1, and TrkC.
- Assessed epidermal innervation patterns and evaluated functional responses in mechanical nociception and thermosensation.
Main Results:
- Bax deletion resulted in increased numbers of TrkA, CGRP, TRPV1, and TrkC immunopositive DRG neurons, all exhibiting cell atrophy.
- Bax-/- mice displayed epidermal hyperinnervation by CGRP-positive fibers and heightened sensitivity to mechanical pain.
- Functional properties of rescued thermoreceptor and mechanoreceptor DRG neurons remained unaltered.
Conclusions:
- Bax deletion effectively rescues all examined DRG neuron types from programmed cell death.
- The expansion of specific DRG neuron populations, particularly CGRP-positive nociceptors, leads to distinct functional consequences, including sensory hypersensitivity.
- These findings highlight phenotype-specific outcomes of developmental cell survival modulation in the sensory nervous system.
