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Updated: Aug 11, 2026
Genetic Study of Axon Regeneration with Cultured Adult Dorsal Root Ganglion Neurons
Published on: August 17, 2012
Survival and phenotypic characteristics of axotomized neurons in spinal ganglia
Yu A Chelyshev1, I S Raginov, D S Guseva
1Department of Histology, Cytology, and Embryology, Kazan' State Medical University.
Abstract:
Trauma to the peripheral processes of sensory neurons of different subpopulations was followed by indirect immunohistochemical analysis of the expression of Bcl-X(L) and Bax, which are, respectively, antiapoptotic and proapoptotic proteins of the Bcl-2 family, and also of the cytokine interleukin-1beta, with the aim of identifying the roles of these substances in controlling apoptosis. The survival abilities of these neurons after central and peripheral axotomy were compared by studying the expression of the high molecular weight component of the neurofilament triplet NF200 and isolectin B4 (IB4). By day 30 after central axotomy, there were no changes in the total numbers of neurons in ganglia L(IV)-L(V) in rats, though there were significant reductions in the numbers of NF200+ neurons. In spinal ganglion L(V) of mice, the proapoptotic protein was detected in the nuclei of 46% of small neurons, which account for 20% of all neurons in the ganglion. By day 30 after nerve compression, Bax was expressed in the nuclei of 30% of neurons and the cytoplasm of 20% of neurons. In intact animals, the antiapoptotic protein Bcl-X(L) was seen in the cytoplasm of 30% of small neurons, as well as in satellite cells surrounding large and intermediate neurons. By day 30 after nerve trauma, Bcl-X(L) was not expressed in spinal ganglion L(V). Interleukin-1beta was present in the cytoplasm of 17% of neurons belonging to the subpopulations of large and intermediate neurons. By day 30 after nerve compression, interleukin-1 beta+ neurons were not identified.
Insights
Peripheral nerve trauma impacts sensory neuron survival by altering apoptosis-related proteins. Studies show reduced neurofilament expression and changes in Bcl-X(L) and Bax levels following injury.
Area of Science:
- Neuroscience
- Cell Biology
Background:
- Sensory neurons exhibit varying survival capacities after axotomy.
- The roles of proapoptotic (Bax) and antiapoptotic (Bcl-X(L)) proteins in neuronal survival are critical.
- Interleukin-1beta's involvement in neuronal apoptosis requires further elucidation.
Purpose of the Study:
- To investigate the roles of Bcl-X(L), Bax, and interleukin-1beta in controlling apoptosis following peripheral nerve trauma.
- To compare the survival of different sensory neuron subpopulations after central and peripheral axotomy.
Main Methods:
- Indirect immunohistochemistry was used to analyze the expression of Bcl-X(L), Bax, and interleukin-1beta.
- Neuronal survival was assessed by examining neurofilament NF200 and isolectin B4 (IB4) expression.
- Studies were conducted on rat and mouse models following central axotomy and nerve compression.
Main Results:
- Central axotomy in rats led to reduced NF200+ neurons without altering total neuron numbers.
- In mice, Bax was detected in small neurons post-axotomy, and nerve compression increased Bax expression.
- Bcl-X(L) expression diminished significantly after nerve trauma, and interleukin-1beta was not detected post-compression.
Conclusions:
- Peripheral nerve trauma significantly impacts apoptosis regulators in sensory neurons.
- The downregulation of antiapoptotic Bcl-X(L) and altered Bax expression suggest a role in neuronal death pathways.
- These findings highlight the complex molecular mechanisms underlying sensory neuron responses to injury.
