Structural basis of sympathetic-sensory coupling in rat and human dorsal root ganglia following peripheral nerve injury

V. Shinder, R. Govrin-Lippmann, S. Cohen, M. Belenky, P. Ilin, K. Fried, H. A. Wilkinson, M. Devor

Research output: Contribution to journalArticlepeer-review

118 Scopus citations

Abstract

Tyrosine hydroxylase immunocytochemistry was used to reveal the sympathetic postganglionic axons that sprout to form basket-like skeins around the somata of some primary sensory neurons in dorsal root ganglia (DRGs) following sciatic nerve injury. Ultrastructural observations in rats revealed that these sprouts grow on the surface of glial lamellae that form on the neurons. Sciatic nerve injury triggers glial cell proliferation in the DRG, and the formation of multilamellar pericellular onion bulb sheaths, primarily around large diameter DRG neurons. We infer that these glia participate in the sprouting process by releasing neurotrophins and expressing growth supportive cell surface molecules. Many DRG cell somata, and their axons in intact nerves and nerve end neuromas, express α2A adrenoreceptors intracytoplasmically and on their membrane surface. However, sympathetic axons never make direct contacts with the soma membrane. The functional coupling known to occur between sympathetic efferents and DRG neurons must therefore be mediated by the diffusion of neurotransmitter molecules in the extracellular space. Sympathetic basket-skeins were observed in DRGs removed from human neuropathic pain patients, but the possibility of a functional relation between these structures and sensory symptoms remains speculative.

Original languageEnglish
Pages (from-to)743-761
Number of pages19
JournalJournal of Neurocytology
Volume28
Issue number9
DOIs
StatePublished - Sep 1999
Externally publishedYes

Bibliographical note

Funding Information:
We thank Dr. Diane Rosin for providing the fi2A antibodies, and Dr. Thomas Smith, for providing human pathological specimens. This work was supported by grants from the German-Israel Foundation for Research and Development (GIF), the United StatesÑIsrael Binational Science Foundation (BSF), the Hebrew University Center for Research on Pain, and the Israel Absorption Ministry/Gileadi Foundation (to VS and MB).

Funding

We thank Dr. Diane Rosin for providing the fi2A antibodies, and Dr. Thomas Smith, for providing human pathological specimens. This work was supported by grants from the German-Israel Foundation for Research and Development (GIF), the United StatesÑIsrael Binational Science Foundation (BSF), the Hebrew University Center for Research on Pain, and the Israel Absorption Ministry/Gileadi Foundation (to VS and MB).

FundersFunder number
German-Israel Foundation for Research and Development
Israel Absorption Ministry/Gileadi Foundation
German-Israeli Foundation for Scientific Research and Development
United States-Israel Binational Science Foundation
Hebrew University of Jerusalem

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