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NEUROLOGY 1983;33:848
© 1983 American Academy of Neurology

Unmyelinated axon subpopulations in the rat peripheral nervous system

David Chad, MD, FRCP (C), Chaudri Rasool, PhD, Walter G. Bradley, DM, FRCP, Paul Good, BS and Seymour Reichlin, MD, PhD

Departments of Neurology (Drs. Chad, Rasool, and Bradley and Mr. Good) and Medicine (Dr. Reichlin) of the Tufts-New England Medical Center, Boston, MA.

using the neurotoxin capsaicin, we examined subpopulations of unmyelinated axons in mixed (sciatic), cutaneous (sural), and muscular (nerve to soleus) nerves. Administration of capsaicin to neonatal rats caused reduction of the sciatic nerve immunoreactive (IR)-substance P (by 45%) and IR-somatostatin (by 84%) contents. This correlated with a substantial reduction in unmyelinated axons in the sciatic and sural nerves (45% and 65%, respectively), although there was no significant decrease in unmyelinated axons in the nerve to soleus. In a parallel study, we have shown that sympathetic ganglia-derived unmyelinated axons account for about 20 to 25% of the total unmyelinated axon population in both the sural nerve and the nerve to soleus. Thus, in the sural nerve, the majority of unmyelinated axons are dorsal root ganglia-derived, contain either substance P or somatostatin, and are capsaicin-sensitive; whereas in the nerve to soleus, the majority of unmyelinated axons are dorsal root ganglia-derived but are insensitive to capsaicin and do not contain substance P or somatostatin. These latter unmyelinated axons presumably contain a yet to be defined neurotransmitter and may be the axons connecting with muscular ergoreceptors, a subpopulation of unmyelinated axons that are biochemically and functionally distinct from the unmyelinated axons of cutaneous nerves.

Address correspondence and reprint requests to Dr. Chad, Department of Neurology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01605.

This work was supported in part by a grant from the MDA. Dr. Chad was a Research Fellow of the MDA.

Portions of this paper were presented at the thirty-fourth annual meeting of the American Academy of Neurology, Washington, DC, April 1982.

Accepted for publication November 1, 1982.




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