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NEUROLOGY 1988;38:452
© 1988 American Academy of Neurology

Spinal cord TRH deficiency is associated with incomplete recovery of denervated muscle in the rat

P. Van den Bergh, MD, J. J. Kelly, Jr., MD, N. Soule, BS, T. L. Munsat, MD, I. M. D. Jackson, MD and R. M. Lechan, MD, PhD

From the Departments of Medicine (Drs. Van den Bergh and Lechan) and Neurology (Drs. Van den Bergh and Kelly, Mr. Soule, and Dr. Munsat), Tufts University, New England Medical Center Hospitals, Boston, MA; and the Department of Medicine (Dr. Jackson), Brown University, Rhode Island Hospital, Providence RI.

The raphe-spinal pathway, which contains co-localized serotonin (5-HT), thyrotropin-releasing hormone (TRH), and several TRH-prohormone-derived non-TRH peptides, projects to the ventral horn of the spinal cord. Pharmacologic ablation of this pathway with the 5-HT neurotoxin, 5, 7-dihydroxytryptamine, in neonatal rats resulted in deficient recovery of plantar foot muscles, functionally denervated with botulinum toxin type A. Failure of reinnervation was suggested by slower and incomplete recovery of the plantar foot compound muscle action potential amplitude and by a reduced mean diameter of plantar foot muscle fibers in ablated rats. These findings indicate that deprivation of alpha motor neurons from descending raphe-spinal input interferes with their ability to respond to muscle-derived signals for reinnervation.

Address correspondence and reprint requests to Dr. Van den Bergh, Neurologue, Service de Médecine Physique et de Réadaptation Motrice, Cliniques Universitaires Saint-Luc, Avenue Hippocrate 10, B-1200 Brussels, Belgium.

Supported by grants from The ALS Association and by grant RR-00054 from the General Clinical Research Centers Program of the Division of Research Resources, NIH.

Received March 19, 1987. Accepted for publication in final form May 28, 1987.




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