Spinal cord TRH deficiency is associated with incomplete recovery of denervated muscle in the rat
Van den Bergh, P.; Kelly, J.J.; Soule, N.; Munsat, T.L.; Jackson, I.M.; Lechan, R.M.
Neurology 38(3): 452-458
1988
ISSN/ISBN: 0028-3878 PMID: 3126409 Document Number: 322506
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.