Abstract
Study design:
Hyperreflexia occurs after spinal cord injury (SCI) and can be assessed by measuring low frequency-dependent depression of the H-reflex. Previous studies showed the time course for the onset of hyperreflexia to occur between 6–28 days in the contusion model of SCI.
Objective:
To determine the time course of the onset of hyperreflexia in the transection model of SCI and examine changes in Connexin-36 (Cx-36) protein levels in the lumbar enlargement of animals.
Setting:
Spinal Cord Injury Mobilization Program of the Center for Translational Neuroscience, the research arm of the Jackson T. Stephens Neuroscience Institute, Little Rock, AR, USA.
Methods:
Adult female rats underwent transection at T10 level. Low frequency-dependent depression of the H-reflex was tested at 7, 14 and 30 days post-transection. Lumbar enlargement tissue was harvested following reflex testing and western blots were performed after immunoprecipitation to compare Cx-36 protein levels.
Results:
Significant decreases in low frequency-dependent depression of the H-reflex were observed in animals tested 14 and 30 days post-transection compared with control animals, but it was not different from control animals at 7 days. Significant decreases in Cx-36 protein levels were observed in animals 7 days post-transection compared with controls.
Conclusion:
Rats transition to a state of hyperreflexia between 7 and 14 days post-transection. Cx-36 protein levels decreased at 7 days post-transection and gradually returned to control levels by 30 days post-transection. These data suggest there may be a relationship between changes in neuronal gap junction protein levels and the delayed onset of hyperreflexia.
Similar content being viewed by others
Log in or create a free account to read this content
Gain free access to this article, as well as selected content from this journal and more on nature.com
or
References
Dietz V . Locomotor recovery after spinal cord injury. Trends Neurosci 1997; 20: 346–347.
Little JW, Ditunno JF, Stiens SA, Harris RM . Incomplete spinal cord injury: neuronal mechanisms of motor recovery and hyperreflexia. Arch Phys Med Rehab 1999; 80: 587–599.
Hultborn H . Spinal reflexes, mechanisms and concepts: from Eccles to Lundberg and beyond. Prog Neurobiol 2006; 78: 215–232.
Calancie B, Broton JG, Klose KJ, Traad M, Difini J, Ayyar DR . Evidence that alterations in presynaptic inhibition contribute to segmental hypo- and hyperexcitability after spinal cord injury in man. Electroencephalogr Clin Neurophysiol 1993; 89: 177–186.
Schindler-Ivens S, Shields RK . Low frequency depression of h-reflexes in humans with acute and chronic spinal-cord injury. Exp Brain Res 2000; 133: 233–241.
Bennett DJ, Li Y, Harvey PJ, Gorassini M . Evidence for plateau potentials in tail motoneurons of awake chronic spinal rats with spasticity. J Neurophysiol 2001; 86: 1972–1982.
Lloyd DP, Wilson VJ . Reflex depression in rhythmically active monosynaptic reflex pathways. J Gen Physiol 1957; 40: 409–426.
Skinner RD, Houle JD, Reese NB, Berry CL, Garcia-Rill E . Effects of exercise and fetal spinal cord implants on the H-Reflex in chronically spinalized adult rats. Brain Res 1996; 729: 127–131.
Thompson FJ, Reier PJ, Lucas CC, Parmer R . Altered patterns of reflex excitability subsequent to contusion injury of the rat spinal cord. J Neurophysiol 1992; 68: 1473–1486.
Malmsten J . Time course of segmental reflex changes after chronic spinal cord hemisection in the rat. Acta Physiol Scand 1983; 119: 435–443.
Leis AA, Zhou HH, Mehta M, Harkey III HL, Paske WC . Behavior of the H-reflex in humans following mechanical perturbation or injury to rostral spinal cord. Muscle Nerve 1996; 19: 1373–1382.
Chang Q, Gonzalez M, Pinter MJ, Balice-Gordon RJ . Gap junctional coupling and patterns of connexin expression among neonatal rat lumbar spinal motor neurons. J Neurosci 1999; 19: 10813–10828.
Walton KD, Navarrete R . Postnatal changes in motoneurone electronic coupling studied in the in vitro rat lumbar spinal cord. J Physiol 1991; 433: 283–305.
Chang Q, Pereda A, Pinter MJ, Balice-Gordon RJ . Nerve injury induces gap junctional coupling among axotomized adult motor neurons. J Neurosci 2000; 20: 674–684.
Lee IH, Lindqvist E, Kiehn O, Widenfalk J, Olson L . Glial and neuronal expression patterns in the rat spinal cord during development and following injury. J Comp Neurol 2005; 489: 1–10.
Reese NB, Skinner RD, Mitchell D, Yates C, Barnes CN, Kiser TS et al. Restoration of frequency-dependent depression of the H-reflex by passive exercise in spinal rats. Spinal Cord 2006; 44: 28–34.
Bradley NS . Animal models offer the opportunity to acquire a new perspective on motor development. Phys Ther 1990; 70: 776–787.
Heister D, Hayar A, Charlesworth A, Yates C, Zhou YH, Garcia-Rill E . Evidence for electrical coupling in the SubCoeruleus(SubC) nucleus. J Neurophysiol 2007; 97: 3142–3147.
Wenner P, O'Donovan MJ . Mechanisms that initiate spontaneous network activity in the developing chick spinal cord. J Neurophysiol 2001; 86: 1481–1498.
Placatonakis DG, Bukovsky AA, Zeng ZH, Kiem HP, Welsh JP . Fundamental role of inferior olive connexin 36 in muscle coherence during tremor. Proc Nat Acad Sci USA 2004; 101: 7164–7169.
Kistler WM, De Jeu MT, Elgersma Y, Van Der Giessen RS, Hensbrock R, Luo C et al. Analysis of Cx36 knockout does not support tenet that olivary gap junctions are required for complex spike synchronization and normal motor performance. Ann NY Acad Sci 2002; 978: 391–404.
Iwahara T, Atsuta Y, Garcia-Rill E, Skinner RD . Spinal cord stimulation-induced locomotion in the adult cat. Brain Res Bull 1991; 28: 99–105.
Hinckley CA, Ziskind-Conhaim L . Electrical coupling between locomotor-related excitatory interneurons in the mammalian spinal cord. J Neurosci 2006; 26: 8477–8483.
Garcia-Rill E, Heister DS, Ye M, Charlesworth A, Hayar A . Electrical coupling: novel mechanism for sleep-wake control. Sleep 2007; 30: 1405–1414.
Yates C, Reese N, Kiser T, Skinner RD, Garcia-Rill E . Modafinil (MOD) normalizes hyperreflexia induced by spinal cord transection in the rat. Neurosci Abst 2007; 33: 405.21.
Acknowledgements
This study was sponsored by NIH Grant RR020146 to the Center for Translational Neuroscience.
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Yates, C., Charlesworth, A., Allen, S. et al. The onset of hyperreflexia in the rat following complete spinal cord transection. Spinal Cord 46, 798–803 (2008). https://doi.org/10.1038/sc.2008.49
Received:
Revised:
Accepted:
Published:
Issue date:
DOI: https://doi.org/10.1038/sc.2008.49
Keywords
This article is cited by
-
Electromagnetic field stimulation facilitates motor neuron excitability, myogenesis and muscle contractility in spinal cord transected rats
Journal of Biosciences (2022)
-
Effects of bioengineered scaffold loaded with neurotrophins and locomotor training in restoring H-reflex responses after spinal cord injury
Experimental Brain Research (2018)
-
Characterisation of Peptide5 systemic administration for treating traumatic spinal cord injured rats
Experimental Brain Research (2017)
-
Implications of Olfactory Lamina Propria Transplantation on Hyperreflexia and Myelinated Fiber Regeneration in Rats with Complete Spinal Cord Transection
Neurochemical Research (2013)
-
The Beneficial Effects of Treadmill Step Training on Activity-Dependent Synaptic and Cellular Plasticity Markers After Complete Spinal Cord Injury
Neurochemical Research (2011)


