Intrathecal dynorphin-A infusion in rat spinal cord causes energy depletion, edema and neurologic dysfunction

Intrathecal dynorphin-A infusion in rat spinal cord causes energy depletion, edema and neurologic... The opioid dynorphin-A (dynA) is thought to contribute to the secondary injury process following spinal cord trauma although little is known about the biochemical mechanisms involved. In the present study, we have used a combination of magnetic resonance imaging (MRI) and spectroscopy (MRS) and hindlimb motor function tests to examine the effects of intrathecal dynA infusion on rat spinal cord. Infusion of 100 nmol of dynA (1–17) caused pronounced edema development as determined by MRI at 24 h after infusion. Infusion of 100 nmol of the dynA (2–17) fragment, which does not have any activity at opiate receptors, also produced profound edema whereas 100 nmol of the low potency κ opiate receptor ligand dynA (1–8) or artificial CSF (ACSF) did not produce any edema. Both dynA (1–17) and dynA (2–17) produced significant hindlimb motor deficits at 24 h when compared to dynA (1–8) and ACSF ( P < 0.05), but the deficits in the dynA (1–17) group were significantly worse than in the dynA (2–17) treated animals ( P < 0.05). Similarly, mortality in the dynA (1–17) treated animals was significantly higher than in the other groups ( P = 0.002). Phosphorus MRS demonstrated that the dynA (1–17) and dynA (2–17) treated animals also had a pronounced decline in high energy phosphates in the spinal cord 24 h after infusion. We conclude that dynA contributes to spinal cord cell death by causing metabolic failure and edema development. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Neurochemistry International Elsevier

Intrathecal dynorphin-A infusion in rat spinal cord causes energy depletion, edema and neurologic dysfunction

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Publisher
Elsevier
Copyright
Copyright © 1995 Elsevier Ltd
ISSN
0197-0186
DOI
10.1016/0197-0186(94)00153-L
Publisher site
See Article on Publisher Site

Abstract

The opioid dynorphin-A (dynA) is thought to contribute to the secondary injury process following spinal cord trauma although little is known about the biochemical mechanisms involved. In the present study, we have used a combination of magnetic resonance imaging (MRI) and spectroscopy (MRS) and hindlimb motor function tests to examine the effects of intrathecal dynA infusion on rat spinal cord. Infusion of 100 nmol of dynA (1–17) caused pronounced edema development as determined by MRI at 24 h after infusion. Infusion of 100 nmol of the dynA (2–17) fragment, which does not have any activity at opiate receptors, also produced profound edema whereas 100 nmol of the low potency κ opiate receptor ligand dynA (1–8) or artificial CSF (ACSF) did not produce any edema. Both dynA (1–17) and dynA (2–17) produced significant hindlimb motor deficits at 24 h when compared to dynA (1–8) and ACSF ( P < 0.05), but the deficits in the dynA (1–17) group were significantly worse than in the dynA (2–17) treated animals ( P < 0.05). Similarly, mortality in the dynA (1–17) treated animals was significantly higher than in the other groups ( P = 0.002). Phosphorus MRS demonstrated that the dynA (1–17) and dynA (2–17) treated animals also had a pronounced decline in high energy phosphates in the spinal cord 24 h after infusion. We conclude that dynA contributes to spinal cord cell death by causing metabolic failure and edema development.

Journal

Neurochemistry InternationalElsevier

Published: May 1, 1995

References

  • Excitotoxic cell death
    Choi, D.W.
  • Opioid and nonopioid mechanisms may contribute to dynorphin's pathophysiological actions in spinal cord injury
    Faden, A.I.
  • A potential role for excitotoxins in the pathophysiology of spinal cord injury
    Faden, A.I.; Simon, R.P.
  • Endogenous opioid immunoreactivity in rat spinal cord following traumatic injury
    Faden, A.I.; Molineaux, C.J.; Rosenberger, J.G.; Jacobs, T.P.; Cox, B.M.
  • Alterations in extracellular amino acids after traumatic spinal cord injury
    Panter, S.S.; Yum, S.W.; Faden, A.I.
  • Excitotoxicity and the NMDA receptor
    Rothman, S.M.; Olney, J.W.
  • Metabolic changes in rabbit spinal cord after trauma: magnetic resonance spectroscopy studies
    Vink, R.; Noble, L.J.; Knoblach, S.M.; Bendall, M.R.; Faden, A.I.

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