N -Methyl- d -aspartate receptors are implicated in hyperresponsiveness following naloxone reversal of alfentanil in isolated rat spinal cord

N -Methyl- d -aspartate receptors are implicated in hyperresponsiveness following naloxone... In isolated neonatal rat spinal cord, naloxone administered after an opioid increases a nociceptive-related slow ventral root potential (sVRP) to levels above pre-drug controls. We studied the role of N -methyl- d -aspartate (NMDA) receptors in this phenomenon, which may be related to acute tolerance and to hyperalgesia on antagonist-precipitated withdrawal. Naloxone (200 nM) alone produced no significant effect on sVRP area, while naloxone (560 nM) increased area to 121 ± 17.5% of control (mean ± SD). Following 200 nM alfentanil, naloxone (200 nM) was associated with a significant rebound in sVRP area to 138 ± 18.0% of pre-drug contro. Hyper-responsiveness developed within 7 min of initial alfentanil exposure. The non-competitive NMDA antagonist MK-801 (20 nM) had no effect on sVRP area when applied alone; higher concentrations produced irreversible depression. MK-801 (20 nM) co-applied with 200 nM alfentanil blocked the rebound increase in sVRP area following naloxone 200 nM and also the increase following naloxone alone (560 nM). The results suggest that alfentanil induces a rapid NMDA receptor-dependent change in spinal cord neuronal excitability. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Neuroscience Letters Elsevier

N -Methyl- d -aspartate receptors are implicated in hyperresponsiveness following naloxone reversal of alfentanil in isolated rat spinal cord

Neuroscience Letters, Volume 189 (2) – Apr 14, 1995

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Publisher
Elsevier
Copyright
Copyright © 1995 Elsevier Ltd
ISSN
0304-3940
DOI
10.1016/0304-3940(95)11465-9
Publisher site
See Article on Publisher Site

Abstract

In isolated neonatal rat spinal cord, naloxone administered after an opioid increases a nociceptive-related slow ventral root potential (sVRP) to levels above pre-drug controls. We studied the role of N -methyl- d -aspartate (NMDA) receptors in this phenomenon, which may be related to acute tolerance and to hyperalgesia on antagonist-precipitated withdrawal. Naloxone (200 nM) alone produced no significant effect on sVRP area, while naloxone (560 nM) increased area to 121 ± 17.5% of control (mean ± SD). Following 200 nM alfentanil, naloxone (200 nM) was associated with a significant rebound in sVRP area to 138 ± 18.0% of pre-drug contro. Hyper-responsiveness developed within 7 min of initial alfentanil exposure. The non-competitive NMDA antagonist MK-801 (20 nM) had no effect on sVRP area when applied alone; higher concentrations produced irreversible depression. MK-801 (20 nM) co-applied with 200 nM alfentanil blocked the rebound increase in sVRP area following naloxone 200 nM and also the increase following naloxone alone (560 nM). The results suggest that alfentanil induces a rapid NMDA receptor-dependent change in spinal cord neuronal excitability.

Journal

Neuroscience LettersElsevier

Published: Apr 14, 1995

References

  • Development of physical dependence on morphine in respect to time and dosage and quantification of the precipitated withdrawal syndrome in rats
    Blasig, J.; Herz, A.; Reinhold, K.; Zieglganberger, S.
  • Enkephalin hyperpolarizes interneurones in the rat hippocampus
    Madison, D.V.; Nicoll, R.A.

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