Related Experiment Videos
Intrathecally administered N-methyl-D-aspartate increases persistent hindlimb flexion in rat
R D Moore1, D J Mokler, B J Winterson
1Department of Physiology, University of New England, College of Osteopathic Medicine, Biddeford, ME 04005.
Neuroscience Letters
|November 9, 1992
Summary
Spinal N-methyl-D-aspartate (NMDA) receptors are crucial for inducing persistent hindlimb flexion in rats. Blocking these receptors with MK-801 prevented this flexion, suggesting their role in spinal cord plasticity.
Area of Science:
- Neuroscience
- Spinal Cord Injury Research
- Pharmacology
Background:
- Persistent hindlimb flexion can be a model for studying spinal cord injury and plasticity.
- N-methyl-D-aspartate (NMDA) receptors are known to play a role in synaptic plasticity and pain signaling.
Purpose of the Study:
- To investigate the role of spinal N-methyl-D-aspartate (NMDA) receptors in the induction of persistent hindlimb flexion.
- To determine if NMDA receptor antagonism can prevent the development of this flexion.
Main Methods:
- Persistent hindlimb flexion was induced in rats via prolonged electrical stimulation.
- Intrathecal administration of NMDA or the NMDA receptor antagonist MK-801 was performed.
- Hindlimb flexion and thermal withdrawal latencies were measured.
Main Results:
- Intrathecal NMDA significantly increased hindlimb flexion post-stimulation and at 3 days, even after spinalization.
- Pretreatment with MK-801 blocked the NMDA-induced enhancement of flexion.
- NMDA administration reduced thermal withdrawal latencies, an effect also blocked by MK-801.
Conclusions:
- Spinal NMDA receptors are essential for the induction of persistent hindlimb flexion.
- NMDA receptor activation contributes to spinal hyperexcitability and altered sensory processing.