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mGluR activation reveals a tonic NMDA component in inflammatory hyperalgesia
S J Boxall1, A Berthele, T R Tölle
1Department of Pharmacology, Novartis Institute for Medical Sciences, London, UK.
Neuroreport
|May 28, 1998
Summary
Metabotropic glutamate receptors (mGluRs) contribute to pain processing. In hyperalgesia, spinal cord mGluR responses are enhanced, suggesting a role for NMDA receptors in inflammatory pain.
Area of Science:
- Neuroscience
- Pharmacology
- Pain Research
Background:
- Metabotropic glutamate receptors (mGluRs) are implicated in spinal nociceptive processing.
- Inflammatory hyperalgesia involves altered spinal cord pain pathways.
Purpose of the Study:
- To investigate the pharmacology of the mGluR agonist (1S,3R)-ACPD in an in vitro model of inflammatory hyperalgesia.
- To determine the influence of hyperalgesia on mGluR-mediated responses in the juvenile rat spinal cord.
Main Methods:
- Used an in vitro juvenile rat hemisected spinal cord preparation.
- Administered the mGluR agonist (1S,3R)-ACPD in a concentration-dependent manner.
- Utilized the NMDA receptor antagonist D-AP5 to probe receptor interactions.
Main Results:
- (1S,3R)-ACPD induced concentration-dependent ventral root depolarization in naive and hyperalgesic rats.
- The maximum response amplitude to (1S,3R)-ACPD was significantly enhanced by 23% in hyperalgesic animals.
- D-AP5 reversed the enhanced response in hyperalgesic animals, indicating NMDA receptor involvement.
Conclusions:
- Spinal mGluR responses are potentiated during inflammatory hyperalgesia.
- A tonic NMDA receptor component contributes to spinal cord function during inflammatory hyperalgesia.
- These findings suggest potential therapeutic targets for managing inflammatory pain.