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Role of NMDA receptors in induction of LTP in spinal WDR neurons after L5 spinal nerve transection in male wistar rats
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Laleh Rezaee   , Homa Manaheji * , *, Shahrbanoo Oryan , Syyed Ali Noorbakhsh , Zahra Bahari |
| 2. Neurophysiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran 3. Department of Physiology, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran |
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Abstract: (13827 Views) |
Introduction: Role of NMDA receptors in persistence of pathological pain is not clear. In addition, long-term potentiation (LTP) has a crucial role in development and maintenance of neuropathic pain. The aim of this study was to investigate the role of glutamate NMDA receptor and electrophysiological changes in spinal dorsal horn following L5 spinal nerve ligation.
Methods: The model of spinal nerve ligation (SNL) was used in this study. In behavioral experiments to evaluate mechanical allodynia, Von frey filaments were used from a day before induction of neuropathy up to 7 days after neuropathy. Memantin 10 mg/Kg, i.p., as NMDA antagonist, was injected one hour before SNL up to 7 days afer SNL. LTP induction and dorsal horn WDR neurons recording was performed by spinal single unit set up on day 7 after high frequeny stimulus (HFS) induction.
Results: SNL induced mechanical allodynia . Daily injection of memantin increased thershold of pain significantly (p < 0.01) at the period of maximum pain (days 5, 6 and 7). Electrophsiological recording showed a significant decrease in the thershold of activation of C and Aδ fibers or LTP induction (p < 0.001) 7 days after SNL, compared to sham group. Daily administration of memantin prevented induction of LTP.
Conclusion: It seems that NMDA receptors are involved in development of plasticity during neuropathic pain. Control of neuropathic pain by memantin might open a new insight in treatment of neuropathic pain.
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| Keywords: Allodynia, LTP, Memantin, NMDA receptors, WDR |
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Full-Text [PDF 572 kb]
(2190 Downloads)
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Type of Study: Original Research |
Subject:
Neuroscience
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