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Jeong Il Choi

Jeong Il Choi

Chonnam National University, South Korea

Title: Spinal 5-HT1A receptor plays a major role in directing serotonergic modulation toward inhibition on mechanical allodynia of carrageenan inflammation

Biography

Biography: Jeong Il Choi

Abstract

Introduction: Descending serotonergic projections may facilitate or inhibit nociceptive processing in the spinal cord depending on several factors. Unlike other pain states, spinal 5-hydroxytryptamine 3 receptors (5-HT3R) were shown to play a limited role in nociceptive transmission of carrageenan-induced inflammatory pain. Instead, a facilitatory role of 5-HT1AR and 5-HT1BR in spinal nociceptive processing was observed during early-phase of carrageenan model. Although the maximum release of 5-HT in spinal cord reaches the maximum 2-3 hours after carrageenan injection (early-phase), its release returns to baseline 8 hours.

Methods: Effects of intrathecal (i.t.) nonspecific 5-HTR agonist, subtype agonist or antagonists (5-HT1AR, 5-HT1BR, 5-HT3R), and 5,7-dihydroxytryptamine (5,7-DHT, a serotonergic neurotoxin) on mechanical allodynia were tested for early- and late-phase allodynia.

Results: Lesioning spinal serotonergic projections with 5,7-DHT induced a significant increase in the intensity of mechanical allodynia at both early and late-phase. This increase was attenuated by i.t. 5-HT. Also, i.t. 5-HT itself produced a significant anti-allodynic effect in late-phase, but not in early-phase. Similarly, i.t. 5-HT1AR agonist (8-OH-DPAT) attenuated the intensity of late-phase allodynia in a dose-dependent manner which was antagonized by 5-HT1AR antagonist (WAY-100635), but produced no effect on the early-phase allodynia. However, other agonists or antagonists of 5-HT1BR and 5-HT3R did not produce any anti or pro-allodynic effects.

Conclusion: Descending serotonergic modulation plays a vital role in inhibition of nociceptive processing during late-phase allodynia, which involves spinal 5-HT1A, but not 5-HT1B or 5-HT3 receptors in carrageenan-induced inflammation. However, the defined role of 5-HT1A and serotonergic inhibition during early-phase remains undetermined.