Serotonin (5-HT) and seritonergic receptors are strategic participants in nociception. Traumatic injury to peripheral tissues which results in arachadonic acid, bradykinin and prostaglandin release, initiates vasodilation and extravisation of serotonin which then binds with 5-HT3 receptors on pain afferents. This sequence has been shown to mediate inflammatory pain both peripherally and centrally and is exclusively excitatory. More recently, Wetzel has shown that gonadal steroids bind to 5-HT3 receptors non-competitively, blocking 5-HT3 receptor sites. This action interrupts propagation of painful stimuli potentially resulting in peripheral inflammatory analgesia. A review of the available literature was performed with the purpose of establishing the location and actions of 5-HT3 receptors in inflammatory pain, discussing the antagonism of 5-HT3 by gonadal steroids and outlining how early estrus might influence inflammatory pain. Of particular interest are the possible effects of elevated serum estrogen levels on 5-HT3 functionality in human pain and the potential for employing 5-HT3 selective drugs as a method of therapy. 5-HT3 receptors are non-competitively bound by circulating gonadal steroids and conduction of peripheral inflammatory pain is reduced or interrupted. Circulating gonadal steroids may affect the potential for conduction of inflammatory pain, enhancing the opportunity for near typical menses.
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