Abstract
The intensity of pain sensation exhibits marked day and night variations. Since the intensity of pain perception is low during dark hours of the night when melatonin levels are high, this hormone has been implicated as one of the prime antinociceptive substances. A number of studies have examined the antinociceptive role of melatonin in acute, inflammatory and neuropathic pain animal models. It has been demonstrated that melatonin exerts antinociceptive actions by acting at both spinal cord and supraspinal levels. The mechanism of antinociceptive actions of melatonin involves opioid, benzodiazepine, α1- and α2-adrenergic, serotonergic and cholinergic receptors. Most importantly however, the involvement of MT1/MT2 melatonergic receptors in the spinal cord has been well documented as an antinociceptive mechanism in a number of animal models of pain perception. Exogenous melatonin has been used effectively in the management of pain in medical conditions such as fibromyalgia, irritable bowel syndrome and migraine and cluster headache. Melatonin has been tried during surgical operating conditions and has been shown to enhance both preoperative and post-operative analgesia. The present review discusses the available evidence indicating that melatonin, acting through MT1/MT2 melatonin receptors, plays an important role in the pathophysiological mechanism of pain.
Highlights
Pain is classically described as an unpleasant sensation
Clinical pain has been divided into two conditions, including inflammatory pain caused by inflammation and neuropathic pain caused by actual injury to the nervous system [2]
Neuropathic pain manifests as allodynia
Summary
Pain is classically described as an unpleasant sensation. By definition “pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage” [1]. Damage or inflammation of tissue releases a variety of inflammatory mediators such as prostaglandins (PGE2), leukotrienes, bradykinin, substance P and inflammatory cytokines like tumor-necrosis factor (TNF-α), ATP and adenosine Each of these substances either directly activates nociceptors or releases local allogenic agents which sensitize nociceptors and enhance the neuronal excitability of pain transmission pathways [9]. The transmission of pain sensation involves nociceptors (the primary sensory nerve endings of Aδ and C fibers) that have their central processes in the dorsal horn of the spinal cord. 168 Current Neuropharmacology, 2012, Vol 10, No 2 descending neural tracts from the brain constitute endogenous pain modulatory systems that inhibit pain transmission signals These pain modulatory systems are activated by opioid and GABAergic mechanisms located in and around the periaqueductal gray region (PAG). Tricyclic antidepressants and gabapentin are often prescribed for the treatment of neuropathic pain with variable results of response [20,21,22], suggesting thereby the need for the development of novel analgesic drugs that can be used for effective treatment and management of inflammatory and neuropathic pain
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