Define The Role Of P2 X Receptors In Nociception

1525 words - 7 pages

Introduction
Nociception is the sensation of pain which is normally a warning signal to brain in respond to a potential hazard. Generally noxious stimulations are detected by specialised high-threshold sensory neurons, which are refer to nociceptors. The signals are then transferred to an electrical potential and conducted to the brain via spinal cord. However sometimes abnormal nociception can lead to a moderate to severe pain although a noxious stimulus is missing. This kind of pain are usually trigger by nerve injury, while the pain sensation remains after the tissue had been healed. Although the prevalence of neuropathic pain is not significant, about 7% to 8% of the European population ...view middle of the document...

The structure of a P2X protein contains two transmembrane domains with intracellular N- and C-terminals and an extracellular loop. On the membrane, P2X receptors are formed as a trimer, with six transmembrane domains forming an ionic channel, and a ligand binding site on the second extracellular loop. The sensitivity of different channels on ATP or the homologues varies, and they also behave differentially once activated. For example P2X7 is less sensitive to ATP, that normally require a high dose of ATP (about 1mM-5mM), while other P2X can respond to micromolar level of ATP. Once activated, the P2X7 mediates a broad and prolonged inwards current and did not desensitise on minutes, while other receptors such P2X4 would desensitise within 10 seconds.

The neuropathic pain usually develops after a periphery nerve injure such as surgery, infection, and diabetes. Accumulating understanding of neuropathic pain accumulated over several decades suggests that, the neurons that undergo molecular or cellular alteration after nerve injury play a crucial role in the pathogenesis of abnormal nociception. The damaged neuron not only show an abnormal plasticity and anatomical reformation, which can generate abnormal electrical potentials, but could also release a number of molecules such as glutamate, GABA or nucleotides. Actually, a higher level of ATP has been found and associated with neuropathic pain (Inoue & Tsuda, 2007). Furthermore, recent research indicated that glial cells are also involved and mediated neuropathic pain, therefore the glial cells that express purinergic receptors might play an important role in neuropathic pain.
Actually, as one of the glial cells together with astrocytes and oligodendrocytes, microglia were underestimated for several decades. Until recently, researchers started to found they are involved in numerous diseases such as ischaemic, neurodegeneration, as well as neuropathic pain. Several purinergic receptors have been detected on microglia including P2X4, P2X7, P2Y6 and P2Y12. Among which the role of P2X4 and P2X7 in neuropathic pain were widely studied, since they can mediate direct electrophysiological responses via their cationic channel.
Microglial P2X4 receptors are suggested to generate allodynia. Although the expression of P2X¬4 receptors on naive microglia is low, injury in spinal cord can activate microglial cells and upregulate their expression P2X4Rs. This was confirmed by Immunohistochemistry experiment, while the expression of P2X4 is failed to be detected on neuron and astrocytes (Tsuda, Shigemoto-Mogami & Koizumi. 2003). In their research, Tsuda and colleagues found tactile allodynia can be inhibited in animal model by specific P2X4 blocker, TPN-ATP at a high concentration, as a comparison, another ATP blocker PPADS which cannot block P2X4 were tested and the allodynia was not reduced. Furthermore, tactile allodynia can be prevented by reducing P2X4 expression using an intrathecally administered...

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