| It is well known that neuron plays a key role in signaling pathway of the central nervous system (CNS). Because of its excitatory characteristic and propagated action potential, neuron has been considered as the only player in signaling transmission. However, glia, another densely populated component in the CNS, has been thought to work as an accessory role and is not involved in signaling pathway. This traditional concept has been challenged by some new findings showing a role of glia in the processing of synaptic development and synaptic transmission. Regarding the roles of glial cells in induction of pain, accumulating evidence shows that astrocyte and microglia in the spinal cord play essential roles in development of neuropathic pain. However, the exact role of glial cells of the spinal cord in development and maintenance of inflammatory pain is controversial and need to be further studied. Moreover, they are neurons whenreceiving peripheral persistent pain information conveyed to the dorsal horn of the spinal cord. Because elderly people are big population suffering from persistent pain and hyperalgesia / allodynia, it is interesting to see whether the function of glial cells were changed with aging, and if any, what roles are played by glial cells when the animals receiving persistent pain stimulation at peripheral? In this study, we combine the behavioral survey with immunocytochemical staining of both neurons (by c-Fos) and astrocytes (by GFAP) to investigate the interactions of neurons and glial cells in the central processing of inflammatory pain information from periphery. To distinguish the roles of neurons and glial cells in different types of pain, we used the bee venom (BV) test to produce persistent spontaneous pain-related behaviors such as paw withdrawal flinching reflex on one hand, and the complete freund's adjuvant (CFA) model to produce peripheral heat and mechanical hyperalgesia / allodynia on the other hand. Moreover, indomethacin (Indo), a non-selective cyclooxygenase (COX) was administrated systemically to block nociceptive information at both peripheral and spinal cord levels, while fluorocitric acid (FCA), an astrocytic metabolic inhibitor, was also used in the same way to destroy functions of astrocyte. The results were as follows: 1. Roles of spinal sensory neuron and astrocyte inprocessing of persistent spontaneous nociception inaged rats0.4% 50 l BV was subcutaneously injected into one hindpaw in aged rats. BV injection could induce a 1 h persistent spontaneous flinching reflex. Systemic administration of Indo or FCA could dramatically inhibit the behavioral spontaneous nociceptive response. By immunohistochemistry, it was observed that the numbers of c-Fos labeled neurons and GFAP labeled astrocytes in the spinal dorsal horn were increased by BV injection. Systemic administration of Indo could inhibit the numbers of both c-Fos labeled neurons and GFAP labeled astrocytes. However, FCA could only inhibit the number of GFAP labeled astrocytes, but not c-Fos labeled neurons. The results indicate that in spinal dorsal horn both neurons and astrocytes are involved in the processing of persistent spontaneous nociception induced by BV. 2. Roles of spinal neurons and astrocytes in generation of hyperalgesia in aged rats50 l CFA was injected into one hindpaw and 4h after injection, thermal and mechanical hyperalgesia appeared. Differently, the former lasted for 1 d, and disappeared in 3 d; but the latter lasted for about 28 d, and then disappeared. After immunohistochemical observation, we found that in the spinal dorsal horn, c-Fos labeled neurons and GFAP labeled astrocytes were activated by CFA injection. Similarly, the former expressed for less than 3 d, but the latter expressed longer than 28 d. When Indo was systemically administrated, it could inhibit mechanical hyperalgesia, but no effect on thermal hyperalgesia.Moreover, systemic administration of FCA could not affect neither mechanical nor thermal hyperalgesia. After immunostaining, we found that Indo could inhibi...
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