Abstract
Neuropathic orofacial pain (NOP) is a debilitating condition. Although the pathophysiology remains unclear, accumulating evidence suggests the involvement of multiple mechanisms in the development of neuropathic pain. Recently, glial cells have been shown to play a key pathogenetic role. Nerve injury leads to an immune response near the site of injury. Satellite glial cells are activated in the peripheral ganglia. Various neural and immune mediators, released at the central terminals of primary afferents, lead to the sensitization of postsynaptic neurons and the activation of glia. The activated glia, in turn, release pro-inflammatory factors, further sensitizing the neurons, and resulting in central sensitization. Recently, we observed the involvement of glia in the alteration of orofacial motor activity in NOP. Microglia and astroglia were activated in the trigeminal sensory and motor nuclei, in parallel with altered motor functions and a decreased pain threshold. A microglial blocker attenuated the reduction in pain threshold, reduced the number of activated microglia, and restored motor activity. We also found an involvement of the astroglial glutamate–glutamine shuttle in the trigeminal motor nucleus in the alteration of the jaw reflex. Neuron–glia crosstalk thus plays an important role in the development of pain and altered motor activity in NOP.
Highlights
Chronic pain is a major public health problem that has a significant impact on both the individual and community [1,2]
Microinjection of methionine sulfoximine, a blocker of glutamine synthetase, decreased the amplitude of the jaw-opening reflex, which was reversed following microinjection of glutamine into the trigeminal motor nucleus [119]. These findings suggest the involvement of the astroglial glutamate–glutamine shuttle in orofacial motor dysfunction, following trigeminal nerve injury (Figure 5) [119,120]
Nerve injury induces immune responses, both peripherally and centrally, which play an important role in the development and maintenance of neuropathic pain
Summary
Chronic pain is a major public health problem that has a significant impact on both the individual and community [1,2]. Neuropathic pain is associated with dysfunction throughout the pain pathway, including the nociceptors, the peripheral ganglia, the brainstem or the spinal cord, the thalamus, and the cerebral cortex [8,9,10,11,12]. Recent studies strongly suggest that the activation of glia in the pain transmission pathway plays a critical role in the initiation and maintenance of neuropathic pain [16,17,18,19]. We discuss the role of glia in the development of neuropathic pain and their involvement in the modulation of orofacial motor activity in the disorder
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