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... the above proteins are involved, either directly or indirectly, DOI: http://dx.doi.org/10. 5772/intechopen.82128 in potassium ion (K + ) buffering and, thus, can influence the level of neuronal excitability, which, in turn, has been associated with neuropathic pain conditions (Figure 7). They also used in vivo RNA interference to reduce the expression of Cx43 (present only in SGCs) in the rat trigeminal ganglion and showed that this resulted in the development of spontaneous pain behavior. ...
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Purpose
Magnetic resonance neurography (MRN) can detect dorsal root ganglia (DRG) hypertrophy in patients with oxaliplatin-induced peripheral neuropathy (OXIPN) but is difficult to apply in clinical daily practice. Aims of this study were (i) to assess whether DRG volume is reliably measurable by routine computed tomography (CT) scans, (ii) to meas...
Despite recent advancements in therapeutic options for disorders of the central nervous system (CNS), the lack of an efficient drug-delivery system (DDS) hampers their clinical application. We hypothesized that liposomes could be optimized for retrograde transport in axons as a DDS from peripheral tissues to the spinal cord and dorsal root ganglia...
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... This exposure of the afferent cell bodies to circulating products, including cytokines, may partly explain why circulating neurotoxic agents (e.g., chemotherapeutics) preferentially accumulate and injure cells within the DRG, inducing a sensory rather than a motor neuropathy (156). DRG neurons are additionally supported by satellite glial cells (SGCs), which envelop them and display gap junction linkages between these two cell types (157). During inflammation, SGCs display enhanced activation, increased TNF production, and neuronal excitability (73). ...
... During inflammation, SGCs display enhanced activation, increased TNF production, and neuronal excitability (73). An increase of gap junctions has been observed in pain-generating conditions, and this correlates with enhanced neuronal excitability (157). Importantly, peripheral inflammation or nerve injury causes DRG neuronal sensitization, leading to a spreading activation of SGCs through gap junctions and to the expression and release of IL-1β from SGCs. ...
... Gap junctions in the DRG can provide direct communications between neuronal cell bodies and SGCs. An increase in gap junctions has been observed in pain condition and seems to enhance neuronal excitability and thus elicit pain (157). Importantly, peripheral inflammation or nerve injury causes sensitization of neurons, innervating peripheral tissues, and spreading of activation of SGCs through gap junctions, which leads to the expression and release of IL-1β from SGCs. ...
A high-intensity potentially tissue-injuring stimulus generates a homotopic response to escape the stimulus and is associated with an affective phenotype considered to represent pain. In the face of tissue or nerve injury, the afferent encoding systems display robust changes in the input–output function, leading to an ongoing sensation reported as painful and sensitization of the nociceptors such that an enhanced pain state is reported for a given somatic or visceral stimulus. Our understanding of the mechanisms underlying this non-linear processing of nociceptive stimuli has led to our appreciation of the role played by the functional interactions of neural and immune signaling systems in pain phenotypes. In pathological states, neural systems interact with the immune system through the actions of a variety of soluble mediators, including cytokines. Cytokines are recognized as important mediators of inflammatory and neuropathic pain, supporting system sensitization and the development of a persistent pathologic pain. Cytokines can induce a facilitation of nociceptive processing at all levels of the neuraxis including supraspinal centers where nociceptive input evokes an affective component of the pain state. We review here several key proinflammatory and anti-inflammatory cytokines/chemokines and explore their underlying actions at four levels of neuronal organization: (1) peripheral nociceptor termini; (2) dorsal root ganglia; (3) spinal cord; and (4) supraspinal areas. Thus, current thinking suggests that cytokines by this action throughout the neuraxis play key roles in the induction of pain and the maintenance of the facilitated states of pain behavior generated by tissue injury/inflammation and nerve injury.
