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Diagram showing primary sensory neuron-satellite glial cell interactions in the spinal/trigeminal ganglion during inflammatory and neuropathic pain. CGRP = calcitonin generelated peptide; Cx = connexin; IL-1b R = interleukin-1b receptor; iNOs = inducible nitric oxide synthase; Kir 4.1 = K +-buffering inwardly rectifying potasium channel; NK1 R = neurokinin 1 receptor; NO = nitric oxide; P2X R = purinergic iontropic channel X subtype receptor; P2Y R = purinergic metabotropic channel Y subtype receptor; SK3 = small conductance Ca 2+-activated K + channel; SP = substance P; TNFa R = tumor necrosis factor a receptor.
Contexts in source publication
Context 1
... immuno- staining (a specific labeling of astroglia in the CNS and satellite cells in the PNS) following inflammation and nerve injury (Zhang and others 2007; Xie and others 2009; Zhang and others 2009). Each DRG neuron has its own sheath, which usually consists of several satellite glial cells tightly enveloping the perikarya of the DRG neurons (Fig. 2). The satellite glial cells are interconnected with each other with connexin-43 (Cx-43) subunit gap junctions and form a morphological unit with the neu- rons. The distance between satellite glial cells and the neuronal surface is very small (about 20 nm), suggesting a close functional relationship between the neurons and satellite ...
Context 2
... pain and chronic inflammatory pain models in rodents ( Interestingly, the behavioral and VG changes produced by IAN-X can be manifested in putative nociceptive pri- mary afferent neurons (e.g., Ad) in the maxillary trigemi- nal division, suggesting mechanisms likely exist in the VG to allow for spread of effects from one division to another (Fig. 2). Satellite glial cells may indeed be involved because the change in Ad primary afferent activity in the IAN-X and ION-CCI model is associated with a variety of changes in satellite glial cell activity (for review, see Bender 2008;Ohara and others 2008). It is also to be noted that some effects of noxious stimulation of orofa- cial ...
Context 3
... in the DRG, gap junctions (Thalakoti and others 2007; Garrett and Durham 2008;Ohara and others 2008) as well as paracrine processes appear to be important in spreading excitation between satellite glial cells as well as to VG neurons. The gap junction is known to be per- meable to Ca 2+ , initiating Ca 2+ waves in adjacent satellite glial cells, and is associated with increases in Cx26, 36, 40, or 43 expression, resulting in an increase in VG neuron excitability (Vit and others 2006). Also, as in the DRG, satellite glial cells in the VG may release mediators (e.g., interleukin 1-b). ...
Context 4
... recent in vivo electrophysiological studies in the pulp inflammatory pain model also have demonstrated a role for P2X mechanisms that may involve microglia in MDH central sensitization (Chiang and others 2005;Xie and others 2007). Medullary application of potent block- ers of the P2X 7 receptor (periodate oxidized ATP or bril- liant blue G) can markedly attenuate the MO-induced central sensitization (Li and others 2008); besides, med- ullary application of ATP can elicit central sensitization- like MDH nociceptive neuronal responses in cases where all other P2X and A1 subtype activities are blocked by pretreatment with suramin (a wide-spectrum P2X and P2Y blocker, except P2X 4,7 subtypes if used at a moder- ate dose) and DPCPX (antagonist of adenosine A1 recep- tor; Itoh and others 2009). These findings indicate an imp ortant role in central sensitization of P2X receptors and the likely involvement also of microglia because P2X 4 and P2X 7 receptors in the MDH (and SDH) are located primarily on microglia (see above). ...
Context 5
... injection of threo-b-benzyloxyas- partate (a glutamate uptake blocker) can produce sponta- neous nociceptive behavior (Liaw and others 2005), and inhibitors of aconitase such as fluoroacetate (FA) that selectively block the astroglial tricarboxylic acid (TCA) cycle prevent formalin-induced hyper algesia and nerve inflammation-induced pain (Milligan and Watkins 2009;Gao and others 2009). However, although methionine sulf- oximine (MSO), an inhibitor of astroglial GS, has been reported to block epilep tiform discharges in cultured hip- pocampal neurons (Bacci and others 2002), no analogous SDH studies on pathological pain have been reported (but such studies have been carried out in the MDH; see below). ...
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