Sodium Channel Expression: A Dynamic Process in Neurons and Non-Neuronal Cells

Black, Joel A.; Sg, Waxman

doi:10.1159/000111403

Cited by 47 publications

(41 citation statements)

References 79 publications

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“…This may reflect the variable functional requirements of these cells in rat and human. A number of reports also have revealed the presence of sodium channel mRNAs in rat brain astrocytes (for reviews, see Black and Waxman, 1996;Sontheimer et al, 1996). Further studies are needed to determine whether similar expression occurs in human glial cells, although sodium currents have been recorded from acutely isolated astrocytes from human cortex and hippocampus and in glial cells from human hippocampal tissue slices (Sontheimer and Waxman, 1993;Bordey and Sontheimer, 1998).…”

Section: Discussionmentioning

confidence: 99%

Distribution of voltage-gated sodium channel ?-subunit and ?-subunit mRNAs in human hippocampal formation, cortex, and cerebellum

et al. 2000

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Section: Discussionmentioning

confidence: 99%

Distribution of voltage-gated sodium channel ?-subunit and ?-subunit mRNAs in human hippocampal formation, cortex, and cerebellum

et al. 2000

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“…The view that odontoblasts could detect and transduce painful stimuli into electric signals questioned the possibility that these cells display excitable properties and possess voltage-gated sodium channels. These later have indeed been detected in non-excitable mineralizing cells (7) like osteoblasts where sodium channel Na v 1.2 mRNA and protein were identified (8). In teeth, voltage-gated Na ϩ channels have been previously evidenced in vitro on dental pulp cell by electrophysiological investigation (9).…”

mentioning

confidence: 86%

Voltage-gated Sodium Channels Confer Excitability to Human Odontoblasts

Allard

Magloire

Couble

et al. 2006

Journal of Biological Chemistry

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Odontoblasts are responsible for the dentin formation. They are suspected to play a role in tooth pain transmission as sensor cells because of their close relationship with nerve, but this role has never been evidenced. We demonstrate here that human odontoblasts in vitro produce voltage-gated tetrodotoxin-sensitive Na ؉ currents in response to depolarization under voltage clamp conditions and are able to generate action potentials. Odontoblasts express neuronal isoforms of ␣2 and ␤2 subunits of sodium channels. Co-cultures of odontoblasts with trigeminal neurons indicate a clustering of ␣2 and ␤2 sodium channel subunits and, at the sites of cell-cell contact, a co-localization of odontoblasts ␤2 subunits with peripherin. In vivo, sodium channels are expressed in odontoblasts. Ankyrin G and ␤2 co-localize, suggesting a link for signal transduction between axons and odontoblasts. Evidence for excitable properties of odontoblasts and clustering of key molecules at the site of odontoblast-nerve contact strongly suggest that odontoblasts may operate as sensor cells that initiate tooth pain transmission.

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“…Within the DRG, several voltage-gated sodium channels are known to be responsible for the TTXs current (PN1, rSCP6/ PN4, rBI, rBII, and rBIII), and these show a wide distribution across large and small neuronal cells (15)(16)(17). Two sensory neuron-specific TTXr sodium channels have been cloned [SNS/PN3 (18,19) and SNS2/NaN (20,21)].…”

mentioning

confidence: 99%

Transcriptional and posttranslational plasticity and the generation of inflammatory pain

Woolf

Costigan

1999

Proc. Natl. Acad. Sci. U.S.A.

498

344

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Inf lammatory pain manifests as spontaneous pain and pain hypersensitivity. Spontaneous pain ref lects direct activation of specific receptors on nociceptor terminals by inf lammatory mediators. Pain hypersensitivity is the consequence of early posttranslational changes, both in the peripheral terminals of the nociceptor and in dorsal horn neurons, as well as later transcription-dependent changes in effector genes, again in primary sensory and dorsal horn neurons. This inf lammatory neuroplasticity is the consequence of a combination of activity-dependent changes in the neurons and specific signal molecules initiating particular signal-transduction pathways. These pathways phosphorylate membrane proteins, changing their function, and activate transcription factors, altering gene expression. Two distinct aspects of sensory neuron function are changed as a result of these processes, basal sensitivity, or the capacity of peripheral stimuli to evoke pain, and stimulus-evoked hypersensitivity, the capacity of certain inputs to generate prolonged alterations in the sensitivity of the system. Posttranslational changes largely alter basal sensitivity. Transcriptional changes both potentiate the system and alter neuronal phenotype. Potentiation occurs as a result of the up-regulation in the dorsal root ganglion of centrally acting neuromodulators and simultaneously in the dorsal horn of their receptors. This means that the response to subsequent inputs is augmented, particularly those that induce stimulus-induced hypersensitivity. Alterations in phenotype includes the acquisition by A fibers of neurochemical features typical of C fibers, enabling these fibers to induce stimulus-evoked hypersensitivity, something only C fiber inputs normally can do. Elucidation of the molecular mechanisms responsible provides new opportunities for therapeutic approaches to managing inf lammatory pain.Pain is a state-dependent sensory experience. Normally, it is generated only by activation of a specific subset of highthreshold peripheral sensory neurons, the nociceptors, hence nociception-the detection of noxious or tissue-damaging stimuli. Nociception is important for being aware of and reacting to potentially or actually damaging stimuli in the environment. Absence of this capacity, as in individuals with congenital analgesia, results in ongoing tissue damage. Pain is also, of course, a major clinical problem. After inflammation or nerve injury, dramatic alterations in the somatosensory system occur, amplifying responses and increasing sensitivity to peripheral stimuli so that pain can now be activated by normally innocuous or low-intensity stimuli. Clinical pain is an expression, then, of plasticity in the somatosensory system, operating at multiple sites and due to diverse mechanisms. The purpose of this paper is to highlight key features of the plasticity of primary sensory neurons and of the synaptic contacts they make with dorsal horn neurons, the mechanisms that operate to produce this plasticity, and how this relates to t...

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Sodium Channel Expression: A Dynamic Process in Neurons and Non-Neuronal Cells

Cited by 47 publications

References 79 publications

Distribution of voltage-gated sodium channel ?-subunit and ?-subunit mRNAs in human hippocampal formation, cortex, and cerebellum

Distribution of voltage-gated sodium channel ?-subunit and ?-subunit mRNAs in human hippocampal formation, cortex, and cerebellum

Voltage-gated Sodium Channels Confer Excitability to Human Odontoblasts

Transcriptional and posttranslational plasticity and the generation of inflammatory pain

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