Abstract
The tetrodotoxin-resistant voltage-gated sodium channel Nav 1.8 is expressed only in nociceptive sensory neurons. This channel has been proposed to contribute significantly to the sensitization of primary sensory neurons after injury. We have studied the nociceptive behaviours of mice carrying a null mutation in the Nav 1.8 gene (Nav 1.8 -/-) in models of peripheral inflammation as well as a model of neuropathic pain. The results from the present studies reveal that Nav 1.8 is a necessary mediator of NGF-induced thermal hyperalgesia but is not essential for PGE2-evoked hypersensitivity. Neuropathic pain behaviours were unchanged in Nav 1.8 -/- mice indicating that this channel is not involved in the alteration of sensory thresholds following peripheral nerve injury.
MeSH terms
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Animals
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Dinoprostone / pharmacology
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Disease Models, Animal
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Female
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Ganglia, Spinal / drug effects*
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Ganglia, Spinal / metabolism
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Ganglia, Spinal / physiopathology
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Hyperalgesia / chemically induced
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Hyperalgesia / genetics*
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Hyperalgesia / metabolism
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Ligation
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Male
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Mice
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Mice, Knockout
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Nerve Growth Factor / pharmacology*
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Neuralgia / genetics*
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Neuralgia / metabolism
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Neuralgia / physiopathology
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Neurons, Afferent / drug effects*
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Neurons, Afferent / metabolism
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Nociceptors / drug effects*
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Nociceptors / metabolism
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Peripheral Nervous System Diseases / genetics
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Peripheral Nervous System Diseases / metabolism
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Peripheral Nervous System Diseases / physiopathology
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Sciatic Nerve / drug effects
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Sciatic Nerve / metabolism
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Sodium Channels / deficiency*
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Sodium Channels / drug effects
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Sodium Channels / genetics
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Tetrodotoxin / pharmacology
Substances
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Sodium Channels
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Tetrodotoxin
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Nerve Growth Factor
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Dinoprostone