Abstract
Trigeminal hyperalgesia frequently appears in diabetic neuralgia altering the transmission of orofacial sensory information. This study was designed to explore the effects of trigeminal hyperalgesia in streptozotocin-induced diabetes monitoring the expression of nitric oxide synthase in the trigeminal ganglion cells. The threshold to heat noxious stimuli decreased in diabetic animals. The number of NADPH-diaphorase (NADPH-d)-positive neurons significantly decreased in the diabetic rats compared with controls. Insulin treatment prevented the decreased nociceptive threshold and reduction of the number of NADPH-d-positive neurons. These findings point out that there is a relationship between the trigeminal nociceptive perception and NADPH-d neuronal expression suggesting that NO may play a role in the pathogenesis of trigeminal sensory neuropathy.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cell Count
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Diabetes Mellitus, Experimental / complications*
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Diabetic Neuropathies / physiopathology*
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Hyperalgesia / physiopathology*
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Hypoglycemic Agents / pharmacology
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Insulin / pharmacology
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Male
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NADP / metabolism
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Neurons / metabolism
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Neurons / pathology
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Nitric Oxide / metabolism*
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Nitric Oxide Synthase / metabolism
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Nociceptors / metabolism
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Nociceptors / pathology
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Nociceptors / physiopathology
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Pain Measurement
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Pain Threshold / drug effects
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Pain Threshold / physiology
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Rats
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Rats, Sprague-Dawley
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Time Factors
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Trigeminal Ganglion / metabolism
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Trigeminal Ganglion / pathology
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Trigeminal Ganglion / physiopathology
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Trigeminal Nerve / metabolism*
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Trigeminal Nerve / pathology
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Trigeminal Nerve / physiopathology*
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Trigeminal Nerve Diseases / physiopathology*
Substances
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Hypoglycemic Agents
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Insulin
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Nitric Oxide
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NADP
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Nitric Oxide Synthase