2001
DOI: 10.1016/s0891-0618(01)00088-6
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Depletion of substance P, neurokinin A and calcitonin gene-related peptide from the contralateral and ipsilateral caudal trigeminal nucleus following unilateral electrical stimulation of the trigeminal ganglion; a possible neurophysiological and neuroanatomical link to generalized head pain

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Cited by 41 publications
(36 citation statements)
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“…Pain SP and NK-1 receptors are present in the dorsal horn of the spinal cord and in nociception spinal SP and neurokinin A play an important role (Samsam et al 2001). Nerve fibers also transmit afferent signals to the CNS in response to inflammation (SP contributes to pain transmission in the CNS in inflammatory processes) (Samsam et al 2001).…”
Section: Alcohol Addictionmentioning
confidence: 99%
“…Pain SP and NK-1 receptors are present in the dorsal horn of the spinal cord and in nociception spinal SP and neurokinin A play an important role (Samsam et al 2001). Nerve fibers also transmit afferent signals to the CNS in response to inflammation (SP contributes to pain transmission in the CNS in inflammatory processes) (Samsam et al 2001).…”
Section: Alcohol Addictionmentioning
confidence: 99%
“…It is believed that activation of TGVS during the head pain phase initiates a chemical cascade of vasoactive neuropeptides such as substance P, calcitonin gene-related peptide, neurokinin A, and nitric oxide. These molecules cause vasodilatation, which can contribute to headaches [17]. The TGVS transmitting migraine pain may be controlled by serotonergic neurons.…”
Section: Serotonin and Its Metabolites In Migrainementioning
confidence: 99%
“…The activation of the primary nociceptive trigeminal afferents leads to peripheral neuropeptide release, calcitonin gene-related peptide (CGRP), neurokinin A and substance P are liberated to the perineural space [71,72], leading to vasodilatation and plasma protein extravasation and to the activation of mast cells and leukocytes collectively termed as neurogenic inflammation [73]. These phenomena are well characterized in animals, however in humans only little direct evidence supports the actual presence of neurogenic inflammation during the attack [74].…”
Section: Headache Phase and Postdromementioning
confidence: 99%