1990
DOI: 10.1016/0306-4522(90)90134-p
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Release, spread and persistence of immunoreactive neurokinin A in the dorsal horn of the cat following noxious cutaneous stimulation. Studies with antibody microprobes

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Cited by 200 publications
(52 citation statements)
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“…Using antibody microprobes, a marked release, spread and persistence of immunoreactive neurokinin A were found all over the dorsal horn after noxious cutaneous stimulation by Duggan et al (1990). These results provided strong evidence for long-distance VT in peptide neurons as far as neurokinin A was concerned.…”
Section: Deficits Of Fast Inactivation Mechanisms Of the Transmittermentioning
confidence: 65%
See 1 more Smart Citation
“…Using antibody microprobes, a marked release, spread and persistence of immunoreactive neurokinin A were found all over the dorsal horn after noxious cutaneous stimulation by Duggan et al (1990). These results provided strong evidence for long-distance VT in peptide neurons as far as neurokinin A was concerned.…”
Section: Deficits Of Fast Inactivation Mechanisms Of the Transmittermentioning
confidence: 65%
“…In contrast, substance P (SP) remained in the substantia gelatinosa where the SP/neurokinin A IR terminals are concentrated. It seemed likely that the slow degradation of neurokinin A versus SP was responsible for these differential effects on neurokinin A (Duggan et al, 1990). This proposal was elegantly supported by the demonstration that a peptidase inhibitor microinjected into the dorsal horn demonstrated the spread of immunoreactive SP over the entire dorsal horn after noxious cutaneous stimulation .…”
Section: Deficits Of Fast Inactivation Mechanisms Of the Transmittermentioning
confidence: 99%
“…This can lead to increased excitability and generation of ectopic discharges [53]. Under these conditions, enhanced activity of primary afferents results in the release of excitatory amino acids and peptides, such as substance P, in the DH, and this increased transmitter release leads to the establishment of central sensitization [11].…”
Section: Introduction Symptomatology and Pathophysiology Of Neuropathmentioning
confidence: 99%
“…Although glutamate is almost certainly the primary mediator of nociceptive transmission at this first synapse, other neurochemicals, notably the tachykinin peptides SP and neurokinin (NK) A, are major contributors (6,7). These peptides are present in a proportion of the small primary afferent neurons that terminate in the outer laminae of the dorsal horn, lamina I and lamina II (8,9); are released by high intensity stimulation (10)(11)(12)(13)(14)(15)(16); enhance the excitability of spinal neurons to noxious inputs (17)(18)(19); and contribute to a 'window' of noxious stimulus-evoked behaviours (20). SP and glutamate colocalize in the terminals of small diameter primary afferent neurons in the dorsal horn (21,22).…”
Section: Pharmacological Controls Of Primarymentioning
confidence: 99%