Research paperAntagonism of nociceptive responses of cat spinal dorsal horn neurons in vivo by the NK-1 receptor antagonists CP-96,345 and CP-99,994, but not by CP-96,344
References (60)
- et al.
Excitatory amino acid receptors and nociceptive neurotransmission in rat spinal cord
Pain
(1990) - et al.
Is the selective non-peptide NK-1 receptor antagonist CP96,345 a peripherally acting analgesic
Regul. Pept.
(1993) - et al.
Facilitatory role of calcitonin gene-related peptide (CGRP) on excitation induced by substance P (SP) and noxious stimuli in rat spinal dorsal horn neurons. An iontophoretic study in vivo
Brain Res.
(1991) - et al.
Inhibition of Ca2+ and K+ channels in sympathetic neurons by neuropeptides and other ganglionic transmitters
Neuron
(1990) - et al.
In vivo release of substance P in cat dorsal horn studied with microdialysis
Neurosci. Lett.
(1987) - et al.
CP-96,345 antagonism of NK1 receptors and smoke-induced protein extravasation in relation to its cardiovascular effects
Eur. J. Pharmac.
(1992) - et al.
Combined application of excitatory amino acids and substance P produces long-lasting changes in responses of primate spinothalamic tract neurons
Brain Res. Rev.
(1993) Neuropeptide release in the spinal cord in response to noxious and non-noxious stimulation
Neuropeptides
(1992)Effects of substance P on functionally identified units in cat spinal cord
Brain Res.
(1976)- et al.
Experimental immunohistochemical studies on the localization and distribution of substance P in cat primary sensory neurons
Brain Res.
(1975)
Tachykinins depress a calcium-dependent potassium conductance in sympathetic preganglionic neurons
Regul. Pept.
Release of substance P into the superficial dorsal horn following nociceptive activation of the hindpaw of the rat
Brain Res.
CP-99,994, a nonpeptide antagonist of the tachykinin NK1 receptor
Regul. Pept.
Intrathecal co-administration of substance P and NMDA augments nociceptive responses in the formalin test
Pain
Substance P augments a persistent slow inward calcium-sensitive current in voltage-clamped spinal dorsal horn neurons of the rat
Brain Res.
Antiinflammatory and analgesic activity of a non-peptide substance P receptor antagonist
Eur. J. Pharmac.
Novel substance P antagonist, CP-96,345, blocks responses of cat spinal dorsal horn neurones to noxious cutaneous stimulation and to substance P
Neurosci. Lett.
Excitatory amino acid receptor mediation of sensory inputs to functionally identified dorsal horn neurons in cat spinal cord
Neuroscience
Effect of substance P in cat dorsal horn neurones activated by noxious stimuli
Brain Res.
Responses of functionally identified neurones in the dorsal horn of the cat spinal cord to substance P, neurokinin A and physalaemin
Neuroscience
The substance P receptor antagonist CP-96,345 interacts with Ca2+ channels
Eur. J. Pharmac.
Substance P and somatostatin inhibit calcium channels in rat sympathetic neurons via different G protein pathways
Neuron
Substance P opens cation channels and closes potassium channels in rat locus coeruleus neurons
Neuroscience
Regional distribution of substance P in the spinal cord and nerve roots of the cat and the effect of dorsal root section
Brain Res.
Analysis of a nonpeptide antagonist for substance P on myenteric neurons of guinea-pig small intestine
Eur. J. Pharmac.
The inhibitory effect of substance P antagonist, CP-96,345, on the late discharges of nociceptive neurons in the rat superficial spinal dorsal horn
Neurosci. Lett.
Intrathecal CP-96,345 blocks reflex facilitation induced in rats by substance P and C-fiber-conditioning stimulation
Eur. J. Pharmac.
Spinal substance P and N-methyl-d-aspartate receptors are coactivated in the induction of central sensitization of the nociceptive flexor reflex
Neuroscience
Stereospecific effects of a nonpeptide NK1 selective antagonist, CP-96,345: antinociception in the absence of motor dysfunction
Life Sci.
Effects of dorsal rhizotomy on neurokinin receptor sub-types in the rat spinal cord: a quantitative autoradiographic study
Brain Res.
Cited by (43)
Resolvin D1 suppresses inflammation-induced hyperexcitability of nociceptive trigeminal neurons associated with mechanical hyperalgesia
2020, Brain Research BulletinCitation Excerpt :Previous studies reported that afterdischarges following noxious mechanical stimulation were observed in SpVc WDR neurons in a chronic inflammation model and these changes are associated with neuronal sensitization during persistent pain (Kitagawa et al., 2005; Tsuboi et al., 2011). In our study, we found that RvD1 abolished the afterdischarge observed following noxious pinch in rats with CFA-induced inflammation; however, the precise mechanism underlying this suppression of pinch-evoked afterdischarges still remains to be determined, A previous study has reported that after administration of substance P/neurokinin-1 receptor antagonist, pinch-evoked afterdischarges of WDR neurons in the spinal cord were inhibited (Radhakrishnan and Henry, 1995). It can be speculated that chronic administration of RvD1 attenuates NK1-receptor mediated afterdischarges of WDR neurons in the SpVc.
Dietary constituent genistein inhibits the hyperexcitability of trigeminal nociceptive neurons associated with mechanical hyperalgesia following orofacial inflammation
2019, Journal of Oral BiosciencesCitation Excerpt :Herein, we found that genistein abolished after-discharges following noxious pinch stimulation in inflamed rats, although the precise mechanism underlying this effect remains unclear. In addition, administration of a substance P (SP) neurokinin-1 (NK1) receptor antagonist inhibits pinch-evoked after-discharges in WDR neurons of the spinal cord [40]. Thus, because genistein can also dose-dependently inhibit SP-induced responses [41], chronic administration of genistein might attenuate the NK1 receptor-mediated after-discharges of WDR neurons in the SpVc under inflammatory conditions.
Oxaliplatin treatment changes the function of sensory nerves in rats
2016, Journal of Pharmacological SciencesCitation Excerpt :Moreover, L-OHP-treated rats showed after-discharges even in response to low mechanical stimuli that did not induce after-discharges in naïve rats. Discharges lasting after stimulation were also observed in the dorsal horn (25–27). The increase in after-discharges was also observed in spared nerve injury model rats (28) and in the spinal dorsal horn of spinal cord injury model rats (29).
Contribution of TRPV1 receptor-expressing fibers to spinal ventral root after-discharges and mechanical hyperalgesia in a spared nerve injury (SNI) rat model
2013, Journal of Pharmacological SciencesSpinal ventral root after-discharges as a pain index: Involvement of NK-1 and NMDA receptors
2006, Brain ResearchCitation Excerpt :It is considered that NK-1 receptor activation by substance P contributed to the generation of after-discharges but not during-discharges. Similar results have been obtained by intracellular recording in the dorsal horn of the cat, in which CP-96,345, a selective NK-1 receptor antagonist, blocked the prolonged excitatory postsynaptic potential following noxious cutaneous stimulation (De Koninck and Henry, 1991; Radhakrishnan and Henry, 1995). NMDA receptors contribute to nociceptive transmission (Dickenson and Sullivan, 1987; Urch et al., 2001).