Peripheral and central distribution of TRPV1, substance P and CGRP of rat corneal neurons

Murata, Yuzo; Masuko, Sadahiko

doi:10.1016/j.brainres.2006.02.035

Cited by 90 publications

(93 citation statements)

References 35 publications

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“…However, considerable interspecies differences are suggested to exist with regard to the colocalization of corneal nerve fiber neuropeptides 19) . Murata and Masuko (2006) 21) demonstrated the coexistence of TRPV1-IR nerve fibers with SP-IR and CGRP-IR nerve fibers in the rat cornea. Recently, considerably more extensive TRPV1-positive fine nerve fibers were identified in the adult rat cornea by immunohistochemical methods 20) and using TRPV1 knock-in mice 23) .…”

Section: Resultsmentioning

confidence: 99%

“…To date, there have been many reports concerning corneal nerve fibers stained by various methods including enzyme detection [1][2][3][4][5][6][7][8][9] , gold impregnation 7,10 -13) , and neuropeptides 5,6,8,14 -20) , lectin IB4 15,20) or capsaicin receptor TRPV1 20,21) localization. Most analyses have been performed on whole mount preparations and paraffin or cryostat sections of the cornea from various mammals.…”

Section: Introductionmentioning

confidence: 99%

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Innervation of TRPV1-, PGP-, and CGRP-immunoreactive nerve fibers in the subepithelial layer of a whole mount preparation of the rat cornea

Hiura

Nakagawa

2012

Okajimas Folia Anat. Jpn.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Innervation of TRPV1-, PGP-, and CGRP-immunoreactive nerve fibers in the subepithelial layer of a whole mount preparation of the rat cornea

Hiura

Nakagawa

2012

Okajimas Folia Anat. Jpn.

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“…TRPV1 is widely expressed in several brain nuclei and human brain endothelial cells (Mezey et al, 2000;Golech et al, 2004). The studies of immunofluorescence show a high degree of colocalization of TRPV1 with CGRP and SP in the brain neurons, such as those in trigeminal ganglionic neurons (Bae et al, 2004) and corneal neurons (Murata, and Masuko, 2006). Recently, TRPV1 has been shown to be associated with cSCS-induced cerebral vasodilation (Yang et al, 2007).…”

Section: Neurohumoral Mechanisms-mentioning

confidence: 99%

Putative mechanisms behind effects of spinal cord stimulation on vascular diseases: A review of experimental studies

Linderoth

Foreman

2008

Autonomic Neuroscience

156

106

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Spinal cord stimulation (SCS) is a widely used clinical technique to treat ischemic pain in peripheral, cardiac and cerebral vascular diseases. The use of this treatment advanced rapidly during the late 80's and 90's, particularly in Europe. Although the clinical benefits of SCS are clear and the success rate remains high, the mechanisms are not yet completely understood. SCS at lumbar spinal segments (L2-L3) produces vasodilation in the lower limbs and feet which is mediated by antidromic activation of sensory fibers and decreased sympathetic outflow. SCS at thoracic spinal segments (T1-T2) induces several benefits including pain relief, reduction in both frequency and severity of angina attacks, and reduced short-acting nitrate intake. The benefits to the heart are not likely due to an increase, or redistribution of local blood flow, rather, they are associated with SCS-induced myocardial protection and normalization of the intrinsic cardiac nervous system. At somewhat lower cervical levels (C3-C6), SCS induces increased blood flow in the upper extremities. SCS at the upper cervical spinal segments (C1-C2) increased cerebral blood flow, which is associated with a decrease in sympathetic activity, an increase in vasomotor center activity and a release of neurohumoral factors. This review will summarize the basic science studies that have contributed to our understanding about mechanisms through which SCS produces beneficial effects when used in the treatment of vascular diseases. Furthermore, this review will particularly focus on the antidromic mechanisms of SCS-induced vasodilation in the lower limbs and feet.

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“…This neuropeptide is involved in nociception, as strongly suggested by experimental findings that a cyclooxygenese inhibitor attenuated a release of CGRP from the trigeminal nucleus caudalis (17), and that a bath application of CGRP also produced a slow action potential in dorsal root ganglion cells (20). Indeed, an intravenous administration of CGRP induces headache in migraineurs (19).…”

Section: Introductionmentioning

confidence: 93%

The effect of neonatal capsaicin treatment on the CGRP-immunoreaction in the trigeminal subnucleus caudalis of mice

2008

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The calcitonin-gene related peptide (CGRP) is a primary afferent neurotransmitter in the trigeminal system. Although a neonatal administration of capsaicin eliminates substance P (SP)-mediated nociceptive responses to induce a permanent functional reduction in C-fibers, little information is available regarding changes in CGRP-immunoreaction in mice undergoing neonatal capsaicin treatment (CP mice). This study examined postnatal changes in the distribution of CGRP-immunoreaction in the trigeminal subnucleus caudalis and trigeminal ganglion of CP mice by immunohistochemical technique and a quantitative analysis. Immunohistochemistry for CGRP in the subnucleus caudalis (Vc) demonstrated two dense distributions of neurons in the CP mice as well as naïve mice: in the marginal layer and the region 400-600 μm deep. The quantitative analysis revealed no significant difference in the density of CGRP immunoreaction between naïve and CP mice 1-8 weeks of age. In the trigeminal ganglion of both groups, the size distribution of CGRPpositive neurons displayed a distribution pattern with one peak in 200-300 μm 2 at week 1 and with two peaks in 200-300 μm 2 and 600-700 μm 2 at week 8 but no significant difference in neural density existed between these regions. When double staining in the naïve mice with CGRP or SP and VR1, a capsaicin receptor, was done, many trigeminal ganglion neurons co-expressed SP-and VR1-immunoreactions, but rarely exhibited CGRP/VR1-co-localization. Taken together with previous data, these current observations suggest that CGRP containing afferent neurons possibly performs differing roles in nociceptive afferent input transmission within the Vc from SP-containing neurons in mice.Calcitonin gene-related peptide (CGRP), widely distributed in central and peripheral nervous systems, has diverse functions including that as a primary afferent neurotransmitter. This neuropeptide is involved in nociception, as strongly suggested by experimental findings that a cyclooxygenese inhibitor attenuated a release of CGRP from the trigeminal nucleus caudalis (17), and that a bath application of CGRP also produced a slow action potential in dorsal root ganglion cells (20). Indeed, an intravenous administration of CGRP induces headache in migraineurs (19). In addition to the nociceptive function, CGRP enhances excitations of wide dynamic range neurons caused by NMDA or AMPA receptor agonist, suggesting a nociceptive modulation role of CGRP (8). Substance P (SP) is also a slow acting neurotransmitter that serves as a modulator of nociceptive transmission (36). CGRP is released from Aδ-and C-fibers while SP is from C-fibers (3,22,23).

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Peripheral and central distribution of TRPV1, substance P and CGRP of rat corneal neurons

Cited by 90 publications

References 35 publications

Innervation of TRPV1-, PGP-, and CGRP-immunoreactive nerve fibers in the subepithelial layer of a whole mount preparation of the rat cornea

Innervation of TRPV1-, PGP-, and CGRP-immunoreactive nerve fibers in the subepithelial layer of a whole mount preparation of the rat cornea

Putative mechanisms behind effects of spinal cord stimulation on vascular diseases: A review of experimental studies

The effect of neonatal capsaicin treatment on the CGRP-immunoreaction in the trigeminal subnucleus caudalis of mice

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