Neurokinin 1 receptor expression in the rat retina

Casini, G.; Rickman, Doug; Sternini, Catia; Brecha, Nicholas C.

doi:10.1002/(sici)1096-9861(19971222)389:3<496::aid-cne10>3.0.co;2-k

Cited by 27 publications

(17 citation statements)

References 62 publications

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“…In the quiescent retina, 20–30% of the amacrine cells express NK1-R (30) and about one third of NK1-R positive cells express substance P (31). However, after RLB trauma the relative expression of substance P or NK1-R is unknown.…”

Section: Resultsmentioning

confidence: 99%

Retinal Laser Burn-Induced Neuropathy Leads to Substance P-Dependent Loss of Ocular Immune Privilege

Lucas

Karamichos

Mathew

et al. 2012

The Journal of Immunology

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Inflammation in the eye is tightly regulated by multiple mechanisms that together contribute to ocular immune privilege. Many studies have shown that it is very difficult to abrogate the immune privileged mechanism called anterior chamber associated immune deviation (ACAID). Previously, we showed that retinal laser burn (RLB) to one eye abrogated immune privilege (ACAID) bilaterally for an extended period of time. In an effort to explain the inflammation in the non-burned eye, we postulated that neuronal signals initiated inflammation in the contralateral eye. Here, we test the role of substance P, a neuroinflamatory peptide, in RLB-induced loss of ACAID. Histological examination of the retina with and without RLB revealed an increase of the substance P-inducible neurokinin 1 receptor (NK1-R) in the retina of first, the burned eye, and then the contralateral eye. Specific antagonists for NK1-R, given locally with antigen within 24h, but not 3,5, or 7 days post RLB treatment, prevented the bilateral loss of ACAID. Substance P Knockout (KO) mice retained their ability to develop ACAID post RLB. These data support the postulate that substance P transmits early inflammatory signals from the RLB eye to the contralateral eye to induce changes to ocular immune privilege and has a central role in the bilateral loss of ACAID. The possibility is raised that blocking of the substance P pathway with NK1-R antagonists post ocular trauma may prevent unwanted and perhaps extended consequences of trauma-induced inflammation in the eye.

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Section: Resultsmentioning

confidence: 99%

Retinal Laser Burn-Induced Neuropathy Leads to Substance P-Dependent Loss of Ocular Immune Privilege

Lucas

Karamichos

Mathew

et al. 2012

The Journal of Immunology

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“…It is likely that NPY released from the retina acts in a paracrine manner on Y receptors in the pigment epithelium. Other neuroactive substances, such as dopamine, somatostatin, and substance P (Witkovsky and Schutte, 1991;Casini et al, 1997;Johnson et al, 1998Johnson et al, , 1999, are also distributed away from their receptors in the retina. For example, in the rat retina, somatostatin is localized to amacrine and displaced amacrine cells and processes that ramify primarily in strata 1 and 5 of the IPL, whereas the somatostatin receptor 2A is localized to cone photoreceptors, horizontal cells, bipolar cells, and amacrine cells (Johnson et al, 1998(Johnson et al, , 1999(Johnson et al, , 2000 and the somatostatin receptor 4 is localized to multistratified ganglion cells (Vila and Brecha, 2001).…”

Section: Npy As a Paracrine Neuromodulator In The Retinamentioning

confidence: 99%

Localization of neuropeptide Y1 receptor immunoreactivity in the rat retina and the synaptic connectivity of Y1 immunoreactive cells

D'Angelo¹,

Oh²,

Chun³

et al. 2002

J of Comparative Neurology

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Neuropeptide Y (NPY), an inhibitory neuropeptide expressed by a moderately dense population of wide-field amacrine cells in the rat retina, acts through multiple (Y1-y6) G-protein-coupled receptors. This study determined the cellular localization of Y1 receptors and the synaptic connectivity of Y1 processes in the inner plexiform layer (IPL) of the rat retina. Specific Y1 immunoreactivity was localized to horizontal cell bodies in the distal inner nuclear layer and their processes in the outer plexiform layer. Immunoreactivity was also prominent in cell processes located in strata 2 and 4, and puncta in strata 4 and 5 of the IPL. Double-label immunohistochemical experiments with calbindin, a horizontal cell marker, confirmed Y1 immunostaining in all horizontal cells. Double-label immunohistochemical experiments, using antibodies to choline acetyltransferase and vesicular acetylcholine transporter to label cholinergic amacrine cell processes, demonstrated that Y1 immunoreactivity in strata 2 and 4 of the IPL was localized to cholinergic amacrine cell processes. Electron microscopic studies of the inner retina showed that Y1-immunostained amacrine cell processes and puncta received synaptic inputs from unlabeled amacrine cell processes (65.2%) and bipolar cell axon terminals (34.8%). Y1-immunoreactive amacrine cell processes most frequently formed synaptic outputs onto unlabeled amacrine cell processes (34.0%) and ganglion cell dendrites (54.1%). NPY immunoreactivity in the rat retina is distributed primarily to strata 1 and 5 of the IPL, and the present findings, thus, suggest that NPY acts in a paracrine manner on Y1 receptors to influence both horizontal and amacrine cells. Indexing termsamacrine cells; choline acetyltransferase; calcium binding protein; horizontal cells; neuropeptides Neuropeptide Y (NPY) has multiple physiologic actions in both the central and peripheral nervous system, including effects on blood flow, memory retention, food intake, epilepsy, and pain (Lundberg et al., 1996;Munglani et al., 1996;Balasubramaniam, 1997;Blomqvist and Herzog, 1997;Thorsell et al., 2000;Furtinger et al., 2001;Naveilhan et al., 2001). These NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript effects are mediated by means of at least five G-protein-coupled receptors, designated as Y1, Y2, Y4, Y5, and y6, which are coupled to pertussis toxin-sensitive inhibitory Gproteins (Lundberg et al., 1996;Munglani et al., 1996;Balasubramaniam, 1997;Blomqvist and Herzog, 1997;Michel et al., 1998). Y-receptors have been localized to specific regions of the central and peripheral nervous system by receptor binding autoradiography, immunohistochemistry, and in situ hybridization (Zhang et al., 1994;Bao et al., 1997;Jacques et al., 1997;Dumont et al., 1998;Hökfelt et al., 1998;Gackenheimer et al., 2001). Y1 receptor is the most studied Y-receptor and it plays key roles in many of the central and peripheral effects of NPY (Lundberg et al., 1996;Munglani et al., 1996;Balasubramaniam, 1997;Blomqvist and H...

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“…SP, NKA, and the NKA‐related peptides are encoded by the preprotachykinin I gene, whereas NKB is encoded by the preprotachykinin II gene (Maggio, 1988; Otsuka and Yoshioka, 1993). These peptides have widespread distribution throughout the peripheral and central nervous systems (for reviews, see Maggio, 1988; Otsuka and Yoshioka, 1993), including the retina (for references, see Casini et al, 1997a). SP, NKA, and NKB appear to act on distinct neurokinin (NK) receptors, termed neurokinin‐1 (NK1), NK2, and NK3, respectively, that belong to the superfamily of G protein‐coupled receptors (Otsuka and Yoshioka, 1993) and are distributed differentially throughout the nervous system and peripheral tissues (Mantyh et al, 1989).…”

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confidence: 99%

“…NK1 and NK3 receptors recently have been localized in the rat retina by using immunohistochemical methods (Casini et al, 1997a; Blumauer and Brecha, 1998) and in situ hybridization histochemistry (Kondoh et al, 1996; Shughrue et al, 1996). NK1, the preferred ligand of which is SP, is expressed by populations of amacrine cells, displaced amacrine cells, interplexiform cells, and ganglion cells.…”

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Developmental expression of neurokinin-1 and neurokinin-3 receptors in the rat retina

et al. 2000

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Tachykinin (TK) peptides act on retinal neurons through neurokinin (NK) receptors. We examined the expression of neurokinin‐1 (NK1; the substance P receptor), NK3 [the neurokinin B (NKB) receptor], and TK peptides in developing rat retinas. NK1 immunolabeling was found in newborn retinas in rare amacrine cells and in putative ganglion cells. At postnatal day 2 (PND 2), NK1 immunostaining was reduced greatly among ganglion cells, and it appeared in many amacrine cells and in fibers in the inner plexiform layer (IPL), with the highest density in laminae 1, 3, and 5. A similar pattern was found at PND 7. At PND 12, interplexiform NK1‐immunoreactive (‐IR) cells were detected, and NK1‐IR fibers in the IPL were concentrated in lamina 2, similar to what was seen in adults. NK3 was expressed mainly by OFF‐cone bipolar cells, and the developmental pattern of NK3 was compared with that of cone bipolar cells that were labeled with antibodies to recoverin. Immature recoverin‐IR cone bipolar cells were seen at PND 2. NK3 immunolabeling was detected first in the outer plexiform layer and in sparse bipolar cell somata at PND 10, when recoverin‐IR cone bipolar cells are nearly mature. By PND 15, both the NK3 immunostaining pattern and the recoverin immunostaining pattern were similar to the patterns seen in adults. TK immunoreactivity was present at PND 0 in amacrine cells and displaced amacrine cells. By PND 10, the morphologic maturation of TK‐IR cells was complete. These findings indicate that, in early postnatal retinas, substance P may act on NK1 receptors, whereas NKB/NK3 interactions are unlikely, suggesting that there are different levels of importance for different TK peptides in the developing retina. J. Comp. Neurol. 421:275–287, 2000. © 2000 Wiley‐Liss, Inc.

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Neurokinin 1 receptor expression in the rat retina

Cited by 27 publications

References 62 publications

Retinal Laser Burn-Induced Neuropathy Leads to Substance P-Dependent Loss of Ocular Immune Privilege

Retinal Laser Burn-Induced Neuropathy Leads to Substance P-Dependent Loss of Ocular Immune Privilege

Localization of neuropeptide Y1 receptor immunoreactivity in the rat retina and the synaptic connectivity of Y1 immunoreactive cells

Developmental expression of neurokinin-1 and neurokinin-3 receptors in the rat retina

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