Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We aimed to provide a detailed analysis of substance P (SP)-containing nerves in the trabecular meshwork by ultrastructural immunohistochemistry and capsaicin treatment for chemical ablation of the sensory nerves. Numerous myelinated and unmyelinated nerves were observed inside the sheets and intertrabecular spaces of the trabecular meshwork, and the inner side of Schlemm's canal. SP-like immunoreactive products were identified in some of these nerves and associated with numerous vesicles of different sizes, a few mitochondria and numerous neurotubili. After the capsaicin treatment, SP-like immunoreactive nerves persisted and no degenerated SP-like immunoreactive nerves were noted. On the basis of the ultrastructural features and the results of capsaicin treatment, it seems that these nerves are most probably autonomic in origin. Autonomic efferent SP-containing nerves are confirmed directly located in the trabecular meshwork; these have not been previously described at electron microscopic level. SP in autonomic efferent nerves might act as a neurotransmitter or neuromodulator for intraocular pressure regulation.
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PMID:Ultrastructural identification of substance P containing nerves in the guinea pig trabecular meshwork. 961 16

Intraocular pressure displays a distinct circadian rhythm in animals and humans, with an increase at night and a decrease during the daytime. In animals, the IOP rhythm has been reported to be synchronized by environmental light and to persist in constant darkness, demonstrating a circadian component controlled by an endogenous pacemaker. The structures involved in the rhythmic regulation of intraocular pressure include the suprachiasmatic nucleus, which controls the activity of sympathetic and parasympathetic ocular innervation. These effectors are responsible for controlling the production (beta-adrenergic system) and the outflow (alpha1-adrenergic, parasympathetic system, prostaglandin) of aqueous humor. The production of aqueous humor is under adrenergic control (alpha1- and beta-receptors). Many neuropeptides such as vasoactive intestinal peptide, substance P, and the atrial natriuretic peptide are also involved in the regulation of intraocular pressure. A better understanding of the circadian regulation of intraocular pressure is needed for an appropriate treatment of ocular hypertension and glaucoma.
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PMID:[The neuroanatomical and physiological bases of variations in intraocular pressure]. 1531 70

Transient retinal ischemia induces loss of retinal ganglion cells, supporting the hypothesis that ischemic conditions contribute to the induction and progression of glaucoma. However, after 60 min of ischemia, also amacrine cells are lost from the inner nuclear layer. The main goal was to determine the relative vulnerability of various amacrine subpopulations by measuring the levels of transcripts that are known to be specifically expressed by different amacrine subpopulations. A 60-min ischemic period was administered to the rat eye by raising the intraocular pressure, followed by a reperfusion period lasting between 2 h and 4 weeks. Total RNA was isolated from the whole retina and expression levels were assessed by real-time quantitative polymerase chain reaction (qPCR). Retinal ischemia/reperfusion has differential effects on the levels of the various transcripts. Three main patterns of changes were identified. (i) A gradual decrease of transcript level without recovery was observed for parvalbumin; this transcript is expressed by the glycinergic AII cells. (ii) A gradual reduction to different levels at 72 h of reperfusion followed by a partial or complete recovery (glycine transporter 1, glutamate decarboxylase, calretinin, and several other transcripts). The glycinergic amacrine cell markers recovered to 65-75% of the control level, while the main GABAergic markers had completely recovered at 4 weeks. (iii) No significant changes of transcript levels were found for markers of several smaller GABAergic subpopulations [including substance P (Tac1), somatostatin, and others]. Expression levels of photoreceptor-, horizontal cell-, and bipolar cell-specific transcripts were not altered. These patterns were confirmed by a cluster analysis of the data. Based on gene expression levels, it may be concluded that amacrine cells are vulnerable to ischemic insults and that the glycinergic amacrine cells are relatively more sensitive to ischemia than the GABAergic population. In particular, the extensive loss of the parvalbumin-containing AII amacrine cells, which serve in the rod pathway, may have functional implications for vision under scotopic conditions. In the accompanying paper [F. Dijk and W. Kamphuis, An immunocytochemical study on specific amacrine subpopulations in the rat retina after ischemia, Brain Res. (2004).], the results are evaluated at the protein level by immunostaining for a selection of the amacrine cell markers.
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PMID:Differential effects of ischemia/reperfusion on amacrine cell subtype-specific transcript levels in the rat retina. 1548 81

Transient retinal ischemia leads to the loss of neurons in the inner retina. In an accompanying paper [F. Dijk, S. Van Leeuwen, W. Kamphuis, Differential effects of ischemia/reperfusion on amacrine cell subtype-specific transcript levels in the rat retina, Brain Res., 1026 (2004) 194-204] we present the results of a study on the effects of experimentally induced retinal ischemia on transcript levels of genes expressed by distinct subpopulations of amacrine cells. In response to 60-min ischemia, three different patterns of changes in transcript levels were found, indicating a differential vulnerability of amacrine subtypes: (i) a gradual decrease of transcript level without recovery (parvalbumin; PV); (ii) a gradual decrease, with varying rates and degrees, followed by partial recovery after 72 h of reperfusion (choline acetyltransferase (ChAT), calretinin (CR) and glycine transporter (Glyt1)); (iii) no significant changes (substance P (SP)). In order to verify whether the degree of cell loss can be predicted from the quantified alterations in gene expression level, immunocytochemical stainings were carried out. A 60-min ischemic period was administered to the rat eye by raising the intraocular pressure, followed by a reperfusion period lasting between 2 h and 4 weeks. Cryosections were immunostained for Glyt1, PV, ChAT, CR, and SP. Double-labelling with apoptosis marker TUNEL was used to demonstrate cell type-specific apoptosis. Following ischemia, the numbers of detected PV-, Glyt1, ChAT-, and CR-immunopositive somata showed a substantial, but differential, reduction at 1-4 weeks after ischemia. The total amount of immunoreactivity present in the inner plexiform layer (IPL) also decreased. The extent of alterations derived from immunocytochemical staining was greater than was anticipated from the decrease of transcript levels. Only for SP, no significant decrease in number of cells or in the intensity of immunoreactivity in IPL was observed, which is in agreement with the absence of significant changes in transcript levels. In conclusion, retinal ischemia/reperfusion differentially affects amacrine cell populations. Although both protein and mRNA levels are reduced, transcript levels are less attenuated. Caution must be applied in the use of real-time quantitative PCR (qPCR) screening as a tool to assess the cellular pattern of neurodegeneration in the retina.
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PMID:An immunocytochemical study on specific amacrine cell subpopulations in the rat retina after ischemia. 1548 82

Antidromic stimulation of the rat trigeminal ganglion triggers the release of substance P (SP) and calcitonin gene-related peptide (CGRP) from sensory nerve terminals of the capsaicin sensitive C-fibers. These pro-inflammatory neuropeptides produce a marked hyperemia in the anterior segment of the eye, accompanied by increased intraocular pressure, breakdown of the blood-aqueous barrier and myosis. To assess the effects of neurogenic inflammation on the retina, specifically on the immunostaining of neurotransmitters and neurotrophins, as well as on the expression of neurotrophin receptors in the retina. RT-PCR was also accomplished in control and stimulated animals to confirm the immunohistochemical results. In the electrically stimulated eyes, immunostaining for SP, CGRP, VIP and nNOS demonstrated a marked increase in the RPE/POS (Retinal Pigment Epithelium/Photoreceptor Outer Segments), in the inner and outer granular layers and in the ganglion cells in comparison to the control eyes. CGRP and SP were found increased in stimulated animals and this result has been confirmed by RT- PCR. Changes in neurotrophin immunostaining and in receptor expression were also observed after electric stimulation of trigeminal ganglia. Decrease of BDNF and NT4 in the outer and inner layers and in ganglion cells was particularly marked. In stimulated rat retinas immunostaining and RT-PCR showed a NGF expression increase. Neurotrophin receptors remained substantially unchanged. These studies demonstrated, for the first time, that antidromic stimulation of the trigeminal ganglion and subsequent neurogenic inflammation affect immunostaining of retinal cell neurotransmitter/neuropeptides and neurotrophins as well as the expression of neurotrophin receptors.
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PMID:Expression of neurotransmitters and neurotrophins in neurogenic inflammation of the rat retina. 1816 54

Extrinsic and intrinsic sources of the autonomic nervous system contribute to choroidal innervation, thus being responsible for the control of choroidal blood flow, aqueous humor production or intraocular pressure. Neuropeptides are involved in this autonomic control, and amongst those, alarin has been recently introduced. While alarin is present in intrinsic choroidal neurons, it is not clear if these are the only source of neuronal alarin in the choroid. Therefore, we here screened for the presence of alarin in human cranial autonomic ganglia, and also in rat, a species lacking intrinsic choroidal innervation. Cranial autonomic ganglia (i.e., ciliary, CIL; pterygopalatine, PPG; superior cervical, SCG; trigeminal ganglion, TRI) of human and rat were prepared for immunohistochemistry against murine and human alarin, respectively. Additionally, double staining experiments for alarin and choline acetyltransferase (ChAT), tyrosine hydroxilase (TH), substance P (SP) were performed in human and rat ganglia for unequivocal identification of ganglia. For documentation, confocal laser scanning microscopy was used, while quantitative RT-PCR was applied to confirm immunohistochemical data and to detect alarin mRNA expression. In humans, alarin-like immunoreactivity (alarin-LI) was detected in intrinsic neurons and nerve fibers of the choroidal stroma, but was lacking in CIL, PPG, SCG and TRI. In rat, alarin-LI was detected in only a minority of cranial autonomic ganglia (CIL: 3.5%; PPG: 0.4%; SCG: 1.9%; TRI: 1%). qRT-PCR confirmed the low expression level of alarin mRNA in rat ganglia. Since alarin-LI was absent in human cranial autonomic ganglia, and only present in few neurons of rat cranial autonomic ganglia, we consider it of low impact in extrinsic ocular innervation in those species. Nevertheless, it seems important for intrinsic choroidal innervation in humans, where it could serve as intrinsic choroidal marker.
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PMID:Alarin in cranial autonomic ganglia of human and rat. 2549 46


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