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)

Calretinin (CR) is a calcium-binding protein purported to have neuroprotective properties. This study was designed to characterize the types of neurons containing CR in two different primary cultures and to determine which, if any, CR-immunoreactive (CR-ir) neurons are resistant to excitotoxic insults. Calretinin-containing neurons in cortical primary cultures derived from E14 rat embryos were not resistant to either kainic acid or a brief calcium overload induced by the calcium ionophore A23187. Equal proportions of CR-ir and GABAergic cortical neurons were lost after a 24-h exposure to 100 or 500 microM kainic acid. A 3 microM, 3-h exposure to A23187 induced equivalent amounts of cell loss in both the total cell and CR-ir cortical neuron culture populations. Cortical cultures grown for 6-7 days were more vulnerable than 12- to 13-day-old cultures to short-term, low-concentration treatments of A23187. Older cultures, however, were more severely affected when examined 24 h after a 3-h exposure to A23187. Calretinin-immunoreactive neurons derived from the diencephalon were relatively more resistant than cortical neurons to kainic acid at 6-7 days in vitro. In cortical or diencephalic cultures, CR was rarely coexpressed with GABA or calbindin D-28k. No vasoactive intestinal peptide, substance P, or parvalbumin was detected in CR-ir neurons in either culture system. We suggest that the presence of CR alone is not sufficient to spare neurons from a toxic calcium overload. Calretinin may still buffer calcium at low concentrations or be a component in a calcium-based signal transduction system.
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PMID:Vulnerability to calcium-induced neurotoxicity in cultured neurons expressing calretinin. 1083 5

Immunohistochemical localization of the substance P receptor (SPR) was examined in the developing rat medulla oblongata, with special reference to the development of substance P (SP)-immunoreactive neurons which form the medullary raphe nuclei. During development, SPR immunoreactivity was detected in cells lying lateral to the medullary midline from embryonic day 13 (E13) to postnatal day 5 (P5). The SPR-positive cell bodies were located close to the fourth ventricle, and bore long processes extending to the ventral pial surface. This SPR immunoreactivity co-localized with staining for monoclonal antibody 1D11, a specific marker of immature astrocytes. Substance P (SP)-immunoreactive neurons were first detected at E14 in the ventrolateral part of the medulla. By E16 their number had increased and they were arrayed in two rows closely parallel to the SPR-immunoreactive processes of non-neuronal cells. By P1, two separate SP-immunoreactive cell clusters could be recognized at the midline, representing dorsally the nascent raphe pallidus and ventrally the raphe obscurus. In addition, many SP-immunoreactive fibers traveled rostrocaudally in the medulla oblongata, juxtaposed to the midline sheets of SPR-immunoreactive long processes. SPR-immunoreactive processes at the midline were also immunoreactive for S-100, a glia-specific calcium-binding protein that is known to promote axonal growth of raphe neurons. These results suggest that SPR-expressing immature glial cells at the medullary midline are involved in the development of SP-immunoreactive raphe neurons, both in the formation of the medullary raphe nuclei and in axon guidance and growth.
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PMID:Immunohistochemical localization of substance P receptors in the midline glia of the developing rat medulla oblongata with special reference to the formation of raphe nuclei. 1087 32

We have recently described large, unipolar neurons (named bullwhip cells) that regulate the proliferation of progenitors in the circumferential marginal zone (CMZ) of the postnatal chicken retina (Fischer et al. [2005] J. Neurosci. 25:10157-10166; [2006] J. Comp. Neurol. 496:479-494). There are only about 240 bullwhip cells in the entire retina, and these cells are easily identified by their unique morphology and immunoreactivity for glucagon, glucagon-like peptide 1 (GLP1), and substance P. The purpose of this study was to elucidate the development of bullwhip cells in the embryonic chicken retina. By using bromodeoxyuridine birth dating, we found that the bullwhip cells are generated very early during retinal development, between E4 and E5. Glucagon peptide was first detected in bullwhip cells at about E10, whereas substance P was not detected in the bullwhip cells until E15. Although glucagon peptide is not present during early stages of retinal development, we detected mRNA for glucagon receptor beginning at E7 and mRNA for GLP1 receptor at E5 through E14. Morphological differentiation of the bullwhip cells begins at about E14 and is completed by E18. The bullwhip cells are greatly overproduced, and nearly 80% of these cells undergo apoptotic cell death during late stages of embryonic development. The bullwhip cells that survive are those that project an axon-like process directly toward the CMZ; the cells that project in an inappropriate direction fail to survive. We conclude that cells fated to become bullwhip neurons are generated long before they begin to differentiate and that their survival depends on the orientation of their primary neurite.
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PMID:Development of bullwhip neurons in the embryonic chicken retina. 1753 34

Epithelial/ectodermal plug formation in the developing nose, ear, and eye regions is followed by canalization/recanalization mediated by cell death. However, the mechanism is not well understood. Recently, substance P (SP)-mediated cell death, rather than cell apoptosis, has been reported in neuronal and non-neuronal cells. Horizontal paraffin sections of 5 human fetuses at 15-16 weeks of gestation were used to examine the entire area of the nose, ear, eye and perineum with immunohistochemistry for SP and its receptor neurokinin-1 (NK-1), and protein gene product (PGP) 9.5 and S100 protein to identify whether the positive cells had neural origins. The deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling (TUNEL) method was also conducted to identify apoptosis. Four SP antibodies were commercially obtained and compared the results. In addition, using the same antibodies for SP, those results were compared with fetal mouse heads (E14-17). Substance P immunoreactivity of one of the 4 antibodies (sc9758) was clearly found in the nasal plug, the epithelium of the anterior nasal cavity, the entire excretory tear duct, the marginal palpebral conjunctiva, the auditory meatal plug, the parotid duct, the external urethral orifice and, the preputial lamella along the future prepuce. Immunoreactivity was usually seen in enlarged round cells in humans. In fetal mouse heads, in spite of negative reaction in all these sites, the midline epithelial seam at the palate fusion and the oral epithelium especially at and near the tooth germ specifically reacted with the sc9758. Nevertheless, the other 3 antibodies did not react at any of those sites both in human and mouse fetuses. NK-1 receptor-positive cells were seen in the nose and meatal plugs and preputial lamella, but not in the tear duct. S100 protein, PGP 9.5, and TUNEL method all demonstrated negative reactivity at any sc9758-positive sites. Consequently, the present immunoreactivity of the sc9758 antibody seemed to be false positive, but it was likely to react with a specific substance in the epithelial or ectodermal cell because of the clearly restricted staining. Which substance it crossed remains unknown.
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PMID:False positive reactivity of a substance P-antibody in the ectodermal/epithelial plug of the nose, ear, eye and perineum of the human and mouse fetuses. 2088 65


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