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  • Mu and delta opioid receptor immunoreactivity and mu receptor regulation in brainstem cells cultured from late fetal and early postnatal rats. 15013624

    Cultured cells from the rat brainstem were used to study opioid receptor (OpR) expression during late fetal and early postnatal development. Mu and delta opioid receptor (MOR and DOR) expression was investigated from embryonic day 16 (E16) to 6 days postnatal (P6). Postnatal neurons showed more intense MOR immunoreactivity (IR) than neurons cultured from fetal brainstem (P 0.006). DOR IR showed a similar pattern, but the differences between fetal and neonatal animals were not statistically significant. Using confocal microscopy, MOR and DOR IR were shown to be present on both the cell membrane and within the cytoplasm, in a similar pattern to the IR seen in SH-SY5Y neuroblastoma cells that endogenously express both MOR and DOR. Double-labeling experiments demonstrated colocalization of MOR and DOR in the same brainstem neurons; however, not all MOR IR regions of a single neuron were also positively stained for DOR, and not all DOR IR regions were also positive for MOR. MOR was down-regulated after a 1- or 2-h treatment with 1 microM DAMGO, a potent mu opioid agonist, in both non-transfected and MOR-transfected SH-SY5Y cells and in primary cell cultures. It was concluded that many brainstem neurons express functional MOR or DOR or coexpress both receptors, although intracellular distributions of the receptors are unique for each receptor type.
    Document Type:
    Reference
    Product Catalog Number:
    AB1774
  • Delta Protocadherin 10 is Regulated by Activity in the Mouse Main Olfactory System. 21897809

    Olfactory sensory neurons (OSNs) are thought to use activity-dependent and independent mechanisms to regulate the expression of axon guidance genes. However, defining the molecular mechanisms that underlie activity-dependent OSN guidance has remained elusive. Only a handful of genes have been identified whose expression is regulated by activity. Interestingly, all of these genes have been shown to play a role in OSN axon guidance, underscoring the importance of identifying other genes regulated by activity. Furthermore, studies suggest that more than one downstream mechanism regulates target gene expression. Thus, both the number of genes regulated by activity and how many total mechanisms control this expression are not well understood. Here we identify delta protocadherin 10 (pcdh10) as a gene regulated by activity. Delta protocadherins are members of the cadherin superfamily, and pcdh10 is known to be important for axon guidance during development. We show pcdh10 is expressed in the nasal epithelium and olfactory bulb in patterns consistent with providing guidance information to OSNs. We use naris occlusion, genetic manipulations, and pharmacological assays to show pcdh10 can be regulated by activity, consistent with activation via the cyclic nucleotide-gated channel. Transgenic analysis confirms a potential role for pcdh10 in OSN axon guidance.
    Document Type:
    Reference
    Product Catalog Number:
    06-519
    Product Catalog Name:
    Anti-phospho-CREB (Ser133) Antibody
  • delta(9)-Tetrahydrocannabinol increases nerve growth factor production by prostate PC-3 cells. Involvement of CB1 cannabinoid receptor and Raf-1. 11168391

    Cannabinoids, the active components of marihuana, exert a variety of effects in humans. Many of these effects are mediated by binding to two types of cannabinoid receptor, CB1 and CB2. Although CB1 is located mainly in the central nervous system, it may also be found in peripheral tissues. Here, we study the effect of cannabinoids in the production of nerve growth factor by the prostate tumor cell line PC-3. We show that addition of Delta(9)-tetrahydrocannabinol to PC-3 cells stimulated nerve growth factor production in a dose-dependent and time-dependent manner. Maximal effect was observed at 0.1 microM Delta(9)-tetrahydrocannabinol and 72 h of treatment. Stimulation was reversed by the CB1 antagonists AM 251 and SR 1411716A. Pre-treatment of cells with pertussis toxin also prevented the effect promoted by Delta(9)-tetrahydrocannabinol. These results indicate that Delta(9)-tetrahydrocannabinol stimulation of nerve growth factor production in these cells was mediated by the cannabinoid CB1 receptor. The implication of Raf-1 activation in the mode of action of Delta(9)-tetrahydrocannabinol is also suggested.
    Document Type:
    Reference
    Product Catalog Number:
    MAB5260-60UG
    Product Catalog Name:
    Anti-Nerve Growth Factor Antibody, clone 27/21
  • DELTA OPIOID RECEPTOR358-372 -2637145

    Document Type:
    Certificate of Analysis
    Lot Number:
    2637145
    Product Catalog Number:
    AG334
    Product Catalog Name:
    Opioid Receptor, δ 358-372, control peptide for AB5505
  • DELTA OPIOID RECEPTOR 358-372 - 3978229

    Document Type:
    Certificate of Analysis
    Lot Number:
    3978229
    Product Catalog Number:
    AG334
    Product Catalog Name:
    Opioid Receptor, δ 358-372, control peptide for AB5505
  • Delta 9-tetrahydrocannabinol suppresses vomiting behavior and Fos expression in both acute and delayed phases of cisplatin-induced emesis in the least shrew. 18721829

    Cisplatin chemotherapy frequently causes severe vomiting in two temporally separated clusters of bouts dubbed the acute and delayed phases. Cannabinoids can inhibit the acute phase, albeit through a poorly understood mechanism. We examined the substrates of cannabinoid-mediated inhibition of both the emetic phases via immunolabeling for serotonin, Substance P, cannabinoid receptors 1 and 2 (CB(1), CB(2)), and the neuronal activation marker Fos in the least shrew (Cryptotis parva). Shrews were injected with cisplatin (10mg/kg i.p.), and one of vehicle, Delta(9)-THC, or both Delta(9)-THC and the CB(1) receptor antagonist SR141716A (2mg/kg i.p.), and monitored for vomiting. Delta(9)-THC-pretreatment caused concurrent decreases in the number of shrews expressing vomiting and Fos-immunoreactivity (Fos-IR), effects which were blocked by SR141716A-pretreatment. Acute phase vomiting induced Fos-IR in the solitary tract nucleus (NTS), dorsal motor nucleus of the vagus (DMNX), and area postrema (AP), whereas in the delayed phase Fos-IR was not induced in the AP at all, and was induced at lower levels in the other nuclei when compared to the acute phase. CB(1) receptor-IR in the NTS was dense, punctate labeling indicative of presynaptic elements, which surrounded Fos-expressing NTS neurons. CB(2) receptor-IR was not found in neuronal elements, but in vascular-appearing structures. All areas correlated with serotonin- and Substance P-IR. These results support published acute phase data in other species, and are the first describing Fos-IR following delayed phase emesis. The data suggest overlapping but separate mechanisms are invoked for each phase, which are sensitive to antiemetic effects of Delta(9)-THC mediated by CB(1) receptors.
    Document Type:
    Reference
    Product Catalog Number:
    AB5636P
    Product Catalog Name:
    Anti-Cannabinoid Receptor 1 Antibody, NT
  • delta Opioid receptor subtypes activate inositol-signaling pathways in the production of antinociception. 9580632

    To analyze the selectivity of delta receptor subtypes to regulate different classes of G proteins, the expression of the alpha-subunits of Gi2, Gi3, Go1, Go2, Gq and G11 transducer proteins was reduced by administration of oligodeoxynucleotides (ODNs) complementary to sequences in their respective mRNAs. Mice receiving antisense ODNs to Gi2 alpha, Gi3 alpha, Go2 alpha and G11 alpha subunits showed an impaired antinociceptive response to all the delta agonists evaluated. An ODN to Go1 alpha specifically blocked the antinociceptive effect of the agonist of delta-1 receptors, [D-Pen2,5]enkephalin (DPDPE), without altering the activity of [D-Ala2]deltorphin II or [D-Ser2]-Leu-enkephalin-Thr (DSLET). In mice treated with an ODN to Gq alpha, the effects of the agonists of delta-2-opioid receptors were reduced, but not those of DPDPE. Thus, Go1 proteins are selectively linked to delta-1-mediated analgesia, and Gq proteins are related to delta-2-evoked antinociception. After impairing the synthesis of Go1 alpha subunits, DPDPE exhibited an antagonistic activity on the antinociception produced by [D-Ala2]deltorphin II. After treatment with ODNs complementary to sequences in Gq alpha or PLC-beta 1 mRNAs, the analgesic capacity of [D-Ala2]deltorphin II was diminished. However, the delta-2-agonist did not alter the antinociceptive activity of DPDPE. An ODN complementary to nucleotides 7 to 26 of the murine delta receptor reduced the analgesic potency of [D-Ala2]deltorphin II, but not that observed for DPDPE. In these mice, [D-Ala2]deltorphin II did not antagonize the effect of DPDPE. These results suggest the existence of different molecular forms of the delta opioid receptor, and the involvement of inositol-signaling pathways in the supraspinal antinociceptive effects of delta agonists.
    Document Type:
    Reference
    Product Catalog Number:
    05-164
    Product Catalog Name:
    Anti-PLCβ-1 Antibody
  • PKC delta, active - 25473CU

    Document Type:
    Certificate of Analysis
    Lot Number:
    25473CU
    Product Catalog Number:
    14-504
    Product Catalog Name:
    PKCδ Protein, active, 10 µg