Identification of polymorphic microsatellite loci in the formosan subterranean termite Coptotermes formosanus Shiraki.
Explore the source record for details and available documents.
Alleles↗
Biomedical subjects
G Henderson
Publications and source records attributed to G Henderson.
A Ras protein from a phytopathogenic fungus causes defects in hyphal growth polarity, and induces tumors in mice.
Ras is a low-molecular-weight guanine nucleotide (GDP/GTP)-binding protein that transduces signals for growth and differentiation in eukaryotes. In mammals, the importance of Ras in regulating growth is underscored by the observation that activating mutations in ras genes are found in many animal tumors. Colletorichum trifolii is a filamentous fungal pathogen of alfalfa which causes anthracnose disease. To investigate signaling pathways that regulate growth and development in this fungus, a gene encoding a Ras homolog (CT-Ras) was cloned from C. trifolii. CT-Ras exhibited extensive amino acid similarity to Ras proteins from higher and lower eukaryotes. A single amino acid change resulting in mutationally activated CT-Ras induced cellular transformation of mouse (NIH 3T3) fibroblasts and tumor formation in nu/nu mice. In Colletotrichum, mutationally activated CT-Ras induced abnormal hyphal proliferation and defects in polarized growth, and significantly reduced differentiation in a nutrient-dependent manner. These results show that C. trifolii Ras is a functional growth regulator in both mammals and fungi, and demonstrate that proper regulation of Ras is required for normal fungal growth and development.
3T3 Cells↗
The latency-related gene of bovine herpesvirus 1 inhibits programmed cell death.
Although viral gene expression occurs in the peripheral nervous system during acute infection, bovine herpesvirus 1 (BHV-1) gene expression is extinguished, many neurons survive, and latency ensues. The only abundant viral transcript expressed during latency is the latency-related (LR) RNA, which is alternatively spliced in trigeminal ganglia during acute infection (L. Devireddy and C. Jones, J. Virol. 72:7294-7301, 1998). A subset of neurons express a protein encoded by the LR gene and the LR protein (LRP) is associated with cyclin-dependent kinase 2 (Cdk2)/cyclin complexes during productive infection (Y. Jiang, A. Hossain, M. T. Winkler, T. Holt, A. Doster, and C. Jones, J. Virol. 72:8133-8142, 1998). LR gene products inhibit cell cycle progression, perhaps as a result of LRP interacting with Cdk2/cyclin complexes. During acute infection, expression of cyclin A occurs in trigeminal ganglionic neurons (L. M. Schang, A. Hossain, and C. Jones, J. Virol. 70:3807-3814, 1996). Inappropriate expression of G(1)- and S-phase cyclins can initiate programmed cell death (PCD), apoptosis, in neurons, suggesting that LR gene products inhibit PCD. To test this hypothesis, we modified an assay to measure PCD frequency in transiently transfected cells. C(6)-ceramide, fumonisin B(1) (FB(1)), or etoposide was used to initiate PCD following transfection of cells with plasmids expressing LR gene products and the beta-galactosidase gene. Transfected cells that survived were quantified by counting beta-galactosidase-positive cells. Plasmids that expressed LR gene products promoted survival of monkey kidney (CV-1), human lung (IMR-90), or mouse neuroblastoma (neuro-2A) cells after induction of PCD. Plasmids with termination codons at the beginning of LR open reading frames or deletion of sequences that mediate splicing of LR RNA did not promote cell survival following PCD induction. We hypothesize that LR gene products play a role in promoting survival of postmitotic neurons during acute infection or reactivation.
Animals↗
Telomerase activity and prognosis in primary breast cancers.
PURPOSE: Recent studies associate telomerase activity with prognostic factors and survival. We compared quantitative telomerase activity in primary tumors with traditional prognostic factors and outcome in a group of invasive but nonmetastatic breast cancers. PATIENTS AND METHODS: Telomerase activity was measured in 203 invasive breast cancers by the quantitative telomeric repeat amplification protocol method. Telomerase expression was compared with 28S rRNA level, tumor content, and clinical variables, including outcome. For clinical correlations, telomerase activity was standardized by two methods: (1) a correction for cellularity using 28S rRNA levels, and (2) a correction for the histologically determined invasive proportion of the specimen. RESULTS: Telomerase activity was found in 82% of breast cancers with measurable 28S rRNA levels. Telomerase activity was associated with the proliferative index (P <.01) of the tumor but not with any other prognostic variable. Neither uncorrected nor corrected telomerase activity was associated with relapse-free or overall survival in this study. CONCLUSION: Telomerase activity level was associated with the proliferative index of invasive breast cancers, but its measurement in samples from this group of nonmetastatic breast cancer patients did not predict survival.
Adult↗
Identification of c-myc promoter-binding protein and X-box binding protein 1 as interleukin-6 target genes in human multiple myeloma cells.
Interleukin-6 (IL-6) is implicated in the in vivo proliferation of malignant plasma cells in multiple myeloma. To define the molecular basis of the IL-6-induced mitogenic response in myeloma cells, we applied STAR (subtractive transcriptional amplification of mRNA), a new differential expression analysis technology, to isolate mRNAs preferentially expressed in IL-6-treated versus untreated cultures of the factor-responsive myeloma cell line U266. From the resulting collection of STAR clones, sequence information was obtained for a total of 72 distinct transcripts. Of these, 29 were found to correspond to known genes, 22 matched expressed sequence tags in public databases and 21 showed no sequence similarity to any existing entries. Among the known genes uncovered in the screen were those encoding proteins that function in cell division, cell signalling and gene/protein expression. Northern blot analysis documented that two transcription factor genes chosen for further study, c-myc promoter-binding protein (MBP-1) and X-box binding protein 1 (XBP-1), were up-regulated in U266 cells about 3-fold relative to the cell cycle-dependent beta-actin gene 12 h after IL-6 treatment. Both genes were also similarly up-regulated by IL-6 in factor-dependent ANBL-6 myeloma cells. These results indicate that MBP-1 and XBP-1 are IL-6 genes in myeloma cells; as such, they may play a role in IL-6-mediated growth control in multiple myeloma.
Base Sequence↗
Somatostatin receptor desensitization in NG108-15 cells. A consequence of receptor sequestration.
In NG108-15 cells inhibition of both N-type calcium channel current and adenylyl cyclase by somatostatin (SRIF) was not sustained but rapidly desensitized in the continued presence of the drug. The degree and rate of desensitization were concentration-dependent, and the desensitization was homologous with respect to the delta-opioid receptor. We have been unable to obtain evidence for the involvement of G protein-coupled receptor kinases (GRKs) in this desensitization. SRIF-induced desensitization of N-type calcium channel currents was not reduced in cells stably overexpressing a dominant negative mutant of GRK2 or following intracellular dialysis with GRK2- and GRK3-blocking peptides or with heparin. Inhibitors of protein kinase A, protein kinase C, and protein kinase G were also without effect. In contrast, both the rate and degree of SRIF-induced desensitization were reduced by pretreatment with phenylarsine oxide or concanavalin A, both inhibitors of receptor endocytosis. Furthermore, SRIF-induced desensitization was enhanced by monensin, which prevents receptor recycling back to the plasma membrane. Similarly, SRIF-induced desensitization of adenylyl cyclase inhibition was not reduced in cells stably overexpressing dominant negative mutant GRK2 but was reduced in cells pretreated with the receptor endocytosis inhibitor hyperosmotic sucrose or concanavalin A. These data are consistent with the view that SRIF-induced desensitization in NG108-15 cells results from receptor internalization.
Adenylyl Cyclase Inhibitors↗
Hyperpolarization-activated cationic currents (Ih) in neurones of the trigeminal mesencephalic nucleus of the rat.
1. We studied the voltage-dependent current activated by membrane hyperpolarization in sensory proprioceptive trigeminal mesencephalic nucleus (MNV) neurones. 2. Membrane hyperpolarization (from -62 to -132 mV in 10 mV steps) activated slowly activating and non-inactivating inward currents. The hyperpolarization-activated currents could be described by activation curves with a half-maximal activation potential (V ) of -93 mV, slope (k) of 8.4 mV, and maximally activated currents (Imax) of around 1 nA. The reversal potential of the hyperpolarization-activated currents was -57 mV. 3. Extracellular Cs+ blocked hyperpolarization-activated currents rapidly and reversibly in a concentration-dependent manner with an IC50 of 100 microM and Hill slope of 0.8. ZD7288 (1 microM; 4-(N-ethyl-N-phenylamino)-1,2-dimethyl-6-(methylamino) pyridinium chloride), the compound developed as an inhibitor of the cardiac hyperpolarization-activated current (If), also blocked the hyperpolarization-activated currents in MNV neurones. Extracellular Ba2+ (1 mM) did not affect hyperpolarization-activated currents. We tested whether the hyperpolarization-activated currents contribute to the somatic membrane properties of MNV neurones by performing some experiments using current-clamp recording. In such experiments application of Cs+ (1 mM) produced no effect on neuronal resting membrane potentials. 4. During the course of our experiments we noticed that activating ATP-gated non-selective cation channels (P2X receptors) caused an inhibition of Ih associated with a V shift of 10 mV in the hyperpolarizing direction. This P2X receptor-mediated inhibition of Ih was blocked in recordings made with the rapid calcium chelator BAPTA (11 mM) in the pipette solution. 5. We conclude that the current activated by membrane hyperpolarization in MNV neurones is Ih on the basis of its similarity to Ih observed in other neuronal preparations. Activation of Ih can account for the anomalous time-dependent inward rectification that has previously been described in MNV neurones.
Animals↗
Glycine and GABAA receptor-mediated synaptic transmission in rat substantia gelatinosa: inhibition by mu-opioid and GABAB agonists.
1. Bicuculline-sensitive and strychnine-sensitive inhibitory postsynaptic currents (IPSCs) could be evoked in neurones of the rat substantia gelatinosa of the spinal trigeminal nucleus pars caudalis. 2. Spontaneous tetrodotoxin (TTX)-insensitive-mediated miniature IPSCs (mIPSCs) blocked by strychnine or bicuculline were also present in many neurones. The decay of the glycine receptor-mediated mIPSCs was fitted by a single exponential, whereas the decay of the GABAA receptor-mediated mIPSCs could in some instances be fitted by a single exponential, but in other instances required two exponentials. 3. An increase in baseline current noise developed during the course of the recording. This noise was abolished by strychnine (1 microM) but was insensitive to bicuculline (10 microM), TTX (0.5 microM), [D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin (DAMGO, 1 microM) or baclofen (30 microM). The single-channel conductance underlying the noise was estimated to be 21 pS. 4. The mu-opioid agonist DAMGO (1-10 microM) reduced the amplitude of the evoked glycine receptor-mediated IPSC and the evoked GABAA receptor-mediated IPSC. The mu-opioid antagonist D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP, 1 microM) reversed the DAMGO inhibition. 5. The GABAB agonist baclofen (30 microM) reduced the amplitude of the evoked glycine receptor-mediated IPSC and the GABAA receptor-mediated IPSC. The inhibition was reversed by the selective GABAB antagonist 3-N[1-(S)-(3,4-dichlorophenyl)ethyl]amino- 2-(S)-hydroxypropyl-P-benzyl-phosphinic acid (CGP 55845A, 1 microM). 6. Both DAMGO and baclofen reduced the frequency of glycine and GABAA receptor-mediated mIPSCs without affecting average amplitude, and increased the percentage of failures of the evoked glycine and GABAA receptor-mediated IPSCs, suggesting a presynaptic site of action.
Analgesics, Opioid↗
NHS performance tables for breast screening.
Explore the source record for details and available documents.
Breast Neoplasms↗
Antioxidant transport by the human placenta.
We investigated the transfer of three antioxidants - melatonin, S-adenosyl methionine (SAM) and various forms of vitamin E - across the term, normal human placenta. The transport technique involved the single, isolated placental cotyledon system in vitro. Melatonin crossed the placental rapidly, equally to the freely diffusible marker, antipyrine. There was no biotransformation of the agent. SAM was transferred slowly, similarly to passively transported L-glucose as a marker. There was a breakdown of SAM to at least one other derivative; the process appeared to be nonenzymatic. Vitamin E was transferred slowly, at a rate only 10% of L-glucose. The natural RRR (nonracemic) form of vitamin E was transported best. Free vitamin, rather than the acetate seems to be transferred best, a finding that will require further study.
Antioxidants↗
The health insurance puzzle: a new approach to assessing patient coverage preferences.
Previous studies of preferences for health insurance benefits have required individuals to make a series of complex and repetitive decisions, and have assumed that all insured benefits are desirable. This study reports the development and testing of a simple, innovative instrument to measure preferences for health insurance benefits. The newly developed instrument (Puzzle) is designed to allow subjects to select health benefits in a way that underscores the trade-offs dictated by budgets and costs. A "puzzle-like" frame representing budget constraints and "puzzle piece" benefit cards proportionately sized to represent the premium price of a single year's coverage comprise the instrument. In a comparison procedure (Money Game), participants "purchase" individual benefits by exchanging "play" money for benefit tokens. The Puzzle's utility was assessed by examining the convergence of results from both instruments and the subject's ratings of and preference for the instruments. One hundred five elderly Medicare enrollees seen in the general Internal Medicine outpatient clinic of a major southeastern teaching hospital were interviewed. Subjects answered interviewer-administered questionnaires and completed both the Puzzle and the Money Game. Both McNemar's test and Kendall's tau-b indicated a high degree of concordance between benefit choices made using the two instruments. Descriptive statistics demonstrated that the Puzzle was clear, easy to use, understandable, and preferred to the Money Game. The results suggest that the Puzzle is a promising tool for assessing health insurance coverage preferences under circumstances of limited expenditures, which can be modified for use with various populations who face limited insurance benefits.
Aged↗
ATP receptor-mediated enhancement of fast excitatory neurotransmitter release in the brain.
ATP-gated cation channels (P2X receptors) exist on the soma of proprioceptive neurons in the trigeminal mesencephalic nucleus (MNV) in the brain stem. However, these pseudomonopolar neurons seem to receive no synaptic input to their soma; we therefore hypothesized that in MNV neurons, the P2X receptors of importance may be those located on their central terminal projections. Here, we show in trigeminal mesencephalic motor nucleus neurons, which receive their major input from the MNV, that both exogenous ATP (1 mM) and high frequency focal stimulation to evoke endogenous ATP release enhanced the frequency of spontaneous fast excitatory postsynaptic currents (EPSCs) with no change in their amplitude. The enhancement was reduced by the antagonists suramin (300 microM) and pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid (30 microM) and persisted when action potential conduction was blocked with tetrodotoxin (1 microM). Thus, functional P2X receptors are expressed on nerve terminals in the brain stem, where they increase the spontaneous release of glutamate onto trigeminal mesencephalic motor nucleus neurons.
Adenosine Triphosphate↗
Antinociceptive and morphine modulatory actions of spinal orphanin FQ.
Orphanin FQ (nociceptin, OFQ), a hepatdecapeptide peptide, has been designated as an endogenous ligand at the orphan receptor ORL1, which lacks affinity for opioid receptor ligands. OFQ-like immunoreactivity has been localized in spinal cord areas that are involved in the processing of nociceptive signals. In this study, the effects of spinally administered OFQ on thermal and mechanical nociceptive stimuli were investigated following intrathecal (i.t.) injection in unanesthetized rats bearing chronic indwelling catheters in the subarachnoid space. Intrathecal OFQ produced two distinct acute actions: an opioid-like antinociceptive effect, and antagonism of morphine-induced antinociception. Chronic administration produces tolerance. Acute actions were as follows. First, injection of OFQ alone in the dose range 10-100 nmol produced sustained antinociceptive effects in the tail-flick (baseline latency 1.5-2 s) and paw-pressure tests. These effects peaked at 45-60 min post-injection, were fully reversible, and were observed in absence of discernable motor impairments. Intrathecal naloxone (5 nmol) significantly attenuated the antinociceptive effects of OFQ (50 nmol i.t.) in tail-flick and paw-pressure tests. A 24-h pretreatment with the irreversible opioid receptor antagonist, beta-flunatrexamine (2 nmol i.t.), also attenuated the antinociceptive effects of OFQ (50, 100 nmol i.t.) and of morphine (7.5 nmol i.t.) in both tests. Low doses (1, 5 nmol) of OFQ, which failed to produce antinociception in the tail-flick test involving a baseline latency of 1.5-2 s, produced a strong antinociceptive response when the baseline latency was increased to 5-6 s. Second, intrathecal OFQ, at doses (0.5, 1.0, and 5.0 nmol) that had no antinociceptive activity in the tail-flick (baseline latency 1.5-2 s) and paw-pressure tests, attenuated the antinociceptive effect of morphine (7.5 nmol i.t.) in these tests. However, a threshold OFQ dose (10 nmol) significantly extended the duration of antinociception induced by morphine (7.5 nmol i.t.) or deltorphin (20 nmol i.t.). Chronic actions were as follows. In rats that were rendered tolerant to spinal morphine, by a continuous intrathecal infusion (7.5 nmol/h) of the agonist for 5 days, the OFQ dose-response curves for its antinociceptive effect in the tail-flick and paw-pressure tests were significantly shifted to the right. In separate experiments, repeated intrathecal injection of OFQ (50 nmol) or morphine (7.5 nmol) produced a significant decline in their antinociceptive effects. Thus, intrathecally administered OFQ produces both development of tolerance to its antinociceptive actions and cross-tolerance to the action of morphine.
Analgesia↗
ATP-gated cation channels (P2X purinoceptors) in trigeminal mesencephalic nucleus neurons of the rat.
1. We have investigated whether receptors for ATP exist on neurones of the trigeminal mesencephalic nucleus (MNV) of the rat using whole-cell and outside-out patch-clamp recording in coronal brainstem slices. 2. With whole-cell recording, the batch application of ATP, adenosine 5'-O-[3-thiotriphosphate] (ATP gamma S) and alpha,beta methylene adenosine triphosphate (alpha beta meATP) caused concentration-dependent inward currents in all cells tested (holding potential, -62 mV), with EC50 values of 437, 15 and 254 microM, respectively. All three agonist-evoked currents developed rapidly (rise time, approximately 10-25 s), desensitized slowly (over approximately 20-50 s), cross-desensitized with each other, were associated with an increase in membrane conductance and were attenuated by the application of suramin (30 microM). 3. The inward current evoked by ATP decreased as the membrane potential was made less negative and had a zero current potential of +1.0 +/- 3.7 mV. The current-voltage relationship showed marked inward rectification. 4. Brief flickery single-channel openings could be resolved in response to ATP (3 microM) in outside-out membrane patches. Unitary current at -82 mV was -1.81 +/- 0.2 pA, which corresponds to a unitary conductance of 22 pS. 5. We conclude that proprioceptive MNV neurones contain ATP-gated cation channels. Such P2X purinoceptors may be involved in the processing of proprioceptive information, thus suggesting a potentially important physiological role of ATP.
Adenosine Triphosphate↗
delta-opioid receptor mobilization of intracellular calcium in SH-SY5Y cells: lack of evidence for delta-receptor subtypes.
delta-opioid receptor agonists mobilize intracellular Ca2+([Ca2+]i) in SH-SY5Y cells when applied in the presence of muscarinic agonists. The putative delta 1 receptor agonist [D-Pen2,D-Pen5]-enkephalin (DPDPE) elevated [Ca2+]i with an EC50 of 11 nM and the putative delta 2 agonist deltorphin II elevated [Ca2+]i, with an EC50 of 14 nM. The maximal elevations of [Ca2+]i caused by both agonists were not different, nor were maximally effective concentrations of DPDPE (1 microM) and deltorphin II (1 microM) applied together more effective than either agonist applied alone. The elevations of [Ca2+]i caused by DPDPE (1 microM) and deltorphin II (1 microM), in the presence of carbachol, desensitized rapidly with continued opioid exposure and the cross-desensitization between PDPDE and deltorphin II was complete. The putative delta 1 selective antagonist 7-benzylidenenaltrexone (BNTX) and the putative delta 2 selective antagonist naltriben both reduced the elevations of [Ca2+]i caused by DPDPE (30 nM) and deltorphin II (10 nM), by greater than 50% at concentrations of less than 10 nM. In SH-SY5Y cells delta-receptor mediated elevation of [Ca2+]i is mediated by a population of receptors, which does not discriminate between agonists and antagonists purportedly selective for delta 1 or delta 2 receptors.
Animals↗
Bradykinin inhibition of N- and L-type calcium channel currents in NG108-15 cells.
The bradykinin regulation of calcium channel currents in NG108-15 neuroblastoma x glioma hybrid cells was examined, in order to determine: (1) which type of bradykinin receptors mediates the inhibition of N-type calcium channels in these cells; and (2) whether bradykinin can modulate other types of calcium channels in these cells. Bradykinin inhibited both N- and L-type calcium channels in NG108-15 cells, with EC50S of 10 +/- 2 nM and 29 +/- 7 nM, respectively. The inhibition of both L- and N-type calcium channels by bradykinin (100 nM) could be completely inhibited by the bradykinin B2 receptor antagonist Hoe 140 (10 nM). Bradykinin appeared to inhibit that portion of the L-type calcium channel current that was also reversibly inhibited by omega-conotoxin GVIA. The bradykinin inhibition of the L-type calcium channel current was partly reduced by pretreatment of the cells with pertussis toxin, whereas the inhibition of the N-type current was pertussis toxin-insensitive. In some cultures it was observed that the bradykinin B1 receptor agonist desArg9bradykinin inhibited the L-type calcium channel current.
Bradykinin↗
Neuropeptide Y Y2 receptor and somatostatin sst2 receptor coupling to mobilization of intracellular calcium in SH-SY5Y human neuroblastoma cells.
1. In this study we have investigated neuropeptide Y (NPY) and somatostatin (SRIF) receptor-mediated elevation of intracellular Ca2+ concentration ([Ca2+]i) in the human neuroblastoma cell line SH-SY5Y. 2. The Ca(2+)-sensitive dye fura 2 was used to measure [Ca2+]i in confluent monolayers of SH-SY5Y cells. Neither NPY (30-100 nM) nor SRIF (100 nM) elevated [Ca2+]i when applied alone. However, when either NPY (300 pM-1 microM) or SRIF (300 pM-1 microM) was applied in the presence of the cholinoceptor agonist carbachol (1 microM or 100 microM) they evoked an elevation of [Ca2+]i above that caused by carbachol alone. 3. The elevation of [Ca2+]i by NPY was independent of the concentration of carbachol. In the presence of 1 microM or 100 microM carbachol NPY elevated [Ca2+]i with a pEC50 of 7.80 and 7.86 respectively. 4. In the presence of 1 microM carbachol the NPY Y2 selective agonist peptide YY(3-36) (PYY(3-36)) elevated [Ca2+]i with a pEC50 of 7.94, the NPY Y1 selective agonist [Leu31, Pro34]-NPY also elevated [Ca2+]i when applied in the presence of carbachol, but only at concentrations > 300 nM. The rank order of potency, PYY(3-36) > or = NPY > > [Leu31, Pro34]-NPY indicates that an NPY Y2-like receptor is involved in the elevation of [Ca2+]i. 5. In the presence of 1 microM carbachol, SRIF elevated [Ca2+]i with a pEC50 of 8.24. The sst2 receptor-preferring analogue BIM-23027 (c[N-Me-Ala-Tyr-D-Trp-Lys-Abu-Phe]) elevated [Ca2+]i with a pEC50 of 8.63, and the sst5-receptor preferring analogue L-362855 (c[Aha-Phe-Trp-D-Trp-Lys-Thr-Phe]) elevated [Ca2+]i with a pEC50 of approximately 6.1. Application of the sst3 receptor-preferring analogue BIM-23056 (D-Phe-Phe-Tyr-D-Trp-Lys-Val-Phe-D-Nal-NH2, 1 microM) to SH-SY5Y cells in the presence of carbachol neither elevated [Ca2+]i nor affected the elevations of [Ca2+]i caused by a subsequent coapplication of SRIF. The rank order of potency, BIM-23026 > or = SRIF > > L-362855 > > > BIM-23026 suggests that an sst2-like receptor is involved in the elevation of [Ca2+]i. 6. Block of carbachol activation of muscarinic receptors with atropine (1 microM) abolished the elevation of [Ca2+]i by the SRIF and NPY. 7. Muscarinic receptor activation, not a rise in [Ca2+]i, was required to reveal the NPY or SRIF response. The Ca2+ channel activator maitotoxin (2 ng ml-1) also elevated [Ca2+]i but subsequent application of either NPY or SRIF in the presence of maitotoxin caused no further changes in [Ca2+]i. 8. The elevations of [Ca2+]i by NPY and SRIF were abolished by pretreatment of the cells with pertussis toxin (200 ng-ml-1, 16 h). This treatment did not significantly affect the response of the cells to carbachol. 9. NPY and SRIF appeared to elevate [Ca2+]i by mobilizing Ca2+ from intracellular stores. Both NPY and SRIF continued to elevate [Ca2+]i when applied in nominally Ca(2+)-free external buffer. Thapsigargin (100 nM), an agent which discharges intracellular Ca2+ stores, also blocked the NPY and SRIF elevations of [Ca2+]i. 10. Delta-Opioid receptor agonists applied in the presence of carbachol also elevate [Ca2+]i in SH-SY5Y cells. When NPY (30 nM) or SRIF (100 nM) was applied together with a maximally effective concentration of the delta-opioid receptor agonist DPDPE ([D-Pen2,5]-enkephalin) (1 microM), the resulting elevations of [Ca2+]i were not greater than those caused by application of DPDPE alone. 11. Thus, in SH-SY5Y cells, NPY and SRIF can mobilize Ca2+ from intracellular stores via activation of NPY Y2 and sst2-like receptors, respectively. Neither NPY nor SRIF elevated [Ca2+]i when applied alone. The requirements for the elevations of [Ca2+]i by NPY and SRIF are the same as those for delta- and mu-opioid receptor and nociceptin receptor mobilization of [Ca2+]i in SH-SY5Y cells.
Brain Neoplasms↗
A new example of a morphine-sensitive neuro-effector junction: adrenergic transmission in the mouse vas deferens. 1972.
Explore the source record for details and available documents.
Adrenergic Fibers↗