Role of the D2 dopamine receptor in molecular adaptation to chronic hypoxia in PC12 cells

[1]  B. Chronwall,et al.  Dopamine D2‐Receptor Isoforms Expressed in AtT20 Cells Inhibit Q‐Type High‐Voltage‐Activated Ca2+ Channels via a Membrane‐Delimited Pathway , 1999, Journal of neurochemistry.

[2]  C. Peers,et al.  Chronic hypoxia enhances the secretory response of rat phaeochromocytoma cells to acute hypoxia , 1999, The Journal of physiology.

[3]  L. Conforti,et al.  Chronic hypoxia reduces adenosine A2A receptor‐mediated inhibition of calcium current in rat PC12 cells via downregulation of protein kinase A , 1998, The Journal of physiology.

[4]  C. Peers,et al.  Hypoxia evokes catecholamine secretion from rat pheochromocytoma PC-12 cells. , 1998, Biochemical and biophysical research communications.

[5]  L. Conforti,et al.  Adenosine modulates hypoxia‐induced responses in rat PC12 cells via the A2A receptor , 1998, The Journal of physiology.

[6]  L. Conforti,et al.  Expression of dopamine D2 receptor in PC-12 cells and regulation of membrane conductances by dopamine. , 1997, American journal of physiology. Cell physiology.

[7]  L. Conforti,et al.  Selective inhibition of a slow‐inactivating voltage‐dependent K+ channel in rat PC 12 cells by hypoxia , 1997, The Journal of physiology.

[8]  V. E. Degtiar,et al.  Receptors couple to L‐type calcium channels via distinct Go proteins in rat neuroendocrine cell lines , 1997, The Journal of physiology.

[9]  D. Millhorn,et al.  Regulation of tyrosine hydroxylase gene expression during hypoxia: role of Ca2+ and PKC. , 1997, Kidney international.

[10]  J. Surmeier,et al.  D2 dopamine receptors reduce N-type Ca2+ currents in rat neostriatal cholinergic interneurons through a membrane-delimited, protein-kinase-C-insensitive pathway. , 1997, Journal of neurophysiology.

[11]  K. Campbell,et al.  Expression and Subunit Interaction of Voltage-Dependent Ca2+ Channels in PC12 Cells , 1996, The Journal of Neuroscience.

[12]  M. Czyzyk-Krzeska,et al.  Membrane depolarization in PC-12 cells during hypoxia is regulated by an O2-sensitive K+ current. , 1996, The American journal of physiology.

[13]  P. Erne,et al.  Involvement of protein kinase C in hypoxia-induced desensitization of the beta-adrenergic system in human endothelial cells. , 1996, Biochemical and Biophysical Research Communications - BBRC.

[14]  K. Mackie,et al.  Modulation of Ca2+ channels by G-protein βγ subunits , 1996, Nature.

[15]  S. Ikeda.  Voltage-dependent modulation of N-type calcium channels by G-protein β γsubunits , 1996, Nature.

[16]  T. Gudermann,et al.  Diversity and selectivity of receptor-G protein interaction. , 1996, Annual review of pharmacology and toxicology.

[17]  D. Clapham,et al.  Ion channel regulation by G proteins. , 1995, Physiological reviews.

[18]  E. Neer.  Heterotrimeric C proteins: Organizers of transmembrane signals , 1995, Cell.

[19]  Bertil Hille,et al.  Modulation of ion-channel function by G-protein-coupled receptors , 1994, Trends in Neurosciences.

[20]  R. Vaughan-Jones,et al.  Effects of hypoxia on membrane potential and intracellular calcium in rat neonatal carotid body type I cells. , 1994, The Journal of physiology.

[21]  M. Czyzyk-Krzeska,et al.  Hypoxia increases rate of transcription and stability of tyrosine hydroxylase mRNA in pheochromocytoma (PC12) cells. , 1994, The Journal of biological chemistry.

[22]  S. Duckles,et al.  Effect of calcium channel blockers on norepinephrine release and modulation by prejunctional D2 dopamine receptors. , 1994, Life sciences.

[23]  N. Berrow,et al.  GABAB receptor modulation of Ca2+ currents in rat sensory neurones by the G protein G(0): antisense oligonucleotide studies. , 1993, The Journal of physiology.

[24]  J. C. Stoof,et al.  Dopamine D2 receptor stimulation differentially affects voltage‐activated calcium channels in rat pituitary melanotropic cells. , 1992, The Journal of physiology.

[25]  J. Bockaert,et al.  Differential G protein-mediated coupling of D2 dopamine receptors to K+ and Ca2+ currents in rat anterior pituitary cells , 1992, Neuron.

[26]  I. Lucki,et al.  Effects of chronic treatment with selective agonists on the subtypes of dopamine receptors , 1992, Brain Research.

[27]  D. Ginty,et al.  Nerve growth factor-induced neuronal differentiation after dominant repression of both type I and type II cAMP-dependent protein kinase activities. , 1991, The Journal of biological chemistry.

[28]  J. López-Barneo,et al.  Feedback Inhibition of Ca2+ Currents by Dopamine in Glomus Cells of the Carotid Body , 1990, The European journal of neuroscience.

[29]  J. Meldolesi,et al.  Calcium channels in undifferentiated PC12 rat pheochromocytoma cells , 1989, FEBS letters.

[30]  D. Walsh,et al.  Protein kinase inhibitor-(6-22)-amide peptide analogs with standard and nonstandard amino acid substitutions for phenylalanine 10. Inhibition of cAMP-dependent protein kinase. , 1989, The Journal of biological chemistry.

[31]  D. A. Brown,et al.  Antibodies to the GTP binding protein, Go, antagonize noradrenaline-induced calcium current inhibition in NG108-15 hybrid cells , 1989, Neuron.

[32]  P. Sternweis,et al.  Differential G protein—mediated coupling of neurotransmitter receptors to Ca2+ channels in rat dorsal root ganglion neurons in vitro , 1989, Neuron.

[33]  G. Aghajanian,et al.  Evidence for G protein mediation of serotonin- and GABAB- induced hyperpolarization of rat dorsal raphe neurons , 1988, Brain Research.

[34]  J. López-Barneo,et al.  Chemotransduction in the carotid body: K+ current modulated by PO2 in type I chemoreceptor cells. , 1988, Science.

[35]  G. Schultz,et al.  Involvement of the guanine nucleotide-binding protein, No, in the inhibitory regulation of neuronal calcium channels. , 1988, Advances in second messenger and phosphoprotein research.

[36]  C. Marsden,et al.  The thermodynamics of agonist and antagonist binding to dopamine D-2 receptors. , 1986, Molecular pharmacology.

[37]  P. Molinoff,et al.  Effects of hypoxia on density of beta-adrenergic receptors. , 1981, Journal of applied physiology: respiratory, environmental and exercise physiology.

[38]  M. M. Bradford.  A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. , 1976, Analytical biochemistry.