S I Walaas

Summary

Affiliation: University of Oslo
Country: Norway

Publications

  1. ncbi request reprint Modulation of calcium-evoked [3H]noradrenaline release from permeabilized cerebrocortical synaptosomes by the MARCKS protein, calmodulin and the actin cytoskeleton
    S I Walaas
    Neurochemical Laboratory, Institute of Basic Medical Sciences, University of Oslo, P O Box 1115 Blindern, N 0317, Oslo, Norway
    Neurochem Int 36:581-93. 2000
  2. ncbi request reprint Regulation of calcium-dependent [3H]noradrenaline release from rat cerebrocortical synaptosomes by protein kinase C and modulation of the actin cytoskeleton
    S I Walaas
    Department Group of Basic Medical Sciences, University of Oslo, Norway
    Neurochem Int 34:221-33. 1999
  3. ncbi request reprint Decrease in phorbol ester-induced potentiation of noradrenaline release in synapsin I-deficient mice
    S I Walaas
    Neurochemical Laboratory, Institute of Basic Medical Science, University of Oslo, Oslo, Norway
    Synapse 36:114-9. 2000
  4. ncbi request reprint Intracerebroventricular administration of quinolinic acid induces a selective decrease of inositol(1,4,5)-trisphosphate receptor in rat brain
    L S Haug
    Neurochemical Laboratory, University of Oslo, Norway
    Neurochem Int 33:109-19. 1998
  5. doi request reprint Synapsin-dependent development of glutamatergic synaptic vesicles and presynaptic plasticity in postnatal mouse brain
    I L Bogen
    Department of Biochemistry, Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, P O Box 1112 Blindern, NO 0317 Oslo, Norway
    Neuroscience 158:231-41. 2009
  6. doi request reprint Non-dioxin-like PCBs inhibit [(3)H]WIN-35,428 binding to the dopamine transporter: a structure-activity relationship study
    M B Wigestrand
    Department of Biochemistry, Institute of Basic Medical Sciences, University of Oslo, NO 0316 Oslo, Norway Electronic address
    Neurotoxicology 39:18-24. 2013
  7. ncbi request reprint Degradation of the type I inositol 1,4,5-trisphosphate receptor by caspase-3 in SH-SY5Y neuroblastoma cells undergoing apoptosis
    L S Haug
    Neurochemical Laboratory, University of Oslo, Oslo, Norway
    J Neurochem 75:1852-61. 2000
  8. doi request reprint Mechanisms of penitrem-induced cerebellar granule neuron death in vitro: possible involvement of GABAA receptors and oxidative processes
    H F Berntsen
    Institute of Basic Medical Sciences, Department of Biochemistry, University of Oslo, P O Box 1112 Blindern, N 0317 Oslo, Norway
    Neurotoxicology 35:129-36. 2013
  9. ncbi request reprint Calcium/phospholipid-dependent protein kinases in rat Sertoli cells: regulation of androgen receptor messenger ribonucleic acid
    A H Ree
    Institute of Medical Biochemistry, Department of Tumor Biology, Norwegian Radium Hospital, Montebello, Oslo, Norway
    Biol Reprod 60:1257-62. 1999
  10. ncbi request reprint Ultrastructural quantification of glutamate receptors at excitatory synapses in hippocampus of synapsin I+II double knock-out mice
    S Gylterud Owe
    Department of Anatomy and Centre for Molecular Biology and Neuroscience CMBN, University of Oslo, P O Box 1105 Blindern, N0317 Oslo, Norway
    Neuroscience 136:769-77. 2005

Collaborators

Detail Information

Publications13

  1. ncbi request reprint Modulation of calcium-evoked [3H]noradrenaline release from permeabilized cerebrocortical synaptosomes by the MARCKS protein, calmodulin and the actin cytoskeleton
    S I Walaas
    Neurochemical Laboratory, Institute of Basic Medical Sciences, University of Oslo, P O Box 1115 Blindern, N 0317, Oslo, Norway
    Neurochem Int 36:581-93. 2000
    ..These results indicate that the MARCKS protein may modulate release from permeabilized noradrenergic synaptosomes, possibly by modulating calmodulin levels and/or the actin cytoskeleton...
  2. ncbi request reprint Regulation of calcium-dependent [3H]noradrenaline release from rat cerebrocortical synaptosomes by protein kinase C and modulation of the actin cytoskeleton
    S I Walaas
    Department Group of Basic Medical Sciences, University of Oslo, Norway
    Neurochem Int 34:221-33. 1999
    ..The results support the existence of two functionally distinct pools of secretory vesicles in noradrenergic CNS nerve terminals, which are regulated in distinct ways by protein kinase C and the actin cytoskeleton...
  3. ncbi request reprint Decrease in phorbol ester-induced potentiation of noradrenaline release in synapsin I-deficient mice
    S I Walaas
    Neurochemical Laboratory, Institute of Basic Medical Science, University of Oslo, Oslo, Norway
    Synapse 36:114-9. 2000
    ..These results indicate that synapsin I plays a role in regulating noradrenaline release...
  4. ncbi request reprint Intracerebroventricular administration of quinolinic acid induces a selective decrease of inositol(1,4,5)-trisphosphate receptor in rat brain
    L S Haug
    Neurochemical Laboratory, University of Oslo, Norway
    Neurochem Int 33:109-19. 1998
    ..The decrease in the level of IP3-receptor immunoreactivity appears to be selective with respect to the other proteins studied, and the IP3-receptor thus shows extreme sensitivity to QUIN neurotoxicity in the neostriatum...
  5. doi request reprint Synapsin-dependent development of glutamatergic synaptic vesicles and presynaptic plasticity in postnatal mouse brain
    I L Bogen
    Department of Biochemistry, Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, P O Box 1112 Blindern, NO 0317 Oslo, Norway
    Neuroscience 158:231-41. 2009
    ....
  6. doi request reprint Non-dioxin-like PCBs inhibit [(3)H]WIN-35,428 binding to the dopamine transporter: a structure-activity relationship study
    M B Wigestrand
    Department of Biochemistry, Institute of Basic Medical Sciences, University of Oslo, NO 0316 Oslo, Norway Electronic address
    Neurotoxicology 39:18-24. 2013
    ..Derived data correlated well with the recently derived neurotoxic equivalency factors (NEQs), indicating the generality and applicability of the NEQ scheme in risk assessments of PCBs. ..
  7. ncbi request reprint Degradation of the type I inositol 1,4,5-trisphosphate receptor by caspase-3 in SH-SY5Y neuroblastoma cells undergoing apoptosis
    L S Haug
    Neurochemical Laboratory, University of Oslo, Oslo, Norway
    J Neurochem 75:1852-61. 2000
    ..These results show that the type I IP(3) receptor is a substrate for caspase-3 in neuronal cells and indicate that apoptotic down-regulation of IP(3) receptor levels may contribute to the pathology of neurodegenerative conditions...
  8. doi request reprint Mechanisms of penitrem-induced cerebellar granule neuron death in vitro: possible involvement of GABAA receptors and oxidative processes
    H F Berntsen
    Institute of Basic Medical Sciences, Department of Biochemistry, University of Oslo, P O Box 1112 Blindern, N 0317 Oslo, Norway
    Neurotoxicology 35:129-36. 2013
    ..A disruption of calcium homeostasis and activation of the JNK pathway may also play a role in penitrem A neurotoxicity...
  9. ncbi request reprint Calcium/phospholipid-dependent protein kinases in rat Sertoli cells: regulation of androgen receptor messenger ribonucleic acid
    A H Ree
    Institute of Medical Biochemistry, Department of Tumor Biology, Norwegian Radium Hospital, Montebello, Oslo, Norway
    Biol Reprod 60:1257-62. 1999
    ..These data suggest that Sertoli cell responses to testosterone may be inhibited by a transiently active PKC with a wide intracellular distribution...
  10. ncbi request reprint Ultrastructural quantification of glutamate receptors at excitatory synapses in hippocampus of synapsin I+II double knock-out mice
    S Gylterud Owe
    Department of Anatomy and Centre for Molecular Biology and Neuroscience CMBN, University of Oslo, P O Box 1105 Blindern, N0317 Oslo, Norway
    Neuroscience 136:769-77. 2005
    ....
  11. ncbi request reprint Decreased inositol (1,4,5)-trisphosphate receptor levels in Alzheimer's disease cerebral cortex: selectivity of changes and possible correlation to pathological severity
    L S Haug
    Neurochemical Laboratory, University of Oslo, Norway
    Neurodegeneration 5:169-76. 1996
    ..These degenerative changes may in part be responsible for the disruption of Ca2+ homeostasis in AD-sensitive neurons...
  12. ncbi request reprint Developmental regulation of two isoforms of Ca(2+)/calmodulin-dependent protein kinase I beta in rat brain
    O P Løseth
    Institute of Medical Biochemistry, University of Oslo, P O Box 1112 Blindern, 0317, Oslo, Norway
    Brain Res 869:137-45. 2000
    ..Our data suggest that the two isoforms of CaM kinase I beta, created by a splicing process occurring within a week around birth, may have distinct pre- and postnatal functions in a distinct set of CNS neurons and excitable tissues...
  13. pmc Protein kinase C and cyclic AMP-dependent protein kinase phosphorylate phospholemman, an insulin and adrenaline-regulated membrane phosphoprotein, at specific sites in the carboxy terminal domain
    S I Walaas
    Neurochemical Laboratory, Institute for Basic Medical Sciences, University of Oslo, Norway
    Biochem J 304:635-40. 1994
    ..Hence, insulin and adrenaline regulate the phosphorylation of phospholemman, presumably through protein kinase C and cAMP-dependent protein kinase, respectively, on partly overlapping phosphorylation sites...