S I Walaas
Affiliation: University of Oslo
- Modulation of calcium-evoked [3H]noradrenaline release from permeabilized cerebrocortical synaptosomes by the MARCKS protein, calmodulin and the actin cytoskeletonS 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...
- Regulation of calcium-dependent [3H]noradrenaline release from rat cerebrocortical synaptosomes by protein kinase C and modulation of the actin cytoskeletonS 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...
- Decrease in phorbol ester-induced potentiation of noradrenaline release in synapsin I-deficient miceS 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...
- Intracerebroventricular administration of quinolinic acid induces a selective decrease of inositol(1,4,5)-trisphosphate receptor in rat brainL 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...
- Synapsin-dependent development of glutamatergic synaptic vesicles and presynaptic plasticity in postnatal mouse brainI 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....
- Non-dioxin-like PCBs inhibit [(3)H]WIN-35,428 binding to the dopamine transporter: a structure-activity relationship studyM 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. ..
- Degradation of the type I inositol 1,4,5-trisphosphate receptor by caspase-3 in SH-SY5Y neuroblastoma cells undergoing apoptosisL 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...
- Mechanisms of penitrem-induced cerebellar granule neuron death in vitro: possible involvement of GABAA receptors and oxidative processesH 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...
- Calcium/phospholipid-dependent protein kinases in rat Sertoli cells: regulation of androgen receptor messenger ribonucleic acidA 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...
- Ultrastructural quantification of glutamate receptors at excitatory synapses in hippocampus of synapsin I+II double knock-out miceS 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....
- Decreased inositol (1,4,5)-trisphosphate receptor levels in Alzheimer's disease cerebral cortex: selectivity of changes and possible correlation to pathological severityL 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...
- Developmental regulation of two isoforms of Ca(2+)/calmodulin-dependent protein kinase I beta in rat brainO 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...
- 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 domainS 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...