Bjørnar Hassel

• Eide, Per Kristian; Mariussen, Espen; Uggerud, Hilde Thelle; Pripp, Are Hugo; Lashkarivand, Aslan & Hassel, Bjørnar [Vis alle 8 forfattere av denne artikkelen] (2021). Clinical application of intrathecal gadobutrol for assessment of cerebrospinal fluid tracer clearance to blood. JCI Insight. ISSN 2379-3708. 6(9), s. 1–13. doi: 10.1172/jci.insight.147063. Fulltekst i vitenarkiv
• Kildal, Emilie; Stadskleiv, Kristine; Boysen, Elin Sundby; Øderud, Tone; Dahl, Inger-Lise & Seeberg, Trine Margrethe [Vis alle 9 forfattere av denne artikkelen] (2021). Increased heart rate functions as a signal of acute distress in non-communicating persons with intellectual disability. Scientific Reports. ISSN 2045-2322. 11(1). doi: 10.1038/s41598-021-86023-6.
• Sumathipala, Dulika Sanjeewani; Strømme, Petter; Gilissen, Christian; Einarsen, Ingunn Holm; Bjørndalen, Hilde & Server, Andrés [Vis alle 10 forfattere av denne artikkelen] (2020). Sudden death in epilepsy and ectopic neurohypophysis in Joubert syndrome 23 diagnosed using SNVs/indels and structural variants pipelines on WGS data: a case report. BMC Medical Genetics. ISSN 1471-2350. 21:96, s. 1–6. doi: 10.1186/s12881-020-01024-y. Fulltekst i vitenarkiv
• Rogne, Ane Gretesdatter; Müller, Ebba Gløersen; Udnæs, Eirin; Sigurdardottir, Solrun; Raudeberg, Rune & Connelly, James Pattrick [Vis alle 8 forfattere av denne artikkelen] (2020). β-Amyloid may accumulate in the human brain after focal bacterial infection: An 18F-flutemetamol positron emission tomography study. European Journal of Neurology. ISSN 1351-5101. 28(3), s. 877–883. doi: 10.1111/ene.14622. Fulltekst i vitenarkiv
• Zhou, Yun; Eid, Tore; Hassel, Bjørnar & Danbolt, Niels Christian (2020). Novel aspects of glutamine synthetase in ammonia homeostasis: Glutamine synthetase and ammonia. Neurochemistry International. ISSN 0197-0186. 140, s. 1–18. doi: 10.1016/j.neuint.2020.104809. Fulltekst i vitenarkiv
• Raheel, Tayyaba Qureshi; Bjørkmo, Mona; Nordengen, Kaja; Gundersen, Vidar; Utheim, Tor Paaske & Watne, Leiv Otto [Vis alle 8 forfattere av denne artikkelen] (2020). Slc38a1 Conveys Astroglia-Derived Glutamine into GABAergic Interneurons for Neurotransmitter GABA Synthesis . Cells. ISSN 2073-4409. 9(7), s. 1–12. doi: 10.3390/cells9071686. Fulltekst i vitenarkiv
• Raheel, Tayyaba Qureshi; Sørensen, Christina; Berghuis, Paul; Jensen, Vidar; Dobszay, Marton B. & Farkas, Tamás [Vis alle 14 forfattere av denne artikkelen] (2019). The glutamine transporter Slc38a1 regulates GABAergic neurotransmission and synaptic plasticity. Cerebral Cortex. ISSN 1047-3211. 29(12), s. 5166–5179. doi: 10.1093/cercor/bhz055. Fulltekst i vitenarkiv
• Hassel, Bjørnar; Rogne, Ane Gretesdatter & Hope, Sigrun (2019). Intellectual disability associated with pyridoxine-responsive epilepsies: The need to protect cognitive development. Frontiers in Psychiatry. ISSN 1664-0640. 10:116, s. 1–8. doi: 10.3389/fpsyt.2019.00116. Fulltekst i vitenarkiv
• Holmøy, Anne Katrin; Johannessen, Cecilie Haggag; Hope, Sigrun; Van Walsem, Marleen Regina; Aanonsen, Nils Olav & Hassel, Bjørnar (2019). Uncovering health and social care needs among myotonic dystrophy patients: Utility of the Needs and Provisions Complexity Scale. Acta Neurologica Scandinavica. ISSN 0001-6314. 139(6), s. 526–532. doi: 10.1111/ane.13086.
• Vohra, Rupali; Dalgaard, Line Marie; Vibæk, Jeppe; Langbøl, Mia Aggergaard; Bergersen, Linda Hildegard & Olsen, Niels Vidiendal [Vis alle 8 forfattere av denne artikkelen] (2019). Potential metabolic markers in glaucoma and their regulation in response to hypoxia. Acta Ophthalmologica. ISSN 1755-375X. s. 1–10. doi: 10.1111/aos.14021.
• Hassel, Bjørnar; Mariussen, Espen; Idland, Ane-Victoria; Dahl, Gry Torsæter; Ræder, Johan & Frihagen, Frede Jon [Vis alle 9 forfattere av denne artikkelen] (2018). CSF sodium at toxic levels precedes delirium in hip fracture patients. Neurotoxicology. ISSN 0161-813X. 69(December), s. 11–16. doi: 10.1016/j.neuro.2018.08.010.
• Zhou, Yun; Dhaher, Roni; Parent, Maxime; Hu, Qiu Xiang; Hassel, Bjørnar & Yee, Siu-Pok [Vis alle 9 forfattere av denne artikkelen] (2018). Selective deletion of glutamine synthetase in the mouse cerebral cortex induces glial dysfunction and vascular impairment that precede epilepsy and neurodegeneration. Neurochemistry International. ISSN 0197-0186. s. 1–12. doi: 10.1016/j.neuint.2018.07.009. Fulltekst i vitenarkiv
• Zhou, Yun; Hassel, Bjørnar; Eid, Tore & Danbolt, Niels Christian (2018). Axon-terminals expressing EAAT2 (GLT-1; Slc1a2) are common in the forebrain and not limited to the hippocampus. Neurochemistry International. ISSN 0197-0186. 123, s. 101–113. doi: 10.1016/j.neuint.2018.03.006. Fulltekst i vitenarkiv
• Morland, Cecilie; Frøland, Anne-Sofie; Nguyen, Mi Mong Tran; Storm-Mathisen, Jon; Gundersen, Vidar & Rise, Frode (2018). Propionate enters GABAergic neurons, inhibits GABA transaminase, causes GABA accumulation and lethargy in a model of propionic acidemia. Biochemical Journal. ISSN 0264-6021. 475(4), s. 749–758. doi: 10.1042/BCJ20170814.
• Hu, Qiu Xiang; Hansen, Sigrid Ottestad; Holmseth, Silvia; Hassel, Bjørnar; Danbolt, Niels Christian & Zhou, Yun (2018). Expression of glutamate transporters in mouse liver, kidney, and intestine. Journal of Histochemistry and Cytochemistry. ISSN 0022-1554. 66(3), s. 189–202. doi: 10.1369/0022155417749828. Fulltekst i vitenarkiv Vis sammendrag

  Glutamate transport activities have been identified not only in the brain, but also in the liver, kidney, and intestine. Although glutamate transporter distributions in the central nervous system are fairly well known, there are still uncertainties with respect to the distribution of these transporters in peripheral organs. Quantitative information is mostly lacking, and few of the studies have included genetically modified animals as specificity controls. The present study provides validated qualitative and semi-quantitative data on the excitatory amino acid transporter (EAAT)1-3 subtypes in the mouse liver, kidney, and intestine. In agreement with the current view, we found high EAAT3 protein levels in the brush borders of both the distal small intestine and the renal proximal tubules. Neither EAAT1 nor EAAT2 was detected at significant levels in murine kidney or intestine. In contrast, the liver only expressed EAAT2 (but 2 C-terminal splice variants). EAAT2 was detected in the plasma membranes of perivenous hepatocytes. These cells also expressed glutamine synthetase. Conditional deletion of hepatic EAAT2 did neither lead to overt neurological disturbances nor development of fatty liver.

• Dahlberg, Daniel; Struys, Eduard A.; Janssen, EE; Mørkrid, Lars; Midttun, Øivind & Hassel, Bjørnar (2017). Cyst Fluid From Cystic, Malignant Brain Tumors: A Reservoir of Nutrients, Including Growth Factor-Like Nutrients, for Tumor Cells. Neurosurgery. ISSN 0148-396X. 80(6), s. 917–924. doi: 10.1093/neuros/nyw101. Vis sammendrag

  BACKGROUND: Brain tumors may have cysts, whose content of nutrients could influence tumor cell microenvironment and growth. OBJECTIVE: To measure nutrients in cyst fluid from glioblastoma multiforme (GBM) and metastatic brain tumors. METHODS: Quantification of nutrients in cyst fluid from 12 to 18 GBMs and 4 to 10 metastatic brain tumors. RESULTS: GBM cysts contained glucose at 2.2 mmol/L (median value; range <0.8-3.5) and glutamine at 1.04 mmol/L (0.17-4.2). Lactate was 7.1 mmol/L (2.4-12.5) and correlated inversely with glucose level (r = -0.77; P < .001). Amino acids, including glutamate, varied greatly, but median values were similar to previously published serum values. Ammonia was 75 μmol/L (11-241). B vitamins were present at previously published serum values, and riboflavin, nicotinamide, pyridoxal 5΄-phosphate, and cobalamin were higher in cyst fluid than in cerebrospinal fluid. Inorganic phosphate was 1.25 mmol/L (0.34-3.44), which was >3 times higher than in ventricular cerebrospinal fluid: 0.35 mmol/L (0.22-0.66; P < .001). Tricarboxylic acid cycle intermediates were in the low micromolar range, except for citrate, which was 240 μmol/L (140-590). In cystic metastatic malignant melanomas and lung tumors values were similar to those in GBMs. CONCLUSION: Tumor cysts may be a nutrient reservoir for brain tumors, securing tumor energy metabolism and synthesis of cell constituents. Serum is one likely source of cyst fluid nutrients. Nutrient levels in tumor cyst fluid are highly variable, which could differentially stimulate tumor growth. Cyst fluid glutamate, lactate, and phosphate may act as tumor growth factors; these compounds have previously been shown to stimulate tumor growth at concentrations found in tumor cyst fluid.

• Hassel, Bjørnar; De Souza, Gustavo Antonio; Stensland, Maria; Ivanovic, Jugoslav; Voie, Øyvind Albert & Dahlberg, Daniel (2017). The proteome of pus from human brain abscesses: Host-derived neurotoxic proteins and the cell-type diversity of CNS pus. Journal of Neurosurgery. ISSN 0022-3085. 129(3), s. 829–837. doi: 10.3171/2017.4.JNS17284. Vis sammendrag

  OBJECTIVE What determines the extent of tissue destruction during brain abscess formation is not known. Pyogenic brain infections cause destruction of brain tissue that greatly exceeds the area occupied by microbes, as seen in experimental studies, pointing to cytotoxic factors other than microbes in pus. This study examined whether brain abscess pus contains cytotoxic proteins that might explain the extent of tissue destruction. METHODS Pus proteins from 20 human brain abscesses and, for comparison, 7 subdural empyemas were analyzed by proteomics mass spectrometry. Tissue destruction was determined from brain abscess volumes as measured by MRI. RESULTS Brain abscess volume correlated with extracellular pus levels of antibacterial proteins from neutrophils and macrophages: myeloperoxidase (r = 0.64), azurocidin (r = 0.61), lactotransferrin (r = 0.57), and cathelicidin (r = 0.52) (p values 0.002-0.018), suggesting an association between leukocytic activity and tissue damage. In contrast, perfringolysin O, a cytotoxic protein from Streptococcus intermedius that was detected in 16 patients, did not correlate with abscess volume (r = 0.12, p = 0.66). The median number of proteins identified in each pus sample was 870 (range 643-1094). Antibiotic or steroid treatment prior to pus evacuation did not reduce the number or levels of pus proteins. Some of the identified proteins have well-known neurotoxic effects, e.g., eosinophil cationic protein and nonsecretory ribonuclease (also known as eosinophil-derived neurotoxin). The cellular response to brain infection was highly complex, as reflected by the presence of proteins that were specific for neutrophils, eosinophils, macrophages, platelets, fibroblasts, or mast cells in addition to plasma and erythrocytic proteins. Other proteins (neurofilaments, myelin basic protein, and glial fibrillary acidic protein) were specific for brain cells and reflected damage to neurons, oligodendrocytes, and astrocytes, respectively. Pus from subdural empyemas had significantly higher levels of plasma proteins and lower levels of leukocytic proteins than pus from intracerebral abscesses, suggesting greater turnover of the extracellular fluid of empyemas and washout of pus constituents. CONCLUSIONS Brain abscess pus contains leukocytic proteins that are neurotoxic and likely participate actively in the excessive tissue destruction inherent in brain abscess formation. These findings underscore the importance of rapid evacuation of brain abscess pus.

• Idland, Ane-Victoria; Wyller, Torgeir Bruun; Støen, Randi; Dahl, Gry Torsæter; Frihagen, Frede Jon & Brækhus, Anne [Vis alle 7 forfattere av denne artikkelen] (2017). Cerebrospinal Fluid Phosphate in Delirium after Hip Fracture. Dementia and Geriatric Cognitive Disorders Extra. ISSN 1664-5464. 7(3), s. 309–317. doi: 10.1159/000478723. Fulltekst i vitenarkiv
• Hassel, Bjørnar & Dingledine, Raymond (2016). A New Approach for Epilepsy. Cerebrum. ISSN 1524-6205. s. 7–16.
• Moen, Marivi Nabong; Fjær, Roar; Hamdani, El Hassan; Lærdahl, Jon Kristen; Menchini, Robin Johansen & Vigeland, Magnus Dehli [Vis alle 12 forfattere av denne artikkelen] (2016). Pathogenic variants in KCTD7 perturb neuronal K+ fluxes and glutamine transport. Brain. ISSN 0006-8950. 139, s. 3109–3120. doi: 10.1093/brain/aww244.
• Watne, Leiv Otto; Idland, Ane-Victoria; Fekkes, Durk; Ræder, Johan; Frihagen, Frede Jon & Ranhoff, Anette Hylen [Vis alle 9 forfattere av denne artikkelen] (2016). Increased CSF levels of aromatic amino acids in hip fracture patients with delirium suggests higher monoaminergic activity. BMC Geriatrics. ISSN 1471-2318. 16(149). doi: 10.1186/s12877-016-0324-0. Fulltekst i vitenarkiv
• Morland, Cecilie; Pettersen, Mi Nguyen & Hassel, Bjørnar (2016). Hyperosmolar sodium chloride is toxic to cultured neurons and causes reduction of glucose metabolism and ATP levels, an increase in glutamate uptake, and a reduction in cytosolic calcium. Neurotoxicology. ISSN 0161-813X. 54, s. 34–43. doi: 10.1016/j.neuro.2016.03.005.
• Dahlberg, Daniel; Ivanovic, Jugoslav & Hassel, Bjørnar (2016). Toxic levels of ammonia in human brain abscess. Journal of Neurosurgery. ISSN 0022-3085. 124(3), s. 854–860. doi: 10.3171/2015.1.JNS142582.
• Solyga, Volker; Western, Elin; Solheim, Hanne; Hassel, Bjørnar & Kerty, Emilia (2015). Posterior kortikal atrofi. Tidsskrift for Den norske legeforening. ISSN 0029-2001. 135(10), s. 949–952. doi: 10.4045/tidsskr.14.1127.
• Dahlberg, Daniel; Mariussen, Espen; Goverud, Ingeborg Løstegaard; Tonjum, Tone; Mæhlen, Jan & Antal, Ellen-Ann (2015). Staphylococcal α-hemolysin is neurotoxic and causes lysis of brain cells in vivo and in vitro. Neurotoxicology. ISSN 0161-813X. 48, s. 61–67. doi: 10.1016/j.neuro.2015.03.001.
• Dahlberg, Daniel; Ivanovic, Jugoslav; Mariussen, Espen & Hassel, Bjørnar (2015). High extracellular levels of potassium and trace metals in human brain abscess. Neurochemistry International. ISSN 0197-0186. 82, s. 28–32. doi: 10.1016/j.neuint.2015.02.003.
• Hassel, Bjørnar; Elsais, Ahmed; Frøland, Anne-Sofie; Taubøll, Erik; Gjerstad, Leif & Quan, Yi [Vis alle 7 forfattere av denne artikkelen] (2015). Uptake and metabolism of fructose by rat neocortical cells in vivo and by isolated nerve terminals in vitro. Journal of Neurochemistry. ISSN 0022-3042. 133(4), s. 572–581. doi: 10.1111/jnc.13079.
• Dahlberg, Daniel; Ivanovic, Jugoslav & Hassel, Bjørnar (2014). High extracellular concentration of excitatory amino acids glutamate and aspartate in human brain abscess. Neurochemistry International. ISSN 0197-0186. 69(1), s. 41–47. doi: 10.1016/j.neuint.2014.03.001.
• Hassel, Bjørnar; Dahlberg, Daniel; Mariussen, Espen; Goverud, Ingeborg Løstegaard; Antal, Ellen-Ann & Tonjum, Tone (2014). Brain infection with Staphylococcus aureus leads to high extracellular levels of glutamate, aspartate, γ-aminobutyric acid, and zinc. Journal of Neuroscience Research. ISSN 0360-4012. 92(12), s. 1792–1800. doi: 10.1002/jnr.23444. Vis sammendrag

  Staphylococcal brain infections may cause mental deterioration and epileptic seizures, suggesting interference with normal neurotransmission in the brain. We injected Staphylococcus aureus into rat striatum and found an initial 76% reduction in the extracellular level of glutamate as detected by microdialysis at 2 hr after staphylococcal infection. At 8 hr after staphylococcal infection, however, the extracellular level of glutamate had increased 12-fold, and at 20 hr it had increased >30-fold. The extracellular level of aspartate and γ-aminobutyric acid (GABA) also increased greatly. Extracellular Zn2+ , which was estimated at ∼2.6 µmol/liter in the control situation, was increased by 330% 1-2.5 hr after staphylococcal infection and by 100% at 8 and 20 hr. The increase in extracellular glutamate, aspartate, and GABA appeared to reflect the degree of tissue damage. The area of tissue damage greatly exceeded the area of staphylococcal infiltration, pointing to soluble factors being responsible for cell death. However, the N-methyl-D-aspartate receptor antagonist MK-801 ameliorated neither tissue damage nor the increase in extracellular neuroactive amino acids, suggesting the presence of neurotoxic factors other than glutamate and aspartate. In vitro staphylococci incubated with glutamine and glucose formed glutamate, so bacteria could be an additional source of infection-related glutamate. We conclude that the dramatic increase in the extracellular concentration of neuroactive amino acids and zinc could interfere with neurotransmission in the surrounding brain tissue, contributing to mental deterioration and a predisposition to epileptic seizures, which are often seen in brain abscess patients.

• Madslien, Elisabeth Henie; Rønning, Helene; Lindback, Toril; Hassel, Bjørnar; Andersson, M.A. & Granum, Per Einar (2013). Lichenysin is produced by most Bacillus licheniformis strains. Journal of Applied Microbiology. ISSN 1364-5072. 115(4), s. 1068–1080. doi: 10.1111/jam.12299.
• (2013). Tetanus: Pathophysiology, Treatment, and the Possibility of Using Botulinum Toxin against Tetanus-Induced Rigidity and Spasms. Toxins. ISSN 2072-6651. 5(1), s. 73–83. doi: 10.3390/toxins5010073.
• Zhou, Yun; Holmseth, Silvia; Guo, C; Hassel, Bjørnar; Höfner, G & Huitfeldt, Henrik [Vis alle 7 forfattere av denne artikkelen] (2012). Deletion of the γ-aminobutyric acid transporter 2 (GAT2 and SLC6A13) gene in mice leads to changes in liver and brain taurine contents. Journal of Biological Chemistry. ISSN 0021-9258. 287(42), s. 35733–35746. doi: 10.1074/jbc.M112.368175.
• (2012). Hans (Hansemann) Tønnesen, en diagnostisk gåte fra Amalie Skram [A description of early hydrocephalus with macrocephaly, cerebral palsy, epilepsy, intellectual disability, and growth retardation by Norwegian novelist Amalie Skram (1846-1905)]. Tidsskrift for Den norske legeforening. ISSN 0029-2001. 132, s. 2632–2635. doi: 10.4045/tidsskr.12.0912.
• (2012). 13C Magnetic Resonance Spectroscopy in Neurobiology - Its Use in Monitoring Brain Energy Metabolism and in Identifying Novel Metabolic Substrates and Metabolic Pathways. InTech. ISSN 0192-303X. http://cdn.intechopen.com/pdfs-wm/30447.pdf. doi: 10.5772/33095.
• Hassel, Bjørnar; Taubøll, Erik; Shaw, Renee; Gjerstad, Leif & Dingledine, Ray (2010). Region-specific changes in gene expression in rat brain after chronic treatment with levetiracetam or phenytoin. Epilepsia. ISSN 0013-9580. 51(9), s. 1714–1720. doi: 10.1111/j.1528-1167.2010.02545.x.
• Hassel, Bjørnar; Tessler, S.; Faull, R. L. M. & Emson, P. C. (2008). Glutamate uptake is reduced in prefrontal cortex in Huntington's disease. Neurochemical Research. ISSN 0364-3190. 33, s. 232–237.
• Herrman, Helle; Brækhus, Anne; Aaserud, Olaf; Aukrust, Pål; Stubhaug, Audun & Hassel, Bjørnar (2008). Early treatment of tetanus-induced trismus with botulinum toxin A. Anesthesia and Analgesia. ISSN 0003-2999. 106, s. 1591–1591. doi: 10.1213/ANE.0b013e31816a30f0.
• Hassel, Bjørnar; Solyga, Volker & Lossius, Andreas (2008). High-affinity choline uptake and acetylcholine-metabolizing enzymes in CNS white matter. A quantitative study. Neurochemistry International. ISSN 0197-0186. 53, s. 193–198. doi: 10.1016/j.neuint.2008.06.008.
• Bough, Kristopher J.; Paquet, Maryse; Pare, Jean-Francois; Hassel, Bjørnar; Smith, Youland & Hall, Randy A. (2007). Evidence against enhanced glutamate transport in the anticonvulsant mechanism of the ketogenic diet. Epilepsy Research. ISSN 0920-1211. 74(2-3), s. 232–236. doi: 10.1016/j.eplepsyres.2007.03.002. Vis sammendrag

  Excessive glutamatergic neurotransmission is considered an underlying factor of epilepsy. Energy-dependent glutamate transporters clear extracellular glutamate to limit neuronal excitability. Evidence suggests that reduced expression and/or activity of glutamate transporters contribute to hyperexcitability and progressive seizure activity in rats. By comparison, treatment with the anticonvulsant ketogenic diet (KD) results in increased mRNA expression of the neuronal glutamate transporter EAAC1, elevated energy reserves, and an increased resistance to seizures in rats. The goal of the current study was to determine whether the expression and/or re-uptake activity of glutamate transporters were elevated in hippocampal tissue of rats after KD treatment. Rats were fed either a ketogenic- or control diet for 4-5 weeks. Western blot analysis showed that protein levels of EAAC1, GLT-1 and GLAST glutamate transporters were not changed in hippocampus, cerebral cortex, or cerebellum after KID. Electron microscopic evidence indicated that the KD did not affect hippocampal EAAC1 distribution. In addition, the re-uptake activity of H-3-glutamate into hippocampal proteoliposomes was similar in both KID and control tissue extracts. These multiple studies suggest that the anticonvulsant nature of the KID does not stem from enhanced glutamate re-uptake. (C) 2007 Elsevier B.V. All rights reserved.

• Henjum, Solveig & Hassel, Bjørnar (2007). High-affinity glycine and glutamate transport in pig forebrain white and gray matter: A quantitative study. Neurochemistry International. ISSN 0197-0186. 50(5), s. 696–702. doi: 10.1016/j.neuint.2007.01.002. Vis sammendrag

  High-affinity uptake of glycine and glutamate modulates glutamatergic neurotransmission in gray matter. N-Methyl-D-aspartate (NMDA) receptors were recently described on white matter oligodendrocytes, therefore uptake of glutamate and glycine in white matter may also modulate NMDA receptor function. We found that glycine uptake in white structures of pig forebrain (corpus callosum, fimbria, subcortical pyramidal tracts, and occipital subcortical white matter) was similar to that in gray structures (frontal and temporal cortices and hippocampus), and that it was sensitive to sarcosine, a GLYT1 inhibitor (IC50 15 mu M). Glutamate uptake in white matter was similar to 10% of that in gray; it was sensitive to dihydrokainate, an EAAT2 inhibitor. The levels of glycine and its precursor serine were similar in white and gray matter: approximately 2 and 1 nmol/mg tissue, respectively. The white matter level of glutamate was similar to 7.6 nmol/mg tissue, or similar to 74% of gray matter levels. The activity of serine hydroxymethyl transferase, which converts serine into glycine, was similar in white and gray matter (11-18 pmol/(mg tissue) min), whereas the white matter activity of phosphate-activated glutaminase, which converts glutamine into glutamate, was similar to 100 pmol/(mg tissue) min, or similar to 34% of gray matter activity. The white matter activity of glutamine synthetase, the glial enzyme that converts glutamate into glutamine, was 20-40 nmol/ (mg tissue) min in neocortex and 5-6 nmol/(mg tissue) min in white matter. The data show that forebrain white matter is equipped to regulate extracellular levels of glycine and glutamate, functions that may modulate white matter NMDA receptor function. (c) 2007 Elsevier Ltd. All rights reserved.

• Henjum, Solveig & Hassel, Bjørnar (2007). High-affinity GABA uptake and GABA-metabolizing enzymes in pig forebrain white matter: A quantitative study. Neurochemistry International. ISSN 0197-0186. 50(2), s. 365–370. doi: 10.1016/j.neuint.2006.09.004. Vis sammendrag

  GABA receptor activation in central nervous white matter may be protective during white matter hypoxia in the adult, and it may modify axonal conduction, especially in the developing brain. GABA uptake is important for the shaping of the GABA signal, but quantitative data are lacking for GABA uptake and GABA-metabolizing enzymes in central nervous white matter. We report that high-affinity uptake of GABA in adult pig corpus callosum, fimbria, subcortical pyramidal tracts, and occipital white matter is similar to 20% of that in temporal cortex gray matter. Tiagabine (0.1 mu M), an antiepileptic drug that specifically inhibits the GAT-I GABA transporter inhibited GABA uptake 50% in temporal cortex and 60-68% in white structures. This finding indicates that GAT-1 is an important GABA transporter in white matter and suggests that white matter GABA uptake is inhibited during tiagabine therapy. GABA transaminase activity in white structures was similar to 20% of neocortical values. Glutamate decarboxylase (GAD) activity in white structures was only 4% of that in neocortex (7-12 pmol/mg tissue x min(-1) versus similar to 200 pmol/mg tissue x min-1). Since white matter activity of citrate synthase of the tricarboxylic acid cycle was similar to 25% of neocortical values (similar to 0.4 nmol/mg tissue x min(-1) versus similar to 1.5 nmol/mg tissue x min(-1)), the low GAD activity suggests a slower metabolic turnover of GABA in white than in gray matter. (c) 2006 Elsevier Ltd. All rights reserved.

• Morland, Cecilie; Henjum, Solveig; Iversen, Evy Grini; Skrede, Knut Kristian & Hassel, Bjørnar (2007). Evidence for a higher glycolytic than oxidative metabolic activity in white matter of rat brain. Neurochemistry International. ISSN 0197-0186. 50(5), s. 703–709.
• Nguyen, Nga H. T.; Gonzalez, Susan Villa & Hassel, Bjørnar (2007). Formation of glycerol from glucose in rat brain and cultured brain cells. Augmentation with kainate or ischemia. Journal of Neurochemistry. ISSN 0022-3042. 101, s. 1694–1700.
• Morland, Cecilie; Boldingh, Karen A; Iversen, Evy Grini & Hassel, Bjørnar (2004). Valproate is neuroprotective against malonate toxicity in rat striatum: an association with augmentation of high-affinity glutamate uptake. Journal of Cerebral Blood Flow and Metabolism. ISSN 0271-678X. 24(11), s. 1226–1234.

Se alle arbeider i Cristin

• Rogne, Ane G.; Dahlberg, Daniel; Udnæs, Eirin; Raudeberg, Rune; Sigurdardottir, Solrun & Hassel, Bjørnar (2019). Cognitive dysfunction in brain abscess patients is not attributable to beta-amyloid deposition.
• Hassel, Bjørnar & Strisland, Frode (2019). Forstå hvordan jeg har det. Sensorteknologi for personer med sterkt begrensende kommunikasjonsevner. Vis sammendrag

  Mennesker med alvorlig grad av utviklingshemming eller andre omfattende funksjonsnedsettelser kan ha sterkt reduserte eller manglende evner til å uttrykke seg verbalt eller på andre måter. De kan derfor ha problemer med å uttrykke smerte eller andre ubehag, og de kan reagere med selvskadende eller aggressiv atferd uten at bakenforliggende årsak blir kjent. Kan enkle fysiologiske målinger, slik som pulsmåling, brukes som en ekstra indikator for å hjelpe tjenestene tolke hva som foregår?

• Aarønæs, Lars; Hassel, Bjørnar; Rogne, Ane & Dahlberg, Daniel (2018). Puss kan gi hjerneskade. [Internett]. Forskning.no.
• (2018). Michelangelos David - et syndrome for fremtiden? I Frich, Jan C; Brean, Are & Dietrichs, Espen (Red.), Hjernen og historien. Det norske medicinske Selskab. ISSN 978-82-92871-84-3. s. 107–113.
• (2018). Religiøs anatomi i hofteregionen. I Frich, Jan C; Brean, Are & Dietrichs, Espen (Red.), Hjernen og historien. Det norske medicinske Selskab. ISSN 978-82-92871-84-3. s. 95–97.
• (2018). Jakobs delirium og overbevisningens nevrobiologi. I Frich, Jan C; Brean, Are & Dietrichs, Espen (Red.), Hjernen og historien. Det norske medicinske Selskab. ISSN 978-82-92871-84-3. s. 87–94.
• Zhou, Yun; Hassel, Bjørnar; Eid, Tore & Danbolt, Niels Christian (2018). Axon-terminals expressing EAAT2 (GLT-1; slc1a2) are common in the forebrain and not limited to the hippocampus.
• Cordero, Patricia Reyes; Rise, Frode & Hassel, Bjørnar (2020). NMR and spectrophotometric investigations of D-glyceraldehyde metabolism via methylglyoxal. Kjemisk Institutt, Universitetet i Oslo. Vis sammendrag

  Aldehydes are toxic carbonylcompoundsthatcanreact with proteins and modify theirfunction, stability and shape, e.g by inducing AGEs production. This class of compounds can be formed intracellularly and can betransported to the extracellular environment. D-glyceraldehyde, a hydroxyaldehyde, can cross thecellmembrane,but the transport mechanism has notyetbeenfullyelucidated.Transport of D-GA across a cell membrane has been studied in isolated nerve terminals from the formation of D-lactate, which is recovered in the extracellular fluid, and the specificity of the aldehyde transport mechanism has been studied by the inhibitory effect of other aldehydes on D-lactate formation from D-GA. However, it is not known whether other aldehydes inhibit the D-GA transport mechanism or if they inhibit the enzymatic reactionsleading from D-GA to D-lactate.The objective of this investigation was to study the enzymatic pathway from D-GA to D-lactate and the effect of differentaldehydes on the enzyme activities in this pathway.By identifying aldehydes that do not inhibit these enzymes, one can more safely assume that they are pure inhibitors of the aldehyde transport mechanism in the cell membrane.The competing aldehydes were acetaldehyde, acrolein, butanal, crotonaldehyde, formaldehyde, L-glyceraldehyde,methylglyoxal and propanal. Another objective was to evaluate the fibrillation of the protein glucagon by various aldehydes. Nuclear magnetic resonance (NMR)spectroscopyand UV spectrophotometry were used to study enzymatic reactions involved in D-GA metabolism. Liquid-state 1H NMR was used to investigate if aldehydes induced fibrillation of glucagon, a protein that readily undergoes fibrillation.The aldehydes that inhibited the phosphorylation of D-glyceraldehyde or the glyoxalase system werebutanal, formaldehyde, methylglyoxaland L-glyceraldehyde. Aldehydes that did not inhibit these enzymes wereacetaldehyde, acrolein, crotonaldehyde and propanal.The latter aldehydes are probably inhibitors of the aldehyde transport mechanism in the cell membrane. None of the aldehydes seemed to initiate the fibrillogenesisof glucagon.

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