Vidar Jensen

• Naik, Aditi; Jensen, Vidar; Bakketun, Cecilie Bugge; Enger, Rune; Hrabetova, Sabina & Hrabe, Jan (2023). BubbleDrive, a low-volume incubation chamber for acute brain slices. Scientific Reports. ISSN 2045-2322. 13(1). doi: 10.1038/s41598-023-45949-9. Full text in Research Archive
• Eltokhi, Ahmed; Bertocchi, Ilaria; Rozov, Andrei; Jensen, Vidar; Borchardt, Thilo & Taylor, Amy [Show all 10 contributors for this article] (2023). Distinct effects of AMPAR subunit depletion on spatial memory. iScience. ISSN 2589-0042. 26(11). doi: 10.1016/j.isci.2023.108116. Full text in Research Archive
• Hjukse, Jarand Berg; Fernández de la Puebla, Mario; Vindedal, Gry Fluge; Sprengel, Rolf; Jensen, Vidar & Nagelhus, Erlend Arnulf [Show all 7 contributors for this article] (2023). Increased membrane Ca²⁺ permeability drives astrocytic Ca²⁺ dynamics during neuronal stimulation at excitatory synapses. Glia. ISSN 0894-1491. 71(12), p. 2770–2781. doi: 10.1002/glia.24450. Full text in Research Archive
• Åbjørsbråten, Knut Sindre; Skaaraas, Gry Helen Enger Syverstad; Cunen, Celine Marie Løken; Bjørnstad, Daniel Marelius; Binder, Kristin Maria Gullestad & Bojarskaite, Laura [Show all 15 contributors for this article] (2022). Impaired astrocytic Ca2+ signaling in awake-behaving Alzheimer’s disease transgenic mice. eLIFE. ISSN 2050-084X. doi: 10.7554/eLife.75055. Full text in Research Archive Show summary

  Increased astrocytic Ca2+ signaling has been shown in Alzheimer’s disease mouse models, but to date no reports have characterized behaviorally induced astrocytic Ca2+ signaling in such mice. Here, we employ an event-based algorithm to assess astrocytic Ca2+ signals in the neocortex of awake-behaving tg-ArcSwe mice and non-transgenic wildtype littermates while monitoring pupil responses and behavior. We demonstrate an attenuated astrocytic Ca2+ response to locomotion and an uncoupling of pupil responses and astrocytic Ca2+ signaling in 15-month-old plaque-bearing mice. Using the genetically encoded fluorescent norepinephrine sensor GRABNE, we demonstrate a reduced norepinephrine signaling during spontaneous running and startle responses in the transgenic mice, providing a possible mechanistic underpinning of the observed reduced astrocytic Ca2+ responses. Our data points to a dysfunction in the norepinephrine–astrocyte Ca2+ activity axis, which may account for some of the cognitive deficits observed in Alzheimer’s disease.

• Hildrestrand, Gunn Annette; Rolseth, Veslemøy; Kunath, Nicolas; Suganthan, Rajikala; Jensen, Vidar & Bugaj, Anna Maria [Show all 24 contributors for this article] (2021). NEIL1 and NEIL2 DNA glycosylases modulate anxiety and learning in a cooperative manner in mice. Communications Biology. ISSN 2399-3642. 4. doi: 10.1038/s42003-021-02864-x. Full text in Research Archive
• Bertocchi, Ilaria; Eltokhi, Ahmed; Rozov, Andrey; Nguyễn Chi, Vivan; Jensen, Vidar & Bus, Thorsten [Show all 23 contributors for this article] (2021). Voltage-independent GluN2A-type NMDA receptor Ca2+ signaling promotes audiogenic seizures, attentional and cognitive deficits in mice. Communications Biology. ISSN 2399-3642. 4, p. 1–21. doi: 10.1038/s42003-020-01538-4. Full text in Research Archive
• Caglayan, Safak; Hashim, Adnan; Cieslar-Pobuda, Artur; Jensen, Vidar; Behringer, Sidney & Talug, Burcu [Show all 16 contributors for this article] (2020). Optic Atrophy 1 Controls Human Neuronal Development by Preventing Aberrant Nuclear DNA Methylation. iScience. ISSN 2589-0042. 23(6). doi: 10.1016/j.isci.2020.101154. Full text in Research Archive Show summary

  Optic atrophy 1 (OPA1), a GTPase at the inner mitochondrial membrane involved in regulating mitochondrial fusion, stability, and energy output, is known to be crucial for neural development: Opa1 heterozygous mice show abnormal brain development, and inactivating mutations in OPA1 are linked to human neurological disorders. Here, we used genetically modified human embryonic and patient-derived induced pluripotent stem cells and reveal that OPA1 haploinsufficiency leads to aberrant nuclear DNA methylation and significantly alters the transcriptional circuitry in neural progenitor cells (NPCs). For instance, expression of the forkhead box G1 transcription factor, which is needed for GABAergic neuronal development, is repressed in OPA1+/− NPCs. Supporting this finding, OPA1+/− NPCs cannot give rise to GABAergic interneurons, whereas formation of glutamatergic neurons is not affected. Taken together, our data reveal that OPA1 controls nuclear DNA methylation and expression of key transcription factors needed for proper neural cell specification.

• Raheel, Tayyaba Qureshi; Sørensen, Christina; Berghuis, Paul; Jensen, Vidar; Dobszay, Marton B. & Farkas, Tamás [Show all 14 contributors for this article] (2019). The glutamine transporter Slc38a1 regulates GABAergic neurotransmission and synaptic plasticity. Cerebral Cortex. ISSN 1047-3211. 29(12), p. 5166–5179. doi: 10.1093/cercor/bhz055. Full text in Research Archive
• Eilert-Olsen, Martine; Hjukse, Jarand Berg; Thoren, Anna; Tang, Wannan; Enger, Rune & Jensen, Vidar [Show all 8 contributors for this article] (2019). Astroglial endfeet exhibit distinct Ca2+ signals during hypoosmotic conditions. Glia. ISSN 0894-1491. 67(12), p. 2399–2409. doi: 10.1002/glia.23692. Full text in Research Archive
• Rosic, Brana; Dukefoss, Didrik Bakke; Åbjørsbråten, Knut Sindre; Tang, Wannan; Jensen, Vidar & Ottersen, Ole Petter [Show all 8 contributors for this article] (2019). Aquaporin-4-independent volume dynamics of astroglial endfeet during cortical spreading depression. Glia. ISSN 0894-1491. 67(6), p. 1113–1121. doi: 10.1002/glia.23604. Full text in Research Archive Show summary

  Cortical spreading depression (CSD) is a slowly propagating wave of depolarization of gray matter. This phenomenon is believed to underlie the migraine aura and similar waves of depolarization may exacerbate injury in a number of neurological disease states. CSD is characterized by massive ion dyshomeostasis, cell swelling, and multiphasic blood flow changes. Recently, it was shown that CSD is associated with a closure of the paravascular space (PVS), a proposed exit route for brain interstitial fluid and solutes, including excitatory and inflammatory substances that increase in the wake of CSD. The PVS closure was hypothesized to rely on swelling of astrocytic endfeet due to their high expression of aquaporin‐4 (AQP4) water channels. We investigated whether CSD is associated with swelling of endfeet around penetrating arterioles in the cortex of living mice. Endfoot cross‐sectional area was assessed by two‐photon microscopy of mice expressing enhanced green fluorescent protein in astrocytes and related to the degree of arteriolar constriction. In anesthetized mice CSD triggered pronounced endfoot swelling that was short‐lasting and coincided with the initial arteriolar constriction. Mice lacking AQP4 displayed volume changes of similar magnitude. CSD‐induced endfoot swelling and arteriolar constriction also occurred in awake mice, albeit with faster kinetics than in anesthetized mice. We conclude that swelling of astrocytic endfeet is a robust event in CSD. The early onset and magnitude of the endfoot swelling is such that it may significantly delay perivascular drainage of interstitial solutes in neurological conditions where CSD plays a pathophysiological role.

• Aryal, Sanjay; Hussain, Suleman; Drevon, Christian A; Nagelhus, Erlend Arnulf; Hvalby, Øyvind & Jensen, Vidar [Show all 8 contributors for this article] (2019). Omega-3 fatty acids regulate plasticity in distinct hippocampal glutamatergic synapses. European Journal of Neuroscience. ISSN 0953-816X. 49(1), p. 40–50. doi: 10.1111/ejn.14224.
• Medin, Tirill; Jensen, Vidar; Skare, Øivind; Storm-Mathisen, Jon; Hvalby, Øyvind Christian & Bergersen, Linda Hildegard (2019). Altered α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor function and expression in hippocampus in a rat model of attention-deficit/hyperactivity disorder (ADHD). Behavioural Brain Research. ISSN 0166-4328. 360, p. 209–215. doi: 10.1016/j.bbr.2018.12.028. Full text in Research Archive Show summary

  Glutamatergic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) carry the bulk of excitatory synaptic transmission. Their modulation plays key roles in synaptic plasticity, which underlies hippocampal learning and memory. A dysfunctional glutamatergic system may negatively affect learning abilities and underlie symptoms of attention-deficit/hyperactivity disorder (ADHD). The aim of this study was to investigate whether the expression and function of AMPARs were altered in ADHD. We recorded AMPAR mediated synaptic transmission at hippocampal excitatory synapses and quantified immunogold labelling density of AMPAR subunits GluA1 and GluA2/3 in a rat model for ADHD; the spontaneously hypertensive rat (SHR). Electrophysiological recordings showed significantly reduced AMPAR mediated synaptic transmission at the CA3-to-CA1 pyramidal cell synapses in stratum radiatum and stratum oriens in SHRs compared to control rats. Electronmicroscopic immunogold quantifications did not show any statistically significant changes in labelling densities of the GluA1 subunit of the AMPAR on dendritic spines in stratum radiatum or in stratum oriens. However, there was a significant increase of the GluA2/3 subunit intracellularly in stratum oriens in SHR compared to control, interpreted as a compensatory effect. The proportion of synapses lacking AMPAR subunit labelling was the same in the two genotypes. In addition, electronmicroscopic examination of tissue morphology showed the density of this type of synapse (i.e., asymmetric synapses on spines), and the average size of the synaptic membranes, to be the same. AMPAR dysfunction, possibly involving molecular changes, in hippocampus may in part reflect altered learning in individuals with ADHD.

• Ringsevjen, Håvard; Hansen, Heidi Marie Umbach; Hussain, Suleman; Hvalby, Øyvind C; Jensen, Vidar & Walaas, S. Ivar [Show all 7 contributors for this article] (2018). Presynaptic increase in IP3 receptor type 1 concentration in the early phase of hippocampal synaptic plasticity. Brain Research. ISSN 0006-8993. 1706, p. 125–134. doi: 10.1016/j.brainres.2018.10.030.
• Bannerman, David M; Borchardt, Thilo; Jensen, Vidar; Rozov, Andrey; Haj Yasein, Nadia & Burnashev, Nail [Show all 12 contributors for this article] (2018). Somatic Accumulation of GluA1-AMPA Receptors Leads to Selective Cognitive Impairments in Mice. Frontiers in Molecular Neuroscience. ISSN 1662-5099. 11. doi: 10.3389/fnmol.2018.00199. Full text in Research Archive
• Hussain, Suleman; Ringsevjen, Håvard; Schupps, M; Hvalby, Øyvind Christian dødsbo; Sørensen, Jakob Balslev & Jensen, Vidar [Show all 7 contributors for this article] (2018). A possible postsynaptic role for SNAP-25 in hippocampal synapses. Brain Structure and Function. ISSN 1863-2653. p. 1–12. doi: 10.1007/s00429-018-1782-2.
• Heuser, Kjell; Nome, Cecilie; Pettersen, Klas; Åbjørsbråten, Knut Sindre; Jensen, Vidar & Tang, Wannan [Show all 10 contributors for this article] (2018). Ca2+ signals in astrocytes facilitate spread of epileptiform activity. Cerebral Cortex. ISSN 1047-3211. 28(11), p. 4036–4048. doi: 10.1093/cercor/bhy196. Full text in Research Archive
• Shimshek, Derya R; Bus, Thorsten; Schupp, Bettina; Jensen, Vidar; Marx, Verena & Layer, Liliana E [Show all 8 contributors for this article] (2017). Different forms of AMPA receptor mediated LTP and their correlation to the spatial working memory formation. Frontiers in Molecular Neuroscience. ISSN 1662-5099. 10. doi: 10.3389/fnmol.2017.00214.
• Enger, Rune; Dukefoss, Didrik Bakke; Tang, Wannan; Pettersen, Klas; Bjørnstad, Daniel Marelius & Helm, Paul Johannes [Show all 11 contributors for this article] (2016). Deletion of aquaporin-4 curtails extracellular glutamate elevation in cortical spreading depression in awake mice. Cerebral Cortex. ISSN 1047-3211. doi: 10.1093/cercor/bhw359.
• Vindedal, Gry Fluge; Thoren, Anna; Jensen, Vidar; Klungland, Arne; Zhang, Yong & Holtzman, Michael [Show all 8 contributors for this article] (2016). Removal of aquaporin-4 from glial and ependymal membranes causes brain water accumulation. Molecular and Cellular Neuroscience. ISSN 1044-7431. 77, p. 47–52. doi: 10.1016/j.mcn.2016.10.004.
• Enger, Rune; Tang, Wannan; Vindedal, Gry Fluge; Jensen, Vidar; Helm, Paul Johannes & Sprengel, Rolf [Show all 8 contributors for this article] (2015). Dynamics of ionic shifts in cortical spreading depression. Cerebral Cortex. ISSN 1047-3211. 25(11), p. 4469–4476. doi: 10.1093/cercor/bhv054. Show summary

  Cortical spreading depression is a slowly propagating wave of near-complete depolarization of brain cells followed by temporary suppression of neuronal activity. Accumulating evidence indicates that cortical spreading depression underlies the migraine aura and that similar waves promote tissue damage in stroke, trauma, and hemorrhage. Cortical spreading depression is characterized by neuronal swelling, profound elevation of extracellular potassium and glutamate, multiphasic blood flow changes, and drop in tissue oxygen tension. The slow speed of the cortical spreading depression wave implies that it is mediated by diffusion of a chemical substance, yet the identity of this substance and the pathway it follows are unknown. Intercellular spread between gap junction-coupled neurons or glial cells and interstitial diffusion of K(+) or glutamate have been proposed. Here we use extracellular direct current potential recordings, K(+)-sensitive microelectrodes, and 2-photon imaging with ultrasensitive Ca(2+) and glutamate fluorescent probes to elucidate the spatiotemporal dynamics of ionic shifts associated with the propagation of cortical spreading depression in the visual cortex of adult living mice. Our data argue against intercellular spread of Ca(2+) carrying the cortical spreading depression wavefront and are in favor of interstitial K(+) diffusion, rather than glutamate diffusion, as the leading event in cortical spreading depression.

• Tang, Wannan; Szokol, Karolina; Jensen, Vidar; Enger, Rune; Trivedi, Chintan A. & Hvalby, Øyvind Christian dødsbo [Show all 10 contributors for this article] (2015). Stimulation-evoked Ca2+ signals in astrocytic processes at hippocampal CA3-CA1 synapses of adult mice are modulated by glutamate and ATP. Journal of Neuroscience. ISSN 0270-6474. 35(7), p. 3016–3021. doi: 10.1523/JNEUROSCI.3319-14.2015. Show summary

  To date, it has been difficult to reveal physiological Ca(2+) events occurring within the fine astrocytic processes of mature animals. The objective of the study was to explore whether neuronal activity evokes astrocytic Ca(2+) signals at glutamatergic synapses of adult mice. We stimulated the Schaffer collateral/commissural fibers in acute hippocampal slices from adult mice transduced with the genetically encoded Ca(2+) indicator GCaMP5E driven by the glial fibrillary acidic protein promoter. Two-photon imaging revealed global stimulation-evoked astrocytic Ca(2+) signals with distinct latencies, rise rates, and amplitudes in fine processes and somata. Specifically, the Ca(2+) signals in the processes were faster and of higher amplitude than those in the somata. A combination of P2 purinergic and group I/II metabotropic glutamate receptor (mGluR) antagonists reduced the amplitude of the Ca(2+) transients by 30-40% in both astrocytic compartments. Blockage of the mGluRs alone only modestly reduced the magnitude of the stimulation-evoked Ca(2+) signals in processes and failed to affect the somatic Ca(2+) response. Local application of group I or I/II mGluR agonists or adenosine triphosphate (ATP) elicited global astrocytic Ca(2+) signals that mimicked the stimulation-evoked astrocytic Ca(2+) responses. We conclude that stimulation-evoked Ca(2+) signals in astrocytic processes at CA3-CA1 synapses of adult mice (1) differ from those in astrocytic somata and (2) are modulated by glutamate and ATP.

• Szokol, Karolina; Heuser, Kjell; Tang, Wannan; Jensen, Vidar; Enger, Rune & Bedner, Peter [Show all 10 contributors for this article] (2015). Augmentation of Ca<sup>2+</sup> signaling in astrocytic endfeet in the latent phase of temporal lobe epilepsy. Frontiers in Cellular Neuroscience. ISSN 1662-5102. 9. doi: 10.3389/fncel.2015.00049. Full text in Research Archive Show summary

  Astrocytic endfeet are specialized cell compartments whose important homeostatic roles depend on their enrichment of water and ion channels anchored by the dystrophin associated protein complex (DAPC). This protein complex is known to disassemble in patients with mesial temporal lobe epilepsy and in the latent phase of experimental epilepsies. The mechanistic underpinning of this disassembly is an obvious target of future therapies, but remains unresolved. Here we show in a kainate model of temporal lobe epilepsy that astrocytic endfeet display an enhanced stimulation-evoked Ca(2+) signal that outlast the Ca(2+) signal in the cell bodies. While the amplitude of this Ca(2+) signal is reduced following group I/II metabotropic receptor (mGluR) blockade, the duration is sustained. Based on previous studies it has been hypothesized that the molecular disassembly in astrocytic endfeet is caused by dystrophin cleavage mediated by Ca(2+) dependent proteases. Using a newly developed genetically encoded Ca(2+) sensor, the present study bolsters this hypothesis by demonstrating long-lasting, enhanced stimulation-evoked Ca(2+) signals in astrocytic endfeet.

• Alazraq, Nadia; Bugge, Cecilie Elisabeth; Jensen, Vidar; Østby, Ivar; Ottersen, Ole Petter & Hvalby, Øyvind Christian [Show all 7 contributors for this article] (2014). Deletion of aquaporin-4 increases extracellular K+ concentration during synaptic stimulation in mouse hippocampus. Brain Structure and Function. ISSN 1863-2653. doi: 10.1007/s00429-014-0767-z.
• Schmeisser, Michael J; Baumann, Bernd; Johannsen, Svenja; Vindedal, Gry Fluge; Jensen, Vidar & Hvalby, Øyvind Christian [Show all 14 contributors for this article] (2012). I kappa B Kinase/Nuclear Factor kappa B-Dependent Insulin-Like Growth Factor 2 (Igf2) Expression Regulates Synapse Formation and Spine Maturation via Igf2 Receptor Signaling. Journal of Neuroscience. ISSN 0270-6474. 32(16), p. 5688–5703. doi: 10.1523/JNEUROSCI.0111-12.2012.
• Bannerman, DM; Bus, T; Taylor, A; Sanderson, D.J.; Schwarz, Inna & Jensen, Vidar [Show all 10 contributors for this article] (2012). Dissecting spatial knowledge from spatial choice by hippocampal NMDA receptor deletion. Nature Neuroscience. ISSN 1097-6256. 15(8), p. 1153–+. doi: 10.1038/nn.3166.
• Herwerth, Marina; Jensen, Vidar; Novak, Martin; Konopka, Witold; Hvalby, Øyvind Christian & Köhr, Georg (2012). D4 Dopamine Receptors Modulate NR2B NMDA Receptors and LTP in Stratum Oriens of Hippocampal CA1. Cerebral Cortex. ISSN 1047-3211. 22(8), p. 1786–1798. doi: 10.1093/cercor/bhr275.
• Haj-Yasein, Nadia Nabil; Jensen, Vidar; Østby, Ivar; Omholt, Stig W; Voipio, Juha & Kaila, Kai [Show all 9 contributors for this article] (2012). Aquaporin-4 regulates extracellular space volume dynamics during high-frequency synaptic stimulation: A gene deletion study in mouse hippocampus. Glia. ISSN 0894-1491. 60(6), p. 867–874. doi: 10.1002/glia.22319. Show summary

  Little is known about the physiological roles of aquaporin-4 (AQP4) in the central nervous system. AQP4 water channels are concentrated in endfeet membranes of astrocytes but also localize to the fine astrocytic processes that abut central synapses. Based on its pattern of expression, we predicted that AQP4 could be involved in controlling water fluxes and changes in extracellular space (ECS) volume that are associated with activation of excitatory pathways. Here, we show that deletion of Aqp4 accentuated the shrinkage of the ECS that occurred in the mouse hippocampal CA1 region during activation of Schaffer collateral/commissural fibers. This effect was found in the stratum radiatum (where perisynaptic astrocytic processes abound) but not in the pyramidal cell layer (where astrocytic processes constitute but a minor volume fraction). For both genotypes the ECS shrinkage was most pronounced in the pyramidal cell layer. Our data attribute a physiological role to AQP4 and indicate that this water channel regulates extracellular volume dynamics in the mammalian brain

• Bogen, Inger Lise; Jensen, Vidar; Hvalby, Øyvind Christian & Walaas, S. Ivar (2011). Glutamatergic neurotransmission in the synapsin I and II double knock-out mouse. Seminars in Cell and Developmental Biology. ISSN 1084-9521. 22(4), p. 400–407. doi: 10.1016/j.semcdb.2011.07.004.
• Haj Yasein, Nadia Nabil; Jensen, Vidar; Vindedal, Gry Fluge; Gundersen, Georg Andreas; Klungland, Arne & Ottersen, Ole Petter [Show all 8 contributors for this article] (2011). Evidence that Compromised K+ Spatial Buffering Contributes to the Epileptogenic Effect of Mutations in the Human Kir4.1 Gene (KCNJ10). Glia. ISSN 0894-1491. 59(11), p. 1635–1642. doi: 10.1002/glia.21205.
• Hvalby, Øyvind Christian; Jensen, Vidar; Kao, Hung-Teh & Walaas, S. Ivar (2010). Synapsin-dependent vesicle recruitment modulated by forskolin, phorbol ester and Ca2+ in mouse excitatory hippocampal synapses. Frontiers in Synaptic Neuroscience. ISSN 1663-3563. 2. doi: 10.3389/fnsyn.2010.00152.
• Jensen, Vidar; Rinholm, Johanne Egge; Johansen, Tine Jeanette; Medin, Tirill; Storm-Mathisen, Jon & Sagvolden, Terje [Show all 8 contributors for this article] (2009). N-methyl-d-aspartate receptor subunit dysfunction at hippocampal glutamatergic synapses in an animal model of attention-deficit/hyperactivity disorder. Neuroscience. ISSN 0306-4522. 158(1), p. 353–364. doi: 10.1016/j.neuroscience.2008.05.016. Show summary

  Attention-deficit/hyperactivity disorder (ADHD) is the most common neurobehavioural disorder among children. ADHD children are hyperactive, impulsive and have problems with sustained attention. These cardinal features are also present in the best validated animal model of ADHD, the spontaneously hypertensive rat (SHR), which is derived from the Wistar Kyoto rat (WKY). Current theories of ADHD relate symptom development to factors that alter learning. N-methyl-d-aspartate receptor (NMDAR) dependent long term changes in synaptic efficacy in the mammalian CNS are thought to represent underlying cellular mechanisms for some forms of learning. We therefore hypothesized that synaptic abnormality in excitatory, glutamatergic synaptic transmission might contribute to the altered behavior in SHRs. We studied physiological and anatomical aspects of hippocampal CA3-to-CA1 synapses in age-matched SHR and WKY (controls). Electrophysiological analysis of these synapses showed reduced synaptic transmission (reduced field excitatory postsynaptic potential for a defined fiber volley size) in SHR, whereas short-term forms of synaptic plasticity, like paired-pulse facilitation, frequency facilitation, and delayed response enhancement were comparable in the two genotypes, and long-term potentiation (LTP) of synaptic transmission was of similar magnitude. However, LTP in SHR was significantly reduced (by 50%) by the NR2B specific blocker CP-101,606 (10 muM), whereas the blocker had no effect on LTP magnitude in the control rats. This indicates that the SHR has a functional predominance of NR2B, a feature characteristic of early developmental stages in these synapses. Quantitative immunofluorescence and electron microscopic postembedding immunogold cytochemistry of the three major NMDAR subunits (NR1, NR2A; and NR2B) in stratum radiatum spine synapses revealed no differences between SHR and WKY. The results indicate that functional impairments in glutamatergic synaptic transmission may be one of the underlying mechanisms leading to the abnormal behavior in SHR, and possibly in human ADHD

• Bogen, Inger Lise; Jensen, Vidar; Hvalby, Øyvind Christian & Walaas, S. Ivar (2009). Synapsin-dependent development of glutamatergic vesicles and presynaptic plasticity in postnatal mouse brain. Neuroscience. ISSN 0306-4522. 158(1), p. 231–241. doi: 10.1016/j.neuroscience.2008.05.055.
• Sagvolden, Terje; Johansen, Espen Borgå; Wøien, Grete; Walaas, S Ivar; Storm-Mathisen, Jon & Bergersen, Linda Hildegard [Show all 14 contributors for this article] (2009). The spontaneously hypertensive rat model of ADHD - The importance of selecting the appropriate reference strain. Neuropharmacology. ISSN 0028-3908. 57(7-8), p. 619–626. doi: 10.1016/j.neuropharm.2009.08.004.
• Owe, Simen Gylterud; Jensen, Vidar; Evergren, E; Ruiz, A; Shupliakov, O & Kullmann, DM [Show all 10 contributors for this article] (2009). Synapsin- and Actin-Dependent Frequency Enhancement in Mouse Hippocampal Mossy Fiber Synapses. Cerebral Cortex. ISSN 1047-3211. 19(3), p. 511–523. doi: 10.1093/cercor/bhn101.
• von Engelhardt, Jacob; Doganci, B; Jensen, Vidar; Hvalby, Øyvind Christian; Göngrich, C & Taylor, A [Show all 12 contributors for this article] (2008). Contribution of Hippocampal and Extra-Hippocampal NR2B-Containing NMDA Receptors to Performance on Spatial Learning Tasks. Neuron. ISSN 0896-6273. 60(5), p. 846–860. doi: 10.1016/j.neuron.2008.09.039.
• Niewoehner, B; Single, FN; Hvalby, Øyvind Christian; Jensen, Vidar; Borgloh, SMZA & Seeburg, PH [Show all 9 contributors for this article] (2007). Impaired spatial working memory but spared spatial reference memory following functional loss of NMDA receptors in the dentate gyrus. European Journal of Neuroscience. ISSN 0953-816X. 25, p. 837–846. doi: 10.1111/j.1460-9568.2007.05312.x.
• Berberich, S; Jensen, Vidar; Hvalby, Øyvind Christian; Seeburg, PH & Kohr, G (2007). The role of NMDAR subtypes and charge transfer during hippocampal UP induction. Neuropharmacology. ISSN 0028-3908. 52, p. 77–86. doi: 10.1016/j.neuropharm.2006.07.016.
• Jensen, Vidar; Hilfiker, S; Ruiz, A; Hvalby, Øyvind Christian & Walaas, Sven Ivar (2007). A delayed response enhancement during hippocampal presynaptic plasticity in mice. Journal of Physiology. ISSN 0022-3751. 583, p. 129–143. doi: 10.1113/jphysiol.2007.131300.
• Faure, C; Corvol, JC; Toutant, M; Valjent, E; Hvalby, Øyvind Christian & Jensen, Vidar [Show all 10 contributors for this article] (2007). Calcineurin is essential for depolarization-induced nuclear translocation and tyrosine phosphorylation of PYK2 in neurons. Journal of Cell Science. ISSN 0021-9533. 120, p. 3034–3044. doi: 10.1242/jcs.009613.
• Humeau, Y; Reisel, D; Johnson, AW; Borchardt, T; Jensen, Vidar & Gebhardt, C [Show all 13 contributors for this article] (2007). A pathway-specific function for different AMPA receptor subunits in amygdala long-term potentiation and fear conditioning. Journal of Neuroscience. ISSN 0270-6474. 27, p. 10947–10956. doi: 10.1523/JNEUROSCI.2603-07.2007.
• Hvalby, Øyvind Christian; Jensen, Vidar; Kao, HT & Walaas, Sven Ivar (2006). Synapsin-regulated synaptic transmission from readily releasable synaptic vesicles in excitatory hippocampal synapses in mice. Journal of Physiology. ISSN 0022-3751. 571, p. 75–82.
• Shimshek, DR; Jensen, Vidar; Celikel, T; Geng, Y; Schupp, B & Bus, T [Show all 11 contributors for this article] (2006). Forebrain-specific glutamate receptor B deletion impairs spatial memory but not hippocampal field long-term potentiation. Journal of Neuroscience. ISSN 0270-6474. 26, p. 8428–8440.
• Pawlak, V; Jensen, Vidar; Schupp, BJ; Kvello, Ane; Hvalby, Øyvind Christian & Seeburg, PH [Show all 7 contributors for this article] (2005). Frequency-dependent impairment of hippocampal LTP from NMDA receptors with reduced calcium permeability. European Journal of Neuroscience. ISSN 0953-816X. 22, p. 476–484.
• Berberich, S; Punnakkal, P; Jensen, Vidar; Pawlak, V; Seeburg, PH & Hvalby, Øyvind Christian [Show all 7 contributors for this article] (2005). Lack of NMDA receptor subtype selectivity for hippocampal long-term potentiation. Journal of Neuroscience. ISSN 0270-6474. 25, p. 6907–6910.
• Jensen, Vidar; Kvello, Ane & Hvalby, Øyvind Christian (2004). Mice with a fra-1 knock-in into the c-fos locus show impaired spatial but regular contextual learning and normal LTP. Brain Research. Molecular Brain Research. ISSN 0169-328X. 130, p. 16–22.
• Krestel, HE; Shimshek, DR; Jensen, Vidar; Nevian, T; Kim, J & Geng, Y [Show all 14 contributors for this article] (2004). A genetic switch for epilepsy in adult mice. Journal of Neuroscience. ISSN 0270-6474. 24, p. 10568–10578.
• Jensen, Vidar; Kaiser, Katharina M.M.; Adelman, Giselind; Borchardt, Thilo; Rozov, Andrei & Burnashev, Nail [Show all 13 contributors for this article] (2003). A juvenile form of postsynaptic hippocampal LTP in mice deficient for the AMPA receptor subunit GluR-A. Journal of Physiology. ISSN 0022-3751. 553, p. 843–856.
• Fleischmann, A; Hvalby, Øyvind Christian; Jensen, Vidar; Strekalova, T; Zacher, C & Layer, L.E. [Show all 12 contributors for this article] (2003). Impaired long-term memory and NR2A-type NMDA receptor-dependent synaptic plasticity in mice lacking c-Fos in the CNS. Journal of Neuroscience. ISSN 0270-6474. 23, p. 9116–9122.
• Köhr, Georg; Jensen, Vidar; Koester, Helmot; Mihaljevic, A; Utvik, JK & Kvello, Ane [Show all 10 contributors for this article] (2003). Intracellular domains of the NMDA receptor subtypes are determinants for long-term potentiation induction. Journal of Neuroscience. ISSN 0270-6474. 23, p. 10791–10799.
• Allen, P. B.; Hvalby, Øyvind Christian; Jensen, Vidar; Errington, M. L.; Ramsay, M. & Chaudhry, Farrukh Abbas [Show all 11 contributors for this article] (2000). Protein phosphatase-1 regulation in the induction of long-term potentiation: heterogeneous molecular mechanisms. Journal of Neuroscience. ISSN 0270-6474. 20, p. 4537–3543.
• Haug, Lise Sofie; Jensen, Vidar; Hvalby, Øyvind Christian; Walaas, Sven Ivar & Østvold, Anne Carine (1999). Phosphorylation of the inositol 1,4,5-trisphosphate receptor by cyclic nucleotide-dependent kinases in vitro and in rat cerebellar slices in situ. Journal of Biological Chemistry. ISSN 0021-9258. 274(11), p. 7467–7473. Show summary

  We have examined cyclic nucleotide-regulated phosphorylation of the neuronal type I inositol 1,4,5-trisphosphate (IP3) receptor immunopurified from rat cerebellar membranes in vitro and in rat cerebellar slices in situ. The isolated IP3 receptor protein was phosphorylated by both cAMP- and cGMP-dependent protein kinases on two distinct sites as determined by thermolytic phosphopeptide mapping, phosphopeptide 1, representing Ser-1589, and phosphopeptide 2, representing Ser-1756 in the rat protein (Ferris, C. D., Cameron, A. M., Bredt, D. S., Huganir, R. L., and Snyder, S. H. (1991) Biochem. Biophys. Res. Commun. 175, 192-198). Phosphopeptide maps show that cAMP-dependent protein kinase (PKA) labeled both sites with the same time course and same stoichiometry, whereas cGMP-dependent protein kinase (PKG) phosphorylated Ser-1756 with a higher velocity and a higher stoichiometry than Ser-1589. Synthetic decapeptides corresponding to the two phosphorylation sites (peptide 1, AARRDSVLAA (Ser-1589), and peptide 2, SGRRESLTSF (Ser-1756)) were used to determine kinetic constants for the phosphorylation by PKG and PKA, and the catalytic efficiencies were in agreement with the results obtained by in vitro phosphorylation of the intact protein. In cerebellar slices prelabeled with [32P]orthophosphate, activation of endogenous kinases by incubation in the presence of cAMP/cGMP analogues and specific inhibitors of PKG and PKA induced in both cases a 3-fold increase in phosphorylation of the IP3 receptor. Thermolytic phosphopeptide mapping of in situ labeled IP3 receptor by PKA showed labeling on the same sites (Ser-1589 and Ser-1756) as in vitro. In contrast to the findings in vitro, PKG preferentially phosphorylated Ser-1589 in situ. Because both PKG and the IP3 receptor are specifically enriched in cerebellar Purkinje cells, PKG may be an important IP3 receptor regulator in vivo.

• Feldmeyer, Dirk; Kask, Kalev; Brusa, Rossella; Kornau, Hans-Kristian; Kolhekar, Rohini & Rozov, Andrei [Show all 11 contributors for this article] (1999). Neurological dysfunction in mice expressing different levels of the Q/R site-unedited AMPA subunit GluR-B. Nature Neuroscience. ISSN 1097-6256. 2(1), p. 57–64.
• Zamamillo, Daniel; Sprengel, Rolf; Hvalby, Øyvind Christian; Jensen, Vidar; Burnashev, Nail & Rozov, Andrei [Show all 16 contributors for this article] (1999). Importance of AMPA Receptors for Hippocampal Synaptic Plasticity But Not for Spatial Learning. Science. ISSN 0036-8075. 284, p. 1805–1811.
• Sprengel, Rolf; Suchanek, B.; Amico, C.; Brusa, R.; Burnashev, Nail & Rozov, Andrei [Show all 15 contributors for this article] (1998). Importance of the intracellular domain of NR2 subunits for NMDA receptor function in vivo. Cell. ISSN 0092-8674. 92, p. 279–289.
• Andersen, Per; Moser, Edvard I. & Jensen, Vidar (1996). Physiologically induced changes of brain temperature and their effect on extracellular field potentials. In Bostock, H.; Kirkwood, P. & Pullen, T. (Ed.), The Neurobiology of Disease. Cambridge University Press. ISSN 0-521-45132-9. p. 221–230.
• Hvalby, Øyvind Christian; Hemmings, H. C. Jr; Paulsen, Ole; Czernik, A.J.; Nairn, A.C. & Godfrain, J.M. [Show all 11 contributors for this article] (1994). Specificity of protein kinase inhibitor peptides and induction of long-term potentiation. Proceedings of the National Academy of Sciences of the United States of America. ISSN 0027-8424. 91, p. 4761–4765.

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• Naik, Aditi; Jensen, Vidar; Bakketun, Cecilie Bugge; Enger, Rune; Hrabetova, Sabina & Hrabe, Jan (2024). Author Correction: BubbleDrive, a low-volume incubation chamber for acute brain slices (Scientific Reports, (2023), 13, 1, (20005), 10.1038/s41598-023-45949-9). Scientific Reports. ISSN 2045-2322. 14(1). doi: 10.1038/s41598-024-52441-5.
• Bertocchi, Ilaria; Eltokhi, Ahmed; Rozov, Andrey; Chi, Vivan Nguyễn; Jensen, Vidar & Bus, Thorsten [Show all 23 contributors for this article] (2021). Erratum: Author Correction: Voltage-independent GluN2A-type NMDA receptor Ca²⁺ signaling promotes audiogenic seizures, attentional and cognitive deficits in mice (Communications biology (2021) 4 1 (59)). Communications Biology. ISSN 2399-3642. 4(1). doi: 10.1038/s42003-021-01717-x.
• Gjerstad, Leif; Jensen, Vidar; Langmoen, Iver Arne; Lømo, Terje; Moser, Edvard Ingjald & Moser, May-Britt [Show all 8 contributors for this article] (2020). Per Andersen. Tidsskrift for Den norske legeforening. ISSN 0029-2001. 9. doi: 10.4045/tidsskr.20.0353.
• Hussain, Suleman; Ringsevjen, Håvard; Schupp, M.; Hvalby, Øyvind Christian dødsbo; Sørensen, J.B. & Jensen, Vidar [Show all 7 contributors for this article] (2019). Correction to: A possible postsynaptic role for SNAP-25 in hippocampal synapses (Brain Structure and Function, (2019), 224, 2, (521-532), 10.1007/s00429-018-1782-2). Brain Structure and Function. ISSN 1863-2653. 224(2). doi: 10.1007/s00429-018-01823-3.
• Bahonjic, Elma; Jensen, Vidar; Hvalby, Øyvind Christian & Walaas, S. Ivar (2013). Distinct hippocampal synaptic vesicle recycling pathways revealed by synapsin I/II-depleted mice.
• Lee, Anee Karin; Dervola, Kine Susann Noren; Roberg, Bjørg Åse; Nielsen, Marit Johanne; Jensen, Vidar & Hvalby, Øyvind Christian [Show all 7 contributors for this article] (2012). Glutamatergic AMPA and NMDA receptor subunits in the hippocampus of rodent models for cognitive dysfunction.
• Owe, Simen Gylterud; Jensen, Vidar; Evergren, Emma; Ruiz, Arnaud; Shupliakov, Oleg & Kullmann, Dimitri [Show all 10 contributors for this article] (2008). Facilitation of glutamate release at hippocampal mossy fibre synapses is dependent on synapsin and actin.
• Gu, Ning; Sausbier, M; Jensen, Vidar; Hvalby, O; Kleppisch, T & Ruth, P [Show all 7 contributors for this article] (2005). Mice lacking BK/KCa1 potassium channels show altered intrinsic excitability but normal synaptic plasticity in hippocampal pyramidal cells. Show summary

  The functions of large conductance (BK) Ca2+-activated K+-channels (KCa1) in CA1 pyramidal cells and synapses were studied in mice with a deletion of the BK channel -subunit gene (BK-/-) by means of field potential recording, sharp electrode intracellular and whole-cell recording from hippocampal slices. We found that, (1) in normal medium, EPSPs evoked by stimulation of Schaffer collaterals were resistant to the BK channel blocker iberiotoxin (IbTX, 100 nM) in both wt and BK-/- cells. (2) There were no significant differences between wt (n=21) and BK-/- (n=18) in the degree or time-course of tetanus-induced long-term potentiation (LTP), nor in paired-pulse facilitation (PPF, 25-420 ms intervals; n=23 and 18, respectively). (3) In the presence of 4-AP, IbTX strongly enhanced the EPSPs evoked by stimulation of Schaffer collaterals, and reduced PPF ratio in wt cells, suggesting an IbTX-induced increase in transmitter release (n=8). This effect of IbTX was absent in BK-/- mice. (4) Moreover, intracellular recordings showed that the repolarization of somatic action potentials was significantly slower in CA1 pyramidal cells from BK-/- mice than in those from wt mice (n=22, p<0.01) and that the fast AHP (fAHP) amplitude was strongly reduced in cells from mutant mice (n=12). (5) IbTX had no effect on spike repolarization or fAHP of CA1 neurons from BK-/- mice, whereas it caused robust spike broadening and block of fAHP in wt cells (n=11). (7) Frequency-dependent spike broadening due to inactivation of the transient BK current was abolished in BK-/- mice (n=12). In conclusion, although BK channels regulate somatic spike repolarization CA1 pyramidal cells and, under certain conditions also control transmitter release at CA1 synapses, they do not appear to affect synaptic facilitation or LTP under basal conditions.

• Jensen, Vidar; Walaas, Sven Ivar; Kao, H.T & Hvalby, Øyvind Christian (2003). Bidirectional regulation of transmitter release induced by synapsins I and II.
• Haug, Lise Sofie; Jensen, Vidar; Hvalby, Øyvind Christian; Walaas, Sven Ivar & Østvold, Anne Carine (1998). Stimulation of cyclic GMP-dependent protein kinase leads to phosphorylation of type I inositol trisphosphate-receptor in rat cerebellar slices.
• Fienberg, A.; Hvalby, Øyvind Christian; Allen, P.; Jensen, Vidar; Ramsay, M. & Morris, Richard G.M. [Show all 8 contributors for this article] (1997). Protein phosphatase inhibitor 1 plays a region specific role in hippocampal LTP induction.
• Skogestad, Sigurd; Einarsrud, Mari-Ann; Fjellvåg, Helmer; Gundersen, Lise-Lotte; Hansen, Trond Vidar & Hemmingsen, Tor [Show all 12 contributors for this article] (2010). Oppfølging av Kjemievalueringen 2009. Forskningsrådet. ISSN 9788212027848.
• Jensen, Vidar (1999). Elements of expression mechanisms of long-term potentiation. ISSN 82-91061-97-1.

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