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  • 1.
    Berntzon, Lotta
    et al.
    Stockholm University, Faculty of Science, Department of Ecology, Environment and Plant Sciences.
    Ronnevi, L. O.
    Bergman, Birgitta
    Stockholm University, Faculty of Science, Department of Ecology, Environment and Plant Sciences.
    Eriksson, Johan
    Stockholm University, Faculty of Science, Department of Ecology, Environment and Plant Sciences.
    DETECTION OF BMAA IN THE HUMAN CENTRAL NERVOUS SYSTEM2015In: Neuroscience, ISSN 0306-4522, E-ISSN 1873-7544, Vol. 292, p. 137-147Article in journal (Refereed)
    Abstract [en]

    Amyotrophic lateral sclerosis (ALS) is an extremely devastating neurodegenerative disease with an obscure etiology. The amino acid beta-N-methyl-L-alanine (BMAA) produced by globally widespread phytoplankton has been implicated in the etiology of human motor neuron diseases. BMAA was recently proven to be present in Baltic Sea food webs, ranging from plankton to larger Baltic Sea organisms, some serving as important food items (fish) for humans. To test whether exposure to BMAA in a Baltic Sea setting is reflected in humans, blood and cerebrospinal fluid (CSF) from individuals suffering from ALS were analyzed, together with sex- and age-matched individuals not inflicted with ALS. Ultra high performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) and multiple reaction monitoring (MRM), in conjunction with diagnostic transitions revealed BMAA in three (12%) of the totally 25 Swedish individuals tested, with no preference for those suffering from ALS. The three BMAA-positive samples were all retrieved from the CSF, while BMAA was not detected in the blood. The data show that BMAA, potentially originating from Baltic Sea phytoplankton, may reach the human central nervous system, but does not lend support to the notion that BMAA is resident specifically in ALS-patients. However, while dietary exposure to BMAA may be intermittent and, if so, difficult to detect, our data provide the first demonstration of BMAA in the central nervous system of human individuals ante mortem quantified with UHPLC-MS/MS, and therefore calls for extended research efforts.

  • 2.
    Cavazzana, Annachiara
    et al.
    Stockholm University, Faculty of Social Sciences, Department of Psychology. TU Dresden, Germany.
    Poletti, Sophia C.
    Guducu, Cagdas
    Larsson, Maria
    Stockholm University, Faculty of Social Sciences, Department of Psychology, Perception and psychophysics.
    Hummel, Thomas
    Electro-olfactogram Responses Before and After Aversive Olfactory Conditioning in Humans2018In: Neuroscience, ISSN 0306-4522, E-ISSN 1873-7544, Vol. 373, p. 199-206Article in journal (Refereed)
    Abstract [en]

    The aim of the present study was to investigate whether repetitive aversive odor conditioning induced changes at the level of the peripheral olfactory system in humans. A total of 51 volunteers participated. A pair of indistinguishable odor enantiomers [(+)-rose oxide and (-)-rose oxide] were used as stimuli. During the pre-conditioning, participants' ability to discriminate between the two odors was assessed using a three-alternative, forced-choice discrimination test. In addition, electro-olfactograms ( EOG) from the olfactory epithelium were recorded. Participants underwent three conditioning sessions on consecutive days. The experimental group received an electrical stimulus to the forearm only following (+)-rose oxide presentation, whereas its enantiomer sibling was never paired with the aversive stimulus; the control group did not receive any electrical stimulation. During the post-conditioning session, their ability to discriminate the two enantiomers was assessed again using the discrimination test and EOG recordings were obtained similarly to the pre-conditioning session. Results showed significant differences in the peripheral electrophysiological responses between the conditioned and the unconditioned stimulus, demonstrating contextually induced changes at the level of the first neuron in the olfactory system.

  • 3. East, Brett S.
    et al.
    Fleming, Gloria
    Peng, Kathy
    Olofsson, Jonas K.
    Stockholm University, Faculty of Social Sciences, Department of Psychology, Perception and psychophysics. Nathan S. Kline Institute, USA; New York University School of Medicine, USA.
    Levy, Efrat
    Mathews, Paul M.
    Wilson, Donald A.
    Human Apolipoprotein E Genotype Differentially Affects Olfactory Behavior and Sensory Physiology in Mice2018In: Neuroscience, ISSN 0306-4522, E-ISSN 1873-7544, Vol. 380, p. 103-110Article in journal (Refereed)
    Abstract [en]

    Apolipoprotein E (ApoE) is an important lipid carrier in both the periphery and the brain. The ApoE epsilon 4 allele (ApoE4) is the single most important genetic risk-factor for Alzheimer's disease (AD) while the epsilon 2 allele (ApoE2) is associated with a lower risk of AD-related neurodegeneration compared to the most common variant, epsilon 3 (ApoE3). ApoE genotype affects a variety of neural circuits; however, the olfactory system appears to provide early biomarkers of ApoE genotype effects. Here, we directly compared olfactory behavior and olfactory system physiology across all three ApoE genotypes in 6-month- and 12-month-old mice with targeted replacement for the human ApoE2, ApoE3, or ApoE4 genes. Odor investigation and habituation were assessed, along with, olfactory bulb and piriform cortical local field potential activity. The results demonstrate that while initial odor investigation was unaffected by ApoE genotype, odor habituation was impaired in E4 relative to E2 mice, with E3 mice intermediate in function. There was also significant deterioration of odor habituation from 6 to 12 months of age regardless of the ApoE genotype. Olfactory system excitability and odor responsiveness were similarly determined by ApoE genotype, with an ApoE4 > ApoE3 > ApoE2 excitability ranking. Although motivated behavior is influenced by many processes, hyper-excitability of ApoE4 mice may contribute to impaired odor habituation, while hypo-excitability of ApoE2 mice may contribute to its protective effects. Given that these ApoE mice do not have AD pathology, our results demonstrate how ApoE affects the olfactory system at early stages, prior to the development of AD.

  • 4. Flohr, E. L. R.
    et al.
    Arshamian, Artin
    Stockholm University, Faculty of Social Sciences, Department of Psychology, Perception and psychophysics.
    Wieser, M. J.
    Hummel, C.
    Larsson, Maria
    Stockholm University, Faculty of Social Sciences, Department of Psychology, Perception and psychophysics.
    Muehlberger, A.
    Hummel, T.
    THE FATE OF THE INNER NOSE: ODOR IMAGERY IN PATIENTS WITH OLFACTORY LOSS2014In: Neuroscience, ISSN 0306-4522, E-ISSN 1873-7544, Vol. 268, p. 118-127Article in journal (Refereed)
    Abstract [en]

    Cerebral activations during olfactory mental imagery are fairly well investigated in healthy participants but little attention has been given to olfactory imagery in patients with olfactory loss. To explore whether olfactory loss leads to deficits in olfactory imagery, neural responses using functional magnetic resonance imaging (fMRI) and self-report measures were investigated in 16 participants with acquired olfactory loss and 19 control participants. Participants imagined both pleasant and unpleasant odors and their visual representations. Patients reported less vivid olfactory but not visual images than controls. Results from neuroimaging revealed that activation patterns differed between patients and controls. While the control group showed stronger activation in olfactory brain regions for unpleasant compared to pleasant odors, the patient group did not. Also, activation in critical areas for olfactory imagery was correlated with the duration of olfactory dysfunction, indicating that the longer the duration of dysfunction, the more the attentional resources were employed. This indicates that participants with olfactory loss have difficulties to perform olfactory imagery in the conventional way. Regular exposure to olfactory information may be necessary to maintain an olfactory imagery capacity.

  • 5.
    Kahsai, Lily
    et al.
    Stockholm University, Faculty of Science, Department of Zoology.
    Carlsson, Mikael A.
    Stockholm University, Faculty of Science, Department of Zoology.
    Winther, Åsa M.
    Stockholm University, Faculty of Science, Department of Zoology.
    Nässel, Dick R.
    Stockholm University, Faculty of Science, Department of Zoology.
    Distribution of metabotropic receptors of serotonin, dopamine, GABA, glutamate, and short neuropeptide F in the central complex of Drosophila2012In: Neuroscience, ISSN 0306-4522, E-ISSN 1873-7544, Vol. 208, p. 11-26Article in journal (Refereed)
    Abstract [en]

    The central complex is a prominent set of midline neuropils in the insect brain, known to be a higher locomotor control center that integrates visual inputs and modulates motor outputs. It is composed of four major neuropil structures, the ellipsoid body (EB), fan-shaped body (FB), noduli (NO), and protocerebral bridge (PB). In Drosophila different types of central complex neurons have been shown to express multiple neuropeptides and neurotransmitters; however, the distribution of corresponding receptors is not known. Here, we have mapped metabotropic, G-protein–coupled receptors (GPCRs) of several neurotransmitters to neurons of the central complex. By combining immunocytochemistry with GAL4 driven green fluorescent protein, we examined the distribution patterns of six different GPCRs: two serotonin receptor subtypes (5-HT1B and 5-HT7), a dopamine receptor (DopR), the metabotropic GABAB receptor (GABABR), the metabotropic glutamate receptor (DmGluRA) and a short neuropeptide F receptor (sNPFR1). Five of the six GPCRs were mapped to different neurons in the EB (sNPFR1 was not seen). Different layers of the FB express DopR, GABABR, DmGluRA, and sNPFR1, whereas only GABABR and DmGluRA were localized to the PB. Finally, strong expression of DopR and DmGluRA was detected in the NO. In most cases the distribution patterns of the GPCRs matched the expression of markers for their respective ligands. In some nonmatching regions it is likely that other types of dopamine and serotonin receptors or ionotropic GABA and glutamate receptors are expressed. Our data suggest that chemical signaling and signal modulation are diverse and highly complex in the different compartments and circuits of the Drosophila central complex. The information provided here, on receptor distribution, will be very useful for future analysis of functional circuits in the central complex, based on targeted interference with receptor expression.

  • 6.
    Larsson, Maria
    et al.
    Stockholm University, Faculty of Social Sciences, Department of Psychology, Perception and psychophysics. Stockholm Brain Institute, Stockholm, Sweden.
    Farde, L.
    Karolinska Institutet.
    Hummel, T.
    University of Dresden Medical School.
    Witt, M.
    University of Dresden Medical School.
    Erixon Lindroth, N.
    Karolinska Institutet.
    Bäckman, Lars
    Karolinska Institutet.
    Age-related loss of olfactory sensitivity: Association to dopamine transporter binding in putamen2009In: Neuroscience, ISSN 0306-4522, E-ISSN 1873-7544, Vol. 161, no 2, p. 422-426Article in journal (Refereed)
    Abstract [en]

    The relationship between age-related reductions in the binding potential for the striatal dopamine transporter (DAT) and age-related deficits in olfactory sensitivity was examined in 12 subjects ranging from 36 to 82 years of age. Positron emission tomography (PET) and the radioligand [11C]β-CIT-FE were used to determine DAT binding in two striatal regions, the caudate and the putamen. The results showed age-related losses of DAT binding from early to late adulthood of similar size for caudate and putamen, and there was a pronounced age deterioration in olfactory sensitivity. Importantly, the age-related olfactory deficit was associated with reductions in DAT binding in putamen, but not caudate. Also, DAT binding in putamen added systematic variance in odor threshold after controlling for age. The findings indicate that DAT binding in putamen is related to age-related olfactory deficits, as well as to odor sensitivity independently of age.

  • 7. Porada, Danja K.
    et al.
    Regenbogen, Christina
    Seubert, Janina
    Freiherr, Jessica
    Lundström, Johan N.
    Stockholm University, Faculty of Humanities, Department of Linguistics. Karolinska Institutet, Sweden; Monell Chemical Senses Center, USA; University of Pennsylvania, USA.
    Multisensory Enhancement of Odor Object Processing in Primary Olfactory Cortex2019In: Neuroscience, ISSN 0306-4522, E-ISSN 1873-7544, Vol. 418, p. 254-265Article in journal (Refereed)
    Abstract [en]

    Identification of an object based on its odor alone is inherently difficult, but becomes easier when other senses provide supporting cues. This suggests that crossmodal sensory input facilitates neural processing of olfactory object information; however, direct evidence is still lacking. Here, we tested the effect of multisensory stimulation on information processing in the human posterior piriform cortex (PPC), a region linked to olfactory object encoding. Participants were exposed to familiar objects in the form of uni-, bi-, and trimodal combinations of odors, videos, and sounds. We hypothesized that the PPC would respond to non-olfactory object information, and that activity would increase linearly with the number of senses providing relevant object information. As predicted, visual object information activated the PPC and activity increased linearly with the number of relevant sensory channels. The crossmodal response pattern thus indicates that the PPC does not exclusively respond to olfactory information, but also to crossmodal object information important for olfactory processing. The continuous activity increase suggests that the PPC further acts as a multisensory binding site where pertinent input from multiple senses results in an increased neural response to the odor object. This potentially represents a neural mechanism for the well-known behavioral improvement present in odor object recognition during concurrent crossmodal sensory stimulation.

  • 8. Yamakawa, Glenn R.
    et al.
    Weerawardhena, Himanthri
    Eyolfson, Eric
    Griep, Yannick
    Stockholm University, Faculty of Social Sciences, Stress Research Institute. The University of Calgary, Canada.
    Antle, Michael C.
    Mychasiuk, Richelle
    Investigating the Role of the Hypothalamus in Outcomes to Repetitive Mild Traumatic Brain Injury: Neonatal Monosodium Glutamate Does Not Exacerbate Deficits2019In: Neuroscience, ISSN 0306-4522, E-ISSN 1873-7544, Vol. 413, p. 264-278Article in journal (Refereed)
    Abstract [en]

    Repetitive mild traumatic brain injury (RmTBI) is a prevalent and costly head injury particularly among adolescents. These injuries may result in long-term consequences, especially during this critical period of development. Insomnia and sleeping difficulties are frequently reported following RmTBI and greatly impair recovery. We sought to develop an animal model of exacerbated deficits following RmTBI by disrupting the hypothalamic circadian system. To accomplish this, we conducted RmTBI on adolescent rats that had received neonatal injections of monosodium glutamate (MSG), a known hypothalamic neurotoxin. We then examined behavioral, circadian, and epigenetic changes. MSG treated rats showed lower anxiety-like behaviors and displayed poor short-term working memory. We also showed changes in the morphology of the circadian clock in the suprachiasmatic nucleus (SCN) vasoactive intestinal polypeptide (VIP) immunostaining. VIP optical density in the SCN increased with MSG but decreased with RmTBI. There were changes in the expression of the clock genes and upregulation of the orexin receptors in response to RmTBI. MSG treated rats had longer telomere lengths than controls. Finally, although both MSG and RmTBI alone produced attenuated circadian amplitudes of activity and body temperature, exacerbated deficits were not identified in animals that received MSG and RmTBI. In sum, both MSG and RmTBI can alter behavior, circadian rhythm amplitude, SCN morphology, and gene expression independently, but the effects do not appear to be additive. Specific damage in the hypothalamus and SCN should be considered when patients experience sleeping problems following RmTBI, as this may improve therapeutic strategies.

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