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  • 1.
    Cselenyi, Zsolt
    et al.
    Karolinska Inst, Sweden; AstraZeneca, Sweden.
    Wallin, Johan
    Karolinska Inst, Sweden.
    Tjerkoski, Jonathan
    Karolinska Inst, Sweden.
    Bloth, Bjorn
    Karolinska Inst, Sweden.
    Svensson, Samuel
    Linköping University, Department of Physics, Chemistry and Biology, Chemistry. Linköping University, Faculty of Science & Engineering. Karolinska Inst, Sweden.
    Nennesmo, Inger
    Karolinska Inst, Sweden.
    Sunnemark, Dan
    Karolinska Inst, Sweden.
    Jelic, Vesna
    Karolinska Inst, Sweden.
    Farde, Lars
    Karolinska Inst, Sweden.
    Svenningsson, Per
    Karolinska Inst, Sweden.
    [C-11]PBB3 binding in A beta(-) or A beta(+) corticobasal syndrome2023In: Synapse, ISSN 0887-4476, E-ISSN 1098-2396, Vol. 77, no 4, article id e22269Article in journal (Refereed)
    Abstract [en]

    Corticobasal syndrome (CBS) is associated with 4-repeat tauopathy and/or Alzheimers disease pathologies. To examine tau and amyloid-beta (A beta) deposits in CBS patients using positron emission tomography (PET). Eight CBS patients and three healthy individuals lacking amyloid pathology underwent PET with [C-11]PBB3 for tau imaging, and [C-11]AZD2184 for A beta. Subcortical and cortical binding of [C-11]PBB3 was compared between A beta(-) and A beta(+) CBS patients and reference group. Postmortem analysis was done in one CBS patient. Three CBS patients were considered A beta(+). Total binding was higher in all patients compared to the reference group. Similar regional binding profiles of [C-11]PBB3 in A beta(+) and A beta(-) CBS patients were found. Elevated [C-11]PBB3 binding in pallidum was observed in all CBS patients. Cortical [C-11]PBB3 binding was higher in A beta(+) compared to A beta(-) patients. Postmortem analysis of a CBS patient revealed corticobasal degeneration neuropathology and [C-11]PBB3 autofluorescence in some tau-positive structures. [C-11]PBB3 is elevated in CBS patients with binding in relevant areas capturing some, but not all, 4-repeat tauopathy in CBS.

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  • 2.
    Skinbjerg, Mette
    et al.
    National Institutes of Health, NIH, Bethesda, MD, USA.
    Ariano, Marjorie A.
    The Chicago Medical School at Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, USA.
    Thorsell, Annika
    National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA.
    Heilig, Markus
    National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA.
    Halldin, Christer
    Karolinska Institutet, Stockholm, Sweden.
    Innis, Robert B.
    National Institute of Mental Health, NIH, Bethesda, MD, USA.
    Sibley, David R.
    National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA.
    Arrestin3 mediates D(2) dopamine receptor internalization2009In: Synapse, ISSN 0887-4476, E-ISSN 1098-2396, Vol. 63, no 7, p. 621-624Article in journal (Refereed)
  • 3.
    Yoshitake, Shimako
    et al.
    Karolinska Institute, Stockholm, Sweden .
    Kuteeva, Eugenia
    Karolinska Institute, Stockholm, Sweden and Atlas Antibodies AB, AlbaNova University Center, Stockholm, Sweden.
    Hokfelt, Tomas
    Karolinska Institute, Stockholm, Sweden .
    Mennicken, Francoise
    AstraZeneca R&D Montréal, Quebec, Canada.
    Theodorsson, Elvar
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Diagnostics, Department of Clinical Chemistry.
    Yamaguchi, Masatoshi
    Fukuoka University, Japan .
    Kehr, Jan
    Karolinska Institute, Stockholm, Sweden and Pronexus Analytical AB, Bromma, Sweden .
    Yoshitake, Takashi
    Karolinska Institute, Stockholm, Sweden and Kagoshima University, Japan .
    Correlation between the effects of local and intracerebroventricular infusions of galanin on 5-HT release studied by microdialysis, and distribution of galanin and galanin receptors in prefrontal cortex, ventral hippocampus, amygdala, hypothalamus, and striatum of awake rats2014In: Synapse, ISSN 0887-4476, E-ISSN 1098-2396, Vol. 68, no 5, p. 179-193Article in journal (Refereed)
    Abstract [en]

    The neuropeptide galanin is implicated in regulation of affective behavior, including modulation of 5-HT signaling. Here, we investigated, by use of microdialysis in freely moving rats, the effects of intracerebral (i.c.) and intracerebroventricular (i.c.v.) infusions of galanin on basal extracellular 5-HT levels in medial prefrontal cortex (mPFC), CA1 area of ventral hippocampus (vHPC), central amygdaloid nucleus (CeA), ventromedial hypothalamic nucleus ventrolateral part (VMHvl), and ventromedial caudate putamen (CPu). These results were compared with a parallel immunohistochemical analysis of the distribution of galanin, 5-HT, and noradrenaline (NA) nerve terminals, and with data on galanin receptors. Galanin i.c.v. significantly decreased the 5-HT levels in mPFC to 79% and in vHPC to 72%. Local infusions of galanin caused a long-lasting decrease in 5-HT levels in vHPC to 88%, and a moderate decrease in CeA, whereas the 5-HT levels in mPFC significantly increased to 121%. These effects of i.c. galanin correlated well with the density of 5-HT and galanin nerve terminals and galanin receptors autoradiography in mPFC, vHPC, and CeA. No effects of i.c. or i.c.v. galanin on 5-HT levels were observed in CPu or VMHvl, in agreement with the low numbers of galanin-positive terminals and low/moderate galanin receptor density. Galanin was often found to coexist in NA, but could never be detected in 5-HT terminals. Together the results show a neuroanatomical correlation between the effects of galanin infusions on 5-HT release and distribution of galanin and its receptors, and that i.c.v. and i.c. administration can give opposite effects on 5-HT release.

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