Maria Lindskog

Maria Lindskog

Anknuten till Forskning
Besöksadress: BioClinicum J10:30, Visionsgatan 4, 17164 Solna
Postadress: H1 Neurobiologi, vårdvetenskap och samhälle, H1 Neurogeriatrik Ankarcrona, 171 77 Stockholm

Om mig

  • Fil. Mag. Uppsala Universitet 1996
    PhD Karolinska Institutet 2001
    PostDoc Kungliga Tekniska Högskolan (Prof. Hällgren-Kotaleski) 2002
    PostDoc Stanford University (Prof. R.W. Tsien) 2002-2006


  • *Lindskog Laboratory*
    If you consider the brain to be an information-processing network, the
    synapse is the contact point where information is transmitted from one neuron
    to another, and thus an important place to tune the network activity through
    regulation of synaptic strength. 80% of the synapses in the brain use
    glutamate as a neurotransmitter, making the tuning of glutamate transmission
    a key mechanism in shaping neural activity and brain function. Most
    importantly, misregulation of glutamatergic transmission has been associated
    with cognitive decline as well as mood disorders. Thus, identification of
    novel regulatory mechanisms can provide much needed targets for treatments
    for diseases where our understanding of the etiology is still limited,
    including Alzheimer’s disease, depression and schizophrenia.
    In my lab we combine electrophysiological recordings in brain slices,
    biochemical analysis and behavior to study the modulation of synaptic
    transmission and plasticity. Currently we are particularly interested in the
    role of astrcoytes, A well accepted theory of astrocyte function proposes
    that astrocytes keep the glutamate transmission balanced by sensing neuronal
    activity and responding by adjusting glutamate uptake or releasing
    gliatransmittors that regulate synaptic function. However, there is still a
    lack of precise information on astrocyte regulation of synaptic activity, and
    strikingly, there is no consensus on what the major function of an astrocyte
    is, neither on how astrocyte function is regulated.
    *Recent publications:*
    Magara S, Holst S, Lundberg S, Roman E, Lindskog M. Altered explorative
    strategies and reactive coping style in the FSL rat model of depression,
    accepted for publicatio [1]n, Front. Behav. Neurosci. 2015
  • 9:89
    Femenía, T., Magara, S., DuPont C.M., Lindskog, M. Effects of the H3
    receptor antagonist clobenpropit in a rat model of depression: the role of
    histamine receptors in the hippocampus, accepted for publication, [2] Int J
    Neuropsychopharmacol. 2015, 18(9)
    Agudelo LZ, Femenía, T, Orhan F, Porsemyr-Palmertz M, Goiny M,
    Martinez.Redondo V, Correia JC, Izadi M, Bhat M, Schppe-Koistinen
    I, Petterson AT, Ferreira DM, Krook A, Barres R, Zierath JR,
    Erhardt S, Lindskog M*, /Ruas JL.* Skeletal muscle PGC-11 modulates
    kynurenine metabolism and mediates resilience to stress-induced depression
    [3]. Cell 2014 159
  • 1 33-45
    *shared last and co-corresponding authors


Alla övriga publikationer


  • Anknuten till Forskning, Neurobiologi, vårdvetenskap och samhälle, Karolinska Institutet, 2023-2024

Examina och utbildning

  • FILOSOFIE DOKTOR, Institutionen för neurovetenskap, Karolinska Institutet, 2001

Nyheter från KI

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