---
res:
  bibo_abstract:
  - "Epilepsy affects about 50 to 65 million people globally. It summarizes a spectrum
    of neurological\r\ndisorders that have in common a hyperactivity of the neuronal
    network resulting in seizures. A common\r\nassumption is that an imbalance between
    neuronal excitation and inhibition is a key mechanism in\r\nseizure generation
    and epileptogeneisis. In at least one-third of the patients, current therapies
    have\r\nproven unsuccessful in treating seizure progression. One potential reason
    could be that the therapies\r\nonly focus on neurons. Recent studies suggest that
    neuronal hyperactivity causes a microglial\r\nresponse, which reinstates brain
    homeostasis. Additionally, interactions between microglia and neurons\r\nhave
    been shown to inhibit neuronal firing and dampen seizure activity. However, the
    exact relationship\r\nbetween microglia and seizure progression in epilepsy is
    yet to be elucidated. A main bottleneck is that\r\nseveral studies investigate
    microglia dynamics in ex vivo slice models, which can severely affect the\r\nmicroglia
    dynamics due to their rapid response to environmental changes. On the other hand,
    in vivo\r\nstudies focus mostly on behavior characterization of the epileptic
    seizure phenotype and their long-term\r\nconsequences on microglia activity leaving
    out the direct consequences of acute seizure activity on\r\nmicroglia dynamics.\r\nHere,
    we perform a pilot study to combine electroencephalography (EEG) and in vivo live
    imaging to\r\ndirectly monitor and correlate the onset of seizure activity with
    microglia response. To induce seizures,\r\nwe take advantage of the kainic acid
    (KA) model, which represents similar neuropathological and\r\nelectroencephalographic
    features seen in human patients with temporal lobe epilepsy (TLE). After\r\nconfirmation
    of induction of the seizure and microglia activity in the hippocampus as a focal
    point, we\r\ninvestigated whether these changes also reached the primary visual
    cortex (V1) as a secondary\r\ngeneralized seizure activity. Indeed, we found that
    microglia changed their morphology at high doses\r\nof KA in the V1. Next, we
    optimized each of the two methodological components: for the EEG recording,\r\nour
    initial attempts under the microscope suffered from extensive electrical noise,
    which overlaid the\r\nactual signal. Thus, we built a customized Faraday-cage
    and confirmed that the signal-to-noise ratio\r\nwas sufficiently reduced to be
    able to record brain oscillatory activity. For the in vivo live imaging of\r\nmicroglia,
    we had to optimize the imaging parameters, so that we would be able to detect
    microglial\r\nprocesses in a sufficient resolution to track their process changes.
    Finally, we combined both\r\nmethodologies with the KA model. We confirmed that
    KA induced seizure activity and found first\r\nindication that those correlate
    with microglia volume changes.\r\nOverall, we have developed a first methodological
    approach, which allows the analysis of the acute\r\neffects of seizure onset on
    microglia. Future studies will have to continue to optimize the drift during\r\nimaging
    recording and the post-image analysis. @eng"
  bibo_authorlist:
  - foaf_Person:
      foaf_givenName: Julie Stefanie
      foaf_name: Murmann, Julie Stefanie
      foaf_surname: Murmann
      foaf_workInfoHomepage: http://www.librecat.org/personId=1d390868-f128-11eb-9611-a0ca5f7833b5
  bibo_doi: 10.15479/at:ista:15352
  dct_date: 2024^xs_gYear
  dct_isPartOf:
  - http://id.crossref.org/issn/2791-4585
  dct_language: eng
  dct_publisher: Institute of Science and Technology Austria@
  dct_title: 'Investigating acute microglia response to seizure activity in vivo:
    Combining 2-Photon imaging and EEG recording@'
...