Poll Group

We investigate diseases of the central nervous system with two research foci (middle panel) from the subcellular to the functional level (left panel) by using cutting-edge two-photon in vivo microscopy, AAV-mediated visualization and manipulation techniques and careful behavioral readouts (right panel). Figure prepared with the help of biorender.com.

It is intriguing how tightly-orchestrated neuronal networks fulfil, what we are appreciating as our mind and what ultimately helps us to define our personality. It is one of our most valuable skills that defines mankind, the ability to create new thoughts and learn from experience. From this it becomes clear that diseases of the central nervous system can present a tremendous burden for individuals and their families. Our group wants to understand the mechanisms of central nervous system (CNS) diseases and their effect on natural processing of information. My group focuses on two research questions: we investigate (A) neuronal circuits involved in spatial and social cognition to decipher their role for behaviour and their impairments in the context of neurodegenerative and neuropsychiatric diseases. We further aim at (B) deciphering the interactions of tumors of the central nervous system with their microenvironment, to identify routes of communication and thus novel treatment strategies. We are using two-photon in vivo microscopy and neuronal manipulation techniques in transgenic mice to investigate structural and functional properties of brain regions in health and disease.

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Methods

  • longitudinal two-photon (2P) microscopy in vivo (mus musculus)
  • AAV-mediated, activity-dependent and temporally controlled expression systems
  • Opto- and chemogenetics
  • Behavioral tests to assess learning and memory recall
  • Immunohistochemistry and confocal microscopy

5 selected publications

  1. Poll S, Mittag M, Musacchio F, Justus LC, Ambrad Giovannetti E, Steffen J, Wagner J, Zohren L, Schoch S, Schmidt B, Jackson WS, Ehninger D, Fuhrmann M. (2020) Memory trace interference impairs recall in a mouse model of AD. Nat. Neurosci. 23: 952-958.
  2. Druart M, Nosten-Bertrand M, Poll S, Crux S, Nebeling F, Delhaye C, Dubois Y, Leboyer M, Tamouza R, Fuhrmann M, Le Magueresse C. (2021) Elevated expression of complement C4 in the mouse prefrontal cortex causes schizophrenia-associated phenotypes. Mol. Psychiatry. 26: 3489-3501.
  3. Pfeiffer T*, Poll S*, Bancelin S*, Angibaud J, Inavalli VK, Keppler K, Mittag M, Fuhrmann M*, Nägerl UV.* (2018) Chronic 2P-STED imaging reveals high turnover of dendritic spines in the hippocampus in vivo. Elife, 7:e34700, *authors contributed equally.
  4. Schmid LC, Mittag M, Poll S, Steffen J, Wagner J, Geis HR, Schwarz I, Schmidt B, Schwarz MK, Remy S, Fuhrmann M. (2016) Dysfunction of somatostatin positive interneurons associated with memory deficits in an Alzheimer’s disease model. Neuron 92(1):114-125.
  5. Gu L, Kleiber S, Schmid L, Nebeling F, Chamoun M, Steffen J, Wagner J, Wagner J, Fuhrmann M. (2014) Long-term in vivo imaging of dendritic spines in the hippocampus reveals structural plasticity. J. Neurosci. 34(42):13948-53.