Empowering the Future of Neuroscience

Empowering the Future of Neurosceince

Fuhrmann Group

My group aims to understand how neurons and innate immune cells in the brain communicate to lay the foundations for cognition and behaviour. We use neurodegenerative and neuropsychiatric disease models to identify new disease relevant mechanisms that may serve for the development of novel therapeutic strategies. Cutting edge in vivo imaging technologies like awake head-fixed Ca2+-imaging and super-resolution 2P-STED imaging enables us to record on the level of individual synapses up to neuronal network. We are able to correlate structural synaptic plasticity and neuronal network activity with precisely measured behaviour. Furthermore, we use state of the art optogenetic and chemogenetic manipulation techniques to modulate neuronal activity. This enables us to causally link neuronal activity with behaviour and cognition. For our large and high dimensional image and video datasets of neuronal activity and behaviour, we apply machine learning and artificial intelligence-based algorithms to perform image analysis and unsupervised behaviour classification. Thereby my group is perfectly suited to ultimately understand how the brain works.

What are we offering?

We perform cutting edge awake two- and three-photon imaging to correlate neuronal activity with behavior.

What are we interested in for collaboration?

We are interested to collaborate on data analyses, microscope inventions and in vivo imaging.

What platforms, analysis tools or facilities do we use and can share?

We are happy to share and help with CaImAn, in vivo imaging and other data analyses.

Discover our homepage here.

To learn more about Prof. Dr. Martin Fuhrmann, follow him on ORCID, Mastodon or Twitter.

Methods

  • Awake head-fixed Ca2+-imaging (two and three photon) during spatial behaviour
  • In vivo super-resolution imaging up to 70 nm x,y-resolution (2P-STED)
  • Opto- and chemogenetics
  • AI-based Image- and Data analysis
  • AAV-based viral tools for cell-type specific manipulation
  • Transgenic mouse lines and behaviour

5 selected publications

  1. Poll, S., Mittag, M., Musacchio, F., Justus, L.C., Ambrad Giovannetti, E., Steffen, J., Wagner, J., Dammer, L., Schoch, S., Schmidt, B., Jackson, W.S., Ehninger, D., Fuhrmann, M. (2020) Memory trace interference impairs recall in a mouse model of AD. Nat Neurosci., 10.1038/s41593-020-0652-4.
  2. Pfeiffer, T., Poll, S., Bancelin, S., Angibaud, J., Inavalli, V.K., Keppler, K., Mittag, M., Fuhrmann, M.*, Nägerl, U.V.* (2018) Chronic 2P-STED imaging reveals high turnover of dendritic spines in the hippocampus in vivo. Elife 7:e34700. *authors contribute equally
  3. Schmid, L.C., Mittag, M., Poll, S., Steffen, J., Wagner, J., Geis, H.R., Schwarz, I., Schmidt, B., Schwarz, M.K., 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.
  4. Gu, L., Kleiber, S., Schmid, L., Nebeling, F., Chamoun, M., Steffen, 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.
  5. Fuhrmann, M., Bittner, T., Jung, C.K., Burgold, S., Page, R.M., Mitteregger, G., Haass, C., LaFerla, F.M., Kretzschmar, H., Herms, J. (2010) Microglial Cx3cr1 knockout prevents neuron loss in a mouse model of Alzheimer’s disease. Nat Neurosci. 13(4):411-3.