Current Research

Spatiotemporal Coupling of Neuronal Activity in Functional Ensembles

Rhythmic activity is a key functional feature of the brain, as evident from the EEG. Meanwhile, many neuroscientists agree that such network oscillations are “meaningful” and provide an important background for temporal coding of information. The basic concept is that synchronized oscillations bind neurons into transient assemblies where co-active neurons constitute transient representations (e.g. spatial memories). In our group we focus on network oscillations in the rodent hippocampus and the adjacent entorhinal cortex. We try elucidating the specific properties of co-active cells which underlie the formation of neuronal assemblies. Experimentally, we are approaching these questions with a variety of electrophysiological methods (tetrodes, patch-clamp, intra- and juxtacellular recordings) and with new life-imaging techniques. Together with our cooperation partners, we also develop new algorithms for data analysis and models of neuronal functions within oscillating networks.
 

Fig. 1: Assembly formation by spatiotemporal activity of sparse neurons

We are also interested in pathological activity patterns, e.g. in epileptic tissue and in mice with altered Alzheimer-related proteins (APP‑/‑/APLP2‑/‑ mice).

Function and plasticity of GABAergic synapses

GABAergic inhibition has a crucial function in the organization of spatiotemporal activity patterns in neuronal networks. The complex organization of central synapses offers multiple mechanisms for regulation and modulation of synaptic strength. We focus on inhibitory synapses in the mammalian CNS which use GABA (gamma-aminobutyric acid) as transmitter. In previous work, we and others have provided evidence that changes in presynaptic GABA content do change the efficacy of inhibitory transmission. The availability of GABA is regulated by its uptake, synthesis and degradation. The relative contribution of these functions can change in situations of enhanced or reduced activity, thereby adapting the efficacy of GABAergic transmission to the degree of activity in the local network. This feedback loop constitutes a mechanism of homeostatic network plasticity. We are presently exploring this concept using various electrophysiological, histological and biochemical techniques.

Fig. 2: Scheme of a GABAergic synapse illustrating different sources of GABA