After a bit of a quiet period we welcome several (new) colleagues to the lab (link).

It is known that dendrites of hippocampal pyramidal cells amplify clustered glutamatergic input. This involves N-methyl-D-aspartate receptors (NMDARs), whose activity also depends on the presence of NMDAR co-agonists such as D-serine.

In our recent study by Bohmbach et al., we discovered an unexpected frequency-dependent excitatory feedback loop between pyramidal cell activity and dendritic amplification of synaptic input. It is mediated by NMDAR co-agonists and astrocytes. Importantly, disrupting this feedback loop at the level of astrocytes impairs spatial memory.

K. Bohmbach, N. Masala, E.M. Schönhense, K. Hill, A.N. Haubrich, A. Zimmer, T. Opitz, H. Beck, C. Henneberger (2022) An astrocytic signaling loop for frequency-dependent control of dendritic integration and spatial learning. Nat. Commun. 13(1):7932. (link)

Congratulations to Kirsten for defending her PhD thesis today. The final verdict after her defense was summa cum laude. Fully deserved, great work!

Again, the defense had to happen entirely online so there was only a very short and adequately socially distanced ceremony. But there will be a time for celebrating more extensively!

Fortunately for us, Kirsten is going to stay with us as a postdoctoral researcher.

Congratulations to Björn for the great defense of his PhD thesis today. The final verdict after his defense, which unfortunately had to happen entirely online, was a fully-deserved summa cum laude. Great work!

Unfortunately for us, Börn has already moved on and is now working as a patent agent. … where he is probably using his experience from our journal clubs to explain each and everyone why there is absolutely nothing new about their recent inventions.

November 2020 marks the official start of The European University Neurotech^EU.

Neurotech^EU will educate students across all levels (bachelor’s, master’s, doctoral as well as life-long learners) and train the next-generation multidisciplinary scientists, scholars and graduates, provide them direct access to cutting-edge infrastructure for fundamental, translational and applied research to help Europe address this unmet challenge.

Synapses in the brain are approached by perisynaptic astrocyte processes, which are important for the clearance of the neurotransmitter glutamate, for instance. But the coverage of synapses by theses astrocytic processes varies considerably from synapse to synapse. In a first recent study, we could demonstrate that stronger synapses are covered less, relative to their size, and uptake of glutamate is less efficient at these synapses, which increases the probability of synaptic crosstalk. In a second recent study, we could reveal that induction of synaptic long-term potentiation, a cellular mechanism underlying learning, but not depression can trigger the withdrawal of astrocytic processes from synapses and increase synaptic crosstalk. Together, both studies show that the geometrical arrangement of synapses and persisynaptic astrocyte processes is dynamically regulated and defines the spatial precision of synaptic transmission.

Herde K, Bohmbach K, Domingos C, Vana N, Komorowska-Müller JA, Passlick S,  Schwarz I, Jackson CJ, Dietrich D, Schwarz MK, Henneberger C (2020) Local efficacy of glutamate uptake decreases with synapse size. Cell Rep. 32(12):108182 (link)

Henneberger C, Bard L, Panatier A, Reynolds J, Kopach O, Medvedev NI, Minge D, Herde MK, Anders S, Kraev I, Heller JP, Rama S, Zheng K, Jensen TP, Sanchez-Romero I, Jackson C, Janovjak H, Ottersen OP, Nagelhus EA, Oliet SHR, Stewart MG, Nägerl UV, Rusakov DA (2020) LTP induction boosts glutamate spillover by driving withdrawal of perisynaptic astroglia. Neuron (in press) (link)

Astroglia can encode their activity by the generation of Ca²⁺ signals, which then trigger or modify various functions of the cell. The signalling pathways that generate Ca²⁺ signals have been explored in detail. However, what controls their amplitude and waveform remains poorly understood. Using an array of optical methods in vitro and in vivo, we, i.e., Claire King, Kirsten Bohmbach and further colleagues have explored how the resting Ca²⁺ concentration controls these signals. We consistently find that peak and amplitude of Ca²⁺ signals display an opposite dependence on the resting Ca²⁺: a previously unrecognized basic rule underlying Ca²⁺ signalling in astroglial. The study has been published in Cell Report.

King CM, Bohmbach K, Minge D, Delekate A, Zheng K, Reynolds J, Rakers C, Zeug A, Petzold GC, Rusakov DA, Henneberger C (2020) Local Resting Ca²⁺ Controls the Scale of Astroglial Ca²⁺ Signals. Cell Rep. 30(10):3466-3477 (link, open access)

For a more in-depth discussion of astrocytic Ca²⁺ signalling please see our recent review.

Semyanov A, Henneberger C, Agarwal A (2020) Making sense of astrocytic calcium signals — from acquisition to interpretation. Nat. Rev. Neurosci. 21(10):551–564. (link)

Astrocytes form networks in which individual astrocytes are coupled to their neighbors via gap junctions. These networks are thought to help buffering rises of extracellular potassium and thereby to control neuronal excitability. Björn Breithausen, a PhD student in our lab, and colleagues have tested if acute pharmacological blockade of gap junctions impairs potassium buffering. In contrast to our expectations, we found that blockade of gap junctions only affected very local and very large extracellular potassium increases, which are usually only found in brain diseases. The study was published in GLIA.

Breithausen B, Kautzmann S, Boehlen A, Steinhäuser C, Henneberger C (2020) Limited contribution of astroglial gap junction coupling to buffering of extracellular K⁺ in CA1 stratum radiatum. Glia. 68(5):918-931 (link, open access)