CBBS Paper of the year 2015
When an error has occurred, acetylcholine is crucial to focus on goal again
The reason for human errors is often a lack of attention and getting distracted by irrelevant information. For instance, if you add salt instead of sugar to a cup of tea, you might have been mislead by the white color and ignored the labeling. Claudia Danielmeier, Gerhard Jocham and Markus Ullsperger from the Otto von Guericke University Magdeburg, Germany, investigated neural processes related to this type of action slips in collaboration with colleagues from Bergen University, Norway, and the university hospital in Cologne, Germany. Previous studies demonstrated that visual brain areas, processing relevant information for reaching a goal, show increasing activity after errors, thereby enhancing attention to relevant information. However, it remained unknown how these adaptations are conveyed. The current study by Danielmeier and colleagues shows that acetylcholine is crucial for neural and behavioral adjustments after errors. Medial frontal brain areas that participate in error detection activate neurons that release acetylcholine in specific parts of the visual cortex. This leads to enhanced processing of relevant and decreased processing of distracting information. The results of this study are important because the role of acetylcholine has so far been neglected in the context of performance monitoring and cognitive control. The findings could also lead to new insights into impairments in Alzheimer’s disease since a lack of acetylcholine is the central underlying problem in this condition.
PMID: 25959965
Winning publication in the field of human research: Danielmeier, Allen, Jocham, Onur, Eichele, Ullsperger, Curr Biol, PMID: 25959965
Winning publication in the field of animal research: Edelmann, Cepeda-Prado, Franck, Lichtenecker, Brigadski, Leßmann, Neuron, PMID: 25959732
Theta burst like stimulations lead to formation of BDNF dependent memory traces
In the study, we used a specific ‘spike-timing-dependent plasticity’ (STDP) protocol in acutely isolated hippocampal slices from rats and mice. This STDP protocol utilises electrical excitation patterns that are also observed during learning processes in the hippocampus ‘in vivo’ (i.e., in the living organism). A typical activity pattern here is the so-called theta rhythm, characterised by short, high-frequency bursts of action potentials in the postsynaptic neuron. In addition to this theta burst stimulation, however, STDP-LTP can also be triggered by single postsynaptic stimulations (single shock). In the study, both STDP protocols were now compared with one another. Surprisingly, significant differences were observed in the molecular mechanisms of the two forms of STDP-LTP: only the STDP-LTP triggered by theta bursts was dependent on the postsynaptic secretion of endogenous BDNF. The released BDNF then led to long-term potentiation of synaptic transmission between the connected neurons. Furthermore, our experiments show that this potentiation is triggered by the binding of the released BDNF to specific postsynaptic receptors (so-called TrkB receptors).
In summary, we were able to demonstrate that theta-burst-like stimulation of neurons triggers the secretion of endogenous BDNF, which acts as a key molecule in the formation of long-lasting memory traces. The findings of this study are of fundamental importance for the development of BDNF-dependent therapeutic approaches for the treatment of neurodegenerative diseases, such as Alzheimer’s disease.
PMID: 25959732