Biology subjects

Leicht, G.

Publications and source records attributed to Leicht, G..

3 recordsLinked to original sources

bioRxiv2024

Source to sensor coupling (SoSeC) as an effective tool to localize interacting sources from EEG and MEG data

A standard approach to estimate interacting sources from EEG or MEG data is to first calculate a coupling between all pairs of voxels on a predefined grid within the brain and then average or maximize this coupling matrix along each column or row. Depending on the chosen coupling measure and grid size this approach can be computationally very costly, in particular when a bias is supposed to be removed. We here suggest to replace this approach by a maximization of coupling between each source and the signal in sensor space. The idea is that any neuronal activity which can be estimated from recorded data must be present in sensor space in the first place. Using the imaginary part of coherency as coupling measure makes sure that we do not confuse this source to sensor coupling with a coupling of a source to itself. We found that this approach is hundreds of times faster than the conventional approach. Results for EEG resting state data indicate that the new approach has more statistical power than the conventional approach. The presentation of this specific method is augmented with a discussion of conceptual issues for various forms of vector beamformers and eLoreta.

neuroscience↗

bioRxiv2024

Post-retrieval noradrenergic activation impairs subsequent memory depending on cortico-hippocampal reactivation

When retrieved, seemingly stable memories can become sensitive to significant events, such as acute stress. The mechanisms underlying these memory dynamics remain poorly understood. Here we show that noradrenergic stimulation after memory retrieval impairs subsequent remembering, depending on hippocampal and cortical signals emerging during retrieval. In a three-day study, we measured brain activity using fMRI during initial encoding, 24h-delayed memory cueing followed by pharmacological elevations of glucocorticoid or noradrenergic activity, and final recall. While post-retrieval glucocorticoids did not affect subsequent memory, the impairing effect of noradrenergic arousal on final recall depended on hippocampal reactivation and category-level reinstatement in ventral temporal cortex during memory cueing. These effects did not require a reactivation of the original memory trace and did not interact with offline reinstatement during rest. Our findings demonstrate that, depending on the retrieval-related neural reactivation of memories, noradrenergic arousal after retrieval can alter the future accessibility of consolidated memories.

neuroscience↗

bioRxiv2021

Glycine attenuates impairments of stimulus-evokedgamma oscillation in the ketaminemodel of schizophrenia

Although a substantial number of studies suggests some clinical benefit concerning negative symptoms in schizophrenia through the modulation of NMDA-receptor function, none of these approaches achieved clinical approval. Given the large body of evidence concerning glutamatergic dysfunction in a subgroup of patients, biomarkers to identify those with a relevant clinical benefit through glutamatergic modulation are urgently needed. A similar reduction of the early auditory evoked gamma-band response (aeGBR) as found in schizophrenia patients can be observed in healthy subjects in the ketamine-model, which addresses the putative excitation / inhibition (E/I) imbalance of the diseases. Moreover, this change in gamma-band oscillations can be related to the emergence of negative symptoms. Accordingly, this study investigated whether glycine-related increases of the aeGBR accompany an improvement concerning negative symptoms in the ketamine-model. The impact of subanesthetic ketamine doses and the pretreatment with glycine was examined in twenty-four healthy male participants while performing a cognitively demanding aeGBR paradigm with 64-channel electroencephalography. Negative Symptoms were assessed through the Positive and Negative Syndrome Scale (PANSS). Ketamine alone caused a reduction of the aeGBR amplitude associated with more pronounced negative symptoms compared to placebo. Pretreatment with glycine attenuated both, the ketamine-induced alterations of the aeGBR amplitude and the increased PANSS negative scores in glycine-responders, classified based on relative aeGBR increase. Thus, we propose that the aeGBR represents a possible biomarker for negative symptoms in schizophrenia related to insufficient glutamatergic neurotransmission. This would allow to identify patients with negative symptoms, who might benefit from glutamatergic treatment.

neuroscience↗