Characterization of GABAA-receptor mediated neurotransmission in the human cortex by paired-pulse TMS-EEG

Király, J.; Premoli, Isabella; Zipser, Carl Moritz; Belardinelli, Paolo; Ziemann, Ulf; Müller‐Dahlhaus, Florian

doi:10.1016/j.clinph.2015.11.146

Cited by 2 publications

(1 citation statement)

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“…TMS showed efficacy as an antidepressant treatment in TRD patients (45), and is also used to experimentally probe cortical inhibition, including short-interval cortical inhibition ( SICI ), long-interval cortical inhibition ( LICI ), and cortical silent period ( CSP ). SICI is similar in duration to GABA A receptor ( GABA A R )-mediated inhibitory post-synaptic potentials (46, 47) and is lengthened by GABA A -acting drugs (48, 49), and is therefore considered to measure GABA A R-mediated neurotransmission. Conversely, the slower LICI and CSP time-courses resemble GABA B receptor ( GABA B R )-mediated post-synaptic potentials (50), and are increased by GABA B R agonists (51, 52), suggesting a reflection of GABA B R-mediated neurotransmission.…”

Section: Gaba Levels and Related Neurophysiological Measures In Deprementioning

confidence: 99%

Somatostatin-Positive Gamma-Aminobutyric Acid Interneuron Deficits in Depression: Cortical Microcircuit and Therapeutic Perspectives

Fee

Banasr

Sibille

2017

Biological Psychiatry

269

217

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The functional integration of external and internal signals forms the basis of information processing and is essential for higher cognitive functions. This occurs in finely-tuned cortical microcircuits whose functions are balanced at the cellular level by excitatory glutamatergic pyramidal neurons and inhibitory γ-aminobutyric acid (GABA) interneurons. The balance of excitation and inhibition, from cellular processes to neural network activity, is characteristically disrupted in multiple neuropsychiatric disorders, including major depressive disorder (MDD), bipolar disorder (BPD), anxiety disorders, and schizophrenia (SCZ). Specifically, nearly three decades of research demonstrate a role for reduced inhibitory GABA level and function across disorders. In MDD, recent evidence from human postmortem and animal studies suggests a selective vulnerability of GABAergic interneurons that co-express the neuropeptide somatostatin (“SST cells/interneurons”). Advances in cell type-specific molecular genetics have now helped to elucidate several important roles for SST interneurons in cortical processing (regulation of pyramidal cell excitatory input) and behavioral control (mood and cognition). Here, we review evidence for altered inhibitory function arising from GABAergic deficits across disorders, and specifically in MDD. We then focus on properties of the cortical microcircuit, wherein SST-positive GABA interneuron deficits may disrupt functioning in several ways. Finally, we discuss the putative origins of SST cell deficits, as informed by recent research, and implications for therapeutic approaches. We conclude that deficits in SST interneurons represent a contributing cellular pathology, and therefore a promising target for normalizing altered inhibitory function in MDD and other disorders with reduced SST cell and GABA functions.

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Section: Gaba Levels and Related Neurophysiological Measures In Deprementioning

confidence: 99%

Somatostatin-Positive Gamma-Aminobutyric Acid Interneuron Deficits in Depression: Cortical Microcircuit and Therapeutic Perspectives

Fee

Banasr

Sibille

2017

Biological Psychiatry

269

217

View full text Add to dashboard Cite

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Brain responsivity provides an individual readout for motor recovery after stroke

Tscherpel

Dern

Hensel

et al. 2020

Brain

103

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Promoting the recovery of motor function and optimizing rehabilitation strategies for stroke patients is closely associated with the challenge of individual prediction. To date, stroke research has identified critical pathophysiological neural underpinnings at the cellular level as well as with regard to network reorganization. However, in order to generate reliable readouts at the level of individual patients and thereby realize translation from bench to bedside, we are still in a need for innovative methods. The combined use of transcranial magnetic stimulation (TMS) and EEG has proven powerful to record both local and network responses at an individual’s level. To elucidate the potential of TMS-EEG to assess motor recovery after stroke, we used neuronavigated TMS-EEG over ipsilesional primary motor cortex (M1) in 28 stroke patients in the first days after stroke. Twenty-five of these patients were reassessed after >3 months post-stroke. In the early post-stroke phase (6.7 ± 2.5 days), the TMS-evoked EEG responses featured two markedly different response morphologies upon TMS to ipsilesional M1. In the first group of patients, TMS elicited a differentiated and sustained EEG response with a series of deflections sequentially involving both hemispheres. This response type resembled the patterns of bilateral activation as observed in the healthy comparison group. By contrast, in a subgroup of severely affected patients, TMS evoked a slow and simplified local response. Quantifying the TMS-EEG responses in the time and time-frequency domain revealed that stroke patients exhibited slower and simple responses with higher amplitudes compared to healthy controls. Importantly, these patterns of activity changes after stroke were not only linked to the initial motor deficit, but also to motor recovery after >3 months post-stroke. Thus, the data revealed a substantial impairment of local effects as well as causal interactions within the motor network early after stroke. Additionally, for severely affected patients with absent motor evoked potentials and identical clinical phenotype, TMS-EEG provided differential response patterns indicative of the individual potential for recovery of function. Thereby, TMS-EEG extends the methodological repertoire in stroke research by allowing the assessment of individual response profiles.

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Characterization of GABAA-receptor mediated neurotransmission in the human cortex by paired-pulse TMS-EEG

Cited by 2 publications

References 0 publications

Somatostatin-Positive Gamma-Aminobutyric Acid Interneuron Deficits in Depression: Cortical Microcircuit and Therapeutic Perspectives

Somatostatin-Positive Gamma-Aminobutyric Acid Interneuron Deficits in Depression: Cortical Microcircuit and Therapeutic Perspectives

Brain responsivity provides an individual readout for motor recovery after stroke

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