Theta-Burst Transcranial Magnetic Stimulation Alters Cortical Inhibition

Benali, Alia; Trippe, Jörn; Weiler, E; Mix, Annika; Petrasch‐Parwez, Elisabeth; Girzalsky, Wolfgang; Eysel, Ulf T.; Erdmann, Ralf; Funke, Klaus

doi:10.1523/jneurosci.1379-10.2011

Cited by 177 publications

(205 citation statements)

References 73 publications

(96 reference statements)

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“…This suggests that TMS delivers a strong volley that predominantly affects inhibitory neurons (55,56), most likely of the parvalbumin-expressing type (57). Because of their soma targeting on pyramidal neurons (58), and possibly because of their far-reaching axonal-dendritic structure (59) enhancing TMS sensitivity (60), these interneurons may impose strong synchronized inhibition in the affected cortical network (10).…”

Section: Discussionmentioning

confidence: 99%

Voltage-sensitive dye imaging of transcranial magnetic stimulation-induced intracortical dynamics

Kozyrev

Eysel

Jancke

2014

Proc. Natl. Acad. Sci. U.S.A.

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Transcranial magnetic stimulation (TMS) is widely used in clinical interventions and basic neuroscience. Additionally, it has become a powerful tool to drive plastic changes in neuronal networks. However, highly resolved recordings of the immediate TMS effects have remained scarce, because existing recording techniques are limited in spatial or temporal resolution or are interfered with by the strong TMS-induced electric field. To circumvent these constraints, we performed optical imaging with voltage-sensitive dye (VSD) in an animal experimental setting using anaesthetized cats. The dye signals reflect gradual changes in the cells' membrane potential across several square millimeters of cortical tissue, thus enabling direct visualization of TMS-induced neuronal population dynamics. After application of a single TMS pulse across visual cortex, brief focal activation was immediately followed by synchronous suppression of a large pool of neurons. With consecutive magnetic pulses (10 Hz), widespread activity within this "basin of suppression" increased stepwise to suprathreshold levels and spontaneous activity was enhanced. Visual stimulation after repetitive TMS revealed long-term potentiation of evoked activity. Furthermore, loss of the "deceleration-acceleration" notch during the rising phase of the response, as a signature of fast intracortical inhibition detectable with VSD imaging, indicated weakened inhibition as an important driving force of increasing cortical excitability. In summary, our data show that high-frequency TMS changes the balance between excitation and inhibition in favor of an excitatory cortical state. VSD imaging may thus be a promising technique to trace TMS-induced changes in excitability and resulting plastic processes across cortical maps with high spatial and temporal resolutions. (1) (TMS) has become a frequently used method for noninvasive diagnostics, therapeutic treatment, and intervention for neurorehabilitation of neurological disorders (2-8). Additionally, TMS has proved a valuable tool in basic brain research as its perturbative effects allow area-selective manipulation of immediate cortical function (9-11), as well as its long-lasting alteration through plasticity and learning protocols (12, 13). However, direct measurements of the TMS-induced cortical dynamics at highly resolved spatiotemporal scales are missing because "online approaches" (14), using modern neuroimaging techniques such as functional MRI (fMRI) (15-18), magnetoencephalography (19), EEG (20), and near-infrared (21) or intrinsic optical imaging (22), are limited in either spatial or temporal resolutions or in both.Here we overcame these limitations, using optical imaging with voltage-sensitive dyes (VSD), which exploits the dye's property to transduce gradual changes in voltage across neuronal membranes into fluorescent light signals. In contrast to imaging methods applicable in humans, this method is invasive but allows avoiding the commonly experienced contamination of signals by artifacts due to the strong ...

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Section: Discussionmentioning

confidence: 99%

Voltage-sensitive dye imaging of transcranial magnetic stimulation-induced intracortical dynamics

Kozyrev

Eysel

Jancke

2014

Proc. Natl. Acad. Sci. U.S.A.

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“…However, a stronger reduction in PV expression obtained with five blocks of iTBS (at 15-minute intervals; Volz and others 2013) can also last for days while the decrease in CB caused by five cTBS blocks recovers more rapidly (Benali and others 2011). Early after iTBS (10-20 minutes) the immediate early gene product c-Fos and presynaptic GAD65 show enhanced expression, indicating that iTBS increases neuronal activity including that of GABAergic neurons (Fig.…”

Section: Modulation Of Cortical Gabaergic Inhibition By Noninvasive Bmentioning

confidence: 82%

“…*P < .05, **P < .01, ***P < .001. Part B of the figure has been redrawn using data of Benali and others (2011) and Hoppenrath and Funke (2013).…”

Section: Modulation Of Cortical Gabaergic Inhibition By Noninvasive Bmentioning

confidence: 99%

GABA—from Inhibition to Cognition: Emerging Concepts

et al. 2017

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Neuroscience aims to elucidate the neural underpinnings of perception, cognition, and adaptive behavior. Neural functioning and plasticity can be studied on different levels of organization and complexity ranging from the molecular and synaptic level to neural circuitry of whole brain networks. Across neuroscience, different methods are being applied to better understand the role of different brain regions, networks, and neurotransmitter systems in the evolution of higher brain functions. γ-Amino-butyric acid (GABA) is the main inhibitory neurotransmitter in the adult mammalian brain, formed by the decarboxylation of glutamate, an enzyme-driven process that primarily takes place in GABAergic interneurons. This synthesis is associated with two different isoforms of the glutamic acid decarboxylase (GAD), GAD65 und GAD67. Both isoforms can be found in most GABAergic neurons. Whereas GAD67 is distributed throughout the cell cytoplasm, GAD65 is highly concentrated in nerve endings, as such GAD65 is critically involved in GABA synthesis targeting vesicular release (Soghomonian and Martin 1998). GABA either binds to GABA A receptors, which are chloride permeable pentameric channels, eliciting a chloride influx 734530N ROXXX10.1177/1073858417734530The NeuroscientistSchmidt-Wilcke et al.

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“…It has been shown that the expression of products of the early genes (c-Fos, zif268), the GA-BA-synthesizing enzymes (GAD65 and GAD67) and also the expression of NMDA-1 receptors in the hippocampus changed under the influence of rTMS in the neocortex of rats, which indicated the initiation of the process of synaptic plasticity [28]. The presence of immediate and long-term reactions to rTMS is confirmed by the results of the current study.…”

Section: Discussionmentioning

confidence: 99%