Neuronal electrical high frequency stimulation enhances GABA outflow from human neocortical slices

Mantovani, M.; Velthoven, Vera Van; Fuellgraf, H.; Feuerstein, Thomas J.; Möser, Andreas

doi:10.1016/j.neuint.2006.02.008

Cited by 30 publications

(28 citation statements)

References 22 publications

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“…In vitro evidence for HFS-induced selective GABA release It has been recently shown that, in human neocortical slices, HFS (124 Hz, pulse width of 100 μs and current of 1 mA) targets axons only and selectively induces the release of GABA, involving facilitatory GABA A autoreceptors (Mantovani et al 2006(Mantovani et al , 2009. This is one of the in vitro supports of the proposed hypothesis of the mechanism of action of DBS-HFS.…”

Section: Proposed Hypothesis: Hfs Selectively Induces Gaba Releasementioning

confidence: 53%

“…In human neocortical slices the presence of a low -per se inactive -concentration of veratridine has also been necessary to reveal the HFS-induced selective GABA release. The HFS duration in vitro was always 10 min (Li et al 2004(Li et al , 2006Mantovani et al 2006Mantovani et al , 2009, i.e. long enough to reflect steady state GABA concentrations with an operative presynaptic autoregulation.…”

Section: Proposed Hypothesis: Hfs Selectively Induces Gaba Releasementioning

confidence: 99%

“…Such a reversal corresponds to a HFSmediated selective GABA release which normalizes the GABAergic projection to the thalamus. In fact, such an increase in the GABAergic neurotransmission may take place according to our own findings in human neocortex slices: The activation of facilitatory GABA A autoreceptors upon HFS, inducing action potentials in GABAergic fibres and subsequent terminal release of GABA, can be assumed for the following reasons: The HFS-evoked GABA release was antagonized (1) by GABA A receptor blockade, (2) by changing the plasmalemmal chloride gradient of the GABA A receptor channels and (3) by tetrodotoxin which abolishes action potentials (Mantovani et al 2006(Mantovani et al , 2009. Thus, HFS of pallido-thalamic GABAergic axons within the GP med may induce, via orthodromic action potentials, the release of GABA from their thalamic terminals; this GABA then leads to even more GABA release due to its activation of facilitatory GABA A autoreceptors on these terminals.…”

Section: Improvement Of Parkinsonian Hypo-or Hyperkinesiamentioning

confidence: 99%

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Selective GABA release as a mechanistic basis of high-frequency stimulation used for the treatment of neuropsychiatric diseases

Feuerstein

Kammerer

Lücking

et al. 2011

Naunyn-Schmiedeberg's Arch Pharmacol

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Electrical high-frequency stimulation (HFS) is applied in many brain areas to treat various clinical syndromes. The nearly identical constellation of stimulation parameters raises the question of a unique mechanism of action of this therapeutic option. The identification of a single HFS mechanism may help to optimize the HFS technology by targeting this single mechanism. Experimentally, only axonal membranes are targets of HFS, but not other membranes of neurons or glial cells. Within all HFS target regions, axons of excitatory glutamatergic and inhibitory GABAergic neurons are present and play roles in all clinical syndromes treated successfully with HFS. Therefore, glutamatergic or GABAergic fibres are likely candidates as mediators of a unique HFS mode of action. The selective involvement of another neuronal fibre type (e.g. monoaminergic, cholinergic, etc.) in the HFS mode of action is highly unlikely since the regional and syndromal dissimilarity of the clinical HFS applications precludes the assumption of such a fibre type as primary HFS site of action. Our recent experimental finding that HFS of human neocortical slices induces the action potential-mediated release of GABA, but not of glutamate, simplifies the possibilities to explain the HFS mode of action, as the explanation now may concentrate on GABAergic axons only. Thus, we are analysing, on the basis of the pathophysiological grounds of the various syndromes treated with deep brain stimulation, whether a selective GABA release is a collective explanation of the mode of action of HFS. We suggest that selective GABA release indeed may needfully and sufficiently explain efficacy and side effects of HFS.

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Section: Proposed Hypothesis: Hfs Selectively Induces Gaba Releasementioning

confidence: 53%

Section: Proposed Hypothesis: Hfs Selectively Induces Gaba Releasementioning

confidence: 99%

Section: Improvement Of Parkinsonian Hypo-or Hyperkinesiamentioning

confidence: 99%

See 1 more Smart Citation

Selective GABA release as a mechanistic basis of high-frequency stimulation used for the treatment of neuropsychiatric diseases

Feuerstein

Kammerer

Lücking

et al. 2011

Naunyn-Schmiedeberg's Arch Pharmacol

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“…Animal studies suggest that HFS induces an increased GABA release by activating local GABAergic neurons whereas glutamate levels appear to remain unchanged in the vicinity of the stimulation electrode [6,7]. Similarly, an enhanced GABA release was also observed during HFS of human neocortical slices [8].…”

Section: Introductionmentioning

confidence: 89%

Biochemical mechanisms of pallidal deep brain stimulation in X-linked dystonia parkinsonism

Tronnier

Domingo

Moll

et al. 2015

Parkinsonism & Related Disorders

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“…GABA A receptor blockade, changing the plasmalemmal chloride gradient of GABA A receptor channels and tetrodotoxin (which abolishes action potentials) antagonized this HFS-evoked GABA release [17,37]. Thus, orthodromic action potentials may be induced in thalamopetal GABAergic axons by HFS within the GP med with subsequent release of GABA from their thalamic terminals; even more GABA release is due to activation by released GABA of facilitatory GABA A autoreceptors on these terminals.…”

Section: Diversity Of Effects Of Hfs In the Gp Medmentioning

confidence: 99%

The mode of action of electrical high frequency stimulation

Kammerer¹,

Hebel²,

Feuerstein³

2010

JBiSE

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Neuronal electrical high frequency stimulation enhances GABA outflow from human neocortical slices

Cited by 30 publications

References 22 publications

Selective GABA release as a mechanistic basis of high-frequency stimulation used for the treatment of neuropsychiatric diseases

Selective GABA release as a mechanistic basis of high-frequency stimulation used for the treatment of neuropsychiatric diseases

Biochemical mechanisms of pallidal deep brain stimulation in X-linked dystonia parkinsonism

The mode of action of electrical high frequency stimulation

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