Correlation between GABAA receptor density and vagus nerve stimulation in individuals with drug-resistant partial epilepsy

Marrosu, Francesco; Serra, Alessandra; Maleci, Alberto; Puligheddu, Monica; Biggio, Giovanni; Piga, M.

doi:10.1016/s0920-1211(03)00107-4

Cited by 160 publications

(89 citation statements)

References 41 publications

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“…5). Moreover, therapeutic response to chronic vagal nerve stimulation in epileptic patients was associated with hippocampal changes in GABA A receptor density (8). In addition, with chronic IGS, we also show significant activation of other limbic regions, namely right OFC and right striatum as well as activation of the right anterior cerebellum.…”

Section: Discussionmentioning

confidence: 55%

Gastric stimulation in obese subjects activates the hippocampus and other regions involved in brain reward circuitry

Wang

Yang

Volkow

et al. 2006

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

147

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The neurobiological mechanisms underlying overeating in obesity are not understood. Here, we assessed the neurobiological responses to an Implantable Gastric Stimulator (IGS), which induces stomach expansion via electrical stimulation of the vagus nerve to identify the brain circuits responsible for its effects in decreasing food intake. Brain metabolism was measured with positron emission tomography and 2-deoxy-2[ 18 F]fluoro-D-glucose in seven obese subjects who had the IGS implanted for 1-2 years. Brain metabolism was evaluated twice during activation (on) and during deactivation (off) of the IGS. The Three-Factor Eating Questionnaire was obtained to measure the behavioral components of eating (cognitive restraint, uncontrolled eating, and emotional eating). The largest difference was in the right hippocampus, where metabolism was 18% higher (P < 0.01) during the ''on'' than ''off'' condition, and these changes were associated with scores on ''emotional eating,'' which was lower during the on than off condition and with ''uncontrolled eating,'' which did not differ between conditions. Metabolism also was significantly higher in right anterior cerebellum, orbitofrontal cortex, and striatum during the on condition. These findings corroborate the role of the vagus nerve in regulating hippocampal activity and the importance of the hippocampus in modulating eating behaviors linked to emotional eating and lack of control. IGS-induced activation of regions previously shown to be involved in drug craving in addicted subjects (orbitofrontal cortex, hippocampus, cerebellum, and striatum) suggests that similar brain circuits underlie the enhanced motivational drive for food and drugs seen in obese and drugaddicted subjects, respectively. brain activation ͉ obesity T he cerebral mechanisms underlying the behaviors that result in pathological overeating and obesity are poorly understood. The regulation of food intake is a complex balance between excitatory and inhibitory processes. The excitatory processes arise from the body's needs for nutrients and calories. The inhibitory processes arise from satiety signals (i.e., electrical and chemical) after food consumption (1). The vagus nerve is one of the ways by which satiety signals are conveyed to the brainstem (2). Gastric and duodenal vagal afferents increase their firing in response to the mechanical pressure from the ingested nutrients and in response to food-induced release of a variety of brain gut peptides (i.e., cholecystokinin and ghrelin). In addition, several neurotransmitters (e.g., serotonin, dopamine, norepinephrine, and opiates) and peptides (i.e., cholecystokinin and corticotrophin releasing factor) are also involved in feeding behaviors (1). It is also recognized that in addition to food's role in fulfilling nutrient requirements, eating also may serve to mitigate stress (comfort food) (3). Disruption in the sensitivity of the brain to these signals could lead to obesity.Recently, the Transcend Implantable Gastric Stimulator (IGS) system, which generates el...

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Section: Discussionmentioning

confidence: 55%

Gastric stimulation in obese subjects activates the hippocampus and other regions involved in brain reward circuitry

Wang

Yang

Volkow

et al. 2006

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

147

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“…Nonetheless, given the causal nature of the brain stimulation technique used in the current study, our findings provide a first direct demonstration for a causal link between the vagus nerve and the subjective experience of flow. Although stimulation of the vagus is, besides NE, also associated with increased GABA release (Ben-Menachem et al 1995;Marrosu et al 2003), to the best of our knowledge there is no indication in the literature that changes in GABA might have been responsible for our results.…”

Section: Discussionmentioning

confidence: 60%

Transcutaneous vagus nerve stimulation (tVNS) modulates flow experience

2017

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“…Chronic VNS has been found to enhance recognition memory and memory storage in humans (Clark et al, 1999) and to increase cortical inhibition by up-regulating the cortical density of g-aminobutyric acid type A (GABA A ) receptors, as assessed by [ 123 I] iomazenil SPECT, in individuals with drug-resistant partial epilepsy (Marrosu et al, 2003). These results suggest that VNS may modulate neuronal plasticity.…”

Section: Discussionmentioning

confidence: 98%

Increase in 20–50Hz (gamma frequencies) power spectrum and synchronization after chronic vagal nerve stimulation

Marrosu¹,

Santoni²,

Puligheddu³

et al. 2005

Clinical Neurophysiology

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Objective: Though vagus nerve stimulation (VNS) is an important option in pharmacoresistant epilepsy, its mechanism of action remains unclear. The observation that VNS desynchronised the EEG activity in animals suggested that this mechanism could be involved in VNS antiepileptic effects in humans. Indeed VNS decreases spiking bursts, whereas its effects on the EEG background remain uncertain. The objective of the present study is to investigate how VNS affects local and inter regional syncronization in different frequencies in pharmacoresistent partial epilepsy. Methods: Digital recordings acquired in 11 epileptic subjects 1 year and 1 week before VNS surgery were compared with that obtained 1 month and 1 year after VNS activation. Power spectrum and synchronization were then analyzed and compared with an epileptic group of 10 patients treated with AEDs only and with 9 non-epileptic patients. Results: VNS decreases the synchronization of theta frequencies (P!0.01), whereas it increases gamma power spectrum and synchronization (!0.001 and 0.01, respectively). Conclusions: The reduction of theta frequencies and the increase in power spectrum and synchronization of gamma bands can be related to VNS anticonvulsant mechanism. In addition, gamma modulation could also play a seizure-independent role in improving attentional performances. Significance: These results suggest that some antiepileptic mechanisms affected by VNS can be modulated by or be the reflection of EEG changes. q

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Correlation between GABAA receptor density and vagus nerve stimulation in individuals with drug-resistant partial epilepsy

Cited by 160 publications

References 41 publications

Gastric stimulation in obese subjects activates the hippocampus and other regions involved in brain reward circuitry

Gastric stimulation in obese subjects activates the hippocampus and other regions involved in brain reward circuitry

Transcutaneous vagus nerve stimulation (tVNS) modulates flow experience

Increase in 20–50Hz (gamma frequencies) power spectrum and synchronization after chronic vagal nerve stimulation

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