Grouping of brain rhythms in corticothalamic systems

Steriade, Mircea

doi:10.1016/j.neuroscience.2005.10.029

Cited by 1,158 publications

(1,054 citation statements)

References 123 publications

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“…The thalamocortical dysrhythmia model (Figure 4) links the symptomatology with abnormal low frequency (< 10 Hz) and gamma band (> 30 Hz) activity in the resting state. Such abnormalities are supported by animal research and are suggested to arise from a cascade of neural events that are initiated by input deafferentation (in the case of TI by hearing loss) (Jeanmonod et al, 1996;Steriade, 2006). Loss of excitatory input results in the membrane potentials of thalamic neurons becoming hyperpolarised.…”

Section: Human Neuroimaging Studiesmentioning

confidence: 98%

The mechanisms of tinnitus: Perspectives from human functional neuroimaging

2009

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In this review, we highlight the contribution of advances in human neuroimaging to the current understanding of central mechanisms underpinning tinnitus and explain how interpretations of neuroimaging data have been guided by animal models. The primary motivation for studying the neural subtrates of tinnitus in humans has been to demonstrate objectively its representation in the central auditory system and to develop a better understanding of its diverse pathophysiology and of the functional interplay between sensory, cognitive and affective systems. The ultimate goal of neuroimaging is to identify subtypes of tinnitus in order to better inform treatment strategies. The three neural mechanisms considered in this review may provide a basis for TI classification. While human neuroimaging evidence strongly implicates the central auditory system and emotional centres in TI, evidence for the precise contribution from the three mechanisms is unclear because the data are somewhat inconsistent. We consider a number of methodological issues limiting the field of human neuroimaging and recommend approaches to overcome potential inconsistency in results arising from poorly matched participants, lack of appropriate controls and low statistical power. AbstractIn this review, we highlight the contribution of advances in human neuroimaging to the current understanding of central mechanisms underpinning tinnitus and explain how interpretations of neuroimaging data have been guided by animal models. The primary motivation for studying the neural subtrates of tinnitus in humans has been to demonstrate objectively its representation in the central auditory system and to develop a better understanding of its diverse pathophysiology and of the functional interplay between sensory, cognitive and affective systems. The ultimate goal of neuroimaging is to identify subtypes of tinnitus in order to better inform treatment strategies. The three neural mechanisms considered in this review may provide a basis for TI classification. While human neuroimaging evidence strongly implicates the central auditory system and emotional centres in TI, evidence for the precise contribution from the three mechanisms is unclear because the data are somewhat inconsistent. We consider a number of methodological issues limiting the field of human neuroimaging and recommend approaches to overcome potential inconsistency in results arising from poorly matched participants, lack of appropriate controls and low statistical power.

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Section: Human Neuroimaging Studiesmentioning

confidence: 98%

The mechanisms of tinnitus: Perspectives from human functional neuroimaging

2009

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“…From a phenomenological point of view, the slow oscillation is an electrophysiological process that is observed at multiple levels of organization in the brain during natural sleep and under certain forms of anesthesia[32,33]. In the human electroencephalogram (EEG), stage 2 sleep is characterized by K-complexes representing single slow oscillation cycles[34,35].…”

Section: Neuronal Substrates Of Slow Oscillationsmentioning

confidence: 99%

“…An important property of the slow oscillation is that it organizes other sleep rhythms, including delta oscillations and spindles[32]. Spindles, which are 7- to 12-Hz thalamocortical oscillations, are known to be triggered by cortical UP states[66].…”

Section: Neuronal Substrates Of Slow Oscillationsmentioning

confidence: 99%

“…In SWS, the thalamocortical system is dominated by stereotyped field potential oscillations in the 0.5- to 4-Hz frequency range, which includes the slow (<1 Hz) oscillation and delta frequencies (1–4 Hz). Analytically described by Steriade and colleagues 17 years ago[29,30,31], the slow oscillation is now thought to be one of the primary organizers of network activity in the thalamocortical system[32] and possibly the key player in off-line memory consolidation during sleep[10,21,26]. In the remainder of this review, we will first discuss the neuronal mechanisms underlying slow oscillations, highlighting the role of dynamic cortico- and thalamocortical coupling to generate this network activity.…”

Section: Introductionmentioning

confidence: 99%

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Integrated Brain Circuits: Neuron-Astrocyte Interaction in Sleep-Related Rhythmogenesis

Halassa

Maschio²,

Beltramo³

et al. 2010

The Scientific World JOURNAL

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Although astrocytes are increasingly recognized as important modulators of neuronal excitability and information transfer at the synapse, whether these cells regulate neuronal network activity has only recently started to be investigated. In this article, we highlight the role of astrocytes in the modulation of circuit function with particular focus on sleep-related rhythmogenesis. We discuss recent data showing that these glial cells regulate slow oscillations, a specific thalamocortical activity that characterizes non-REM sleep, and sleep-associated behaviors. Based on these findings, we predict that our understanding of the genesis and tuning of thalamocortical rhythms will necessarily go through an integrated view of brain circuits in which non-neuronal cells can play important neuromodulatory roles.

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“…As the neurophysiological underpinnings to the complex waveforms of the EEG are just beginning to be elucidated [148], the mechanism behind how neurofeedback exerts its effect on these systems remains unclear. The sensorimotor rhythm develops when a subject is motionless yet remains attentive.…”

Section: Neurofeedbackmentioning

confidence: 99%

Techniques and devices to restore cognition

Serruya

Kahana

2008

Behavioural Brain Research

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Executive planning, the ability to direct and sustain attention, language and several types of memory may be compromised by conditions such as stroke, traumatic brain injury, cancer, autism, cerebral palsy and Alzheimer's disease. No medical devices are currently available to help restore these cognitive functions. Recent findings about the neurophysiology of these conditions in humans coupled with progress in engineering devices to treat refractory neurological conditions imply that the time has arrived to consider the design and evaluation of a new class of devices. Like their neuromotor counterparts, neurocognitive prostheses might sense or modulate neural function in a non-invasive manner or by means of implanted electrodes. In order to paint a vision for future device development, it is essential to first review what can be achieved using behavioral and external modulatory techniques. While non-invasive approaches might strengthen a patient's remaining intact cognitive abilities, neurocognitive prosthetics comprised of direct brain-computer interfaces could in theory physically reconstitute and augment the substrate of cognition itself.

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Grouping of brain rhythms in corticothalamic systems

Cited by 1,158 publications

References 123 publications

The mechanisms of tinnitus: Perspectives from human functional neuroimaging

The mechanisms of tinnitus: Perspectives from human functional neuroimaging

Integrated Brain Circuits: Neuron-Astrocyte Interaction in Sleep-Related Rhythmogenesis

Techniques and devices to restore cognition

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