Looking back: corticothalamic feedback and early visual processing

Cudeiro, Javier; Sillito, Adam M.

doi:10.1016/j.tins.2006.05.002

Cited by 121 publications

(82 citation statements)

References 90 publications

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“…Certainly, cortical neurons are sensitive to general anesthetics, 62,63 and cortical inhibition could influence thalamic activity via the descending corticofugal pathway. 64 A study that concluded that cortical changes in the EEG preceded changes in thalamic local field potentials at loss of consciousness supports this view but, interestingly, a recent study concluded the opposite during sleep onset. 65 Alternatively, anesthetics are known to hyperpolarize thalamocortical neurons, [66][67][68][69][70] and this could lead directly to the delta oscillations and spindle activity that are observed during anesthesia.…”

Section: Sleep and General Anesthesia 143mentioning

confidence: 98%

Sleep and general anesthesia

Franks

Zecharia

2010

Can J Anesth/J Can Anesth

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Purpose The mechanisms through which general anesthetics cause reversible loss of consciousness are characterized poorly. In this review, we examine the evidence that anesthetic-induced loss of consciousness may be caused by actions on the neuronal pathways that produce natural sleep. Principal findings It is clear that many general anesthetics produce effects in the brain (detected on electroencephalogram recordings) that are similar to those seen during non-rapid eye movement non-(REM) sleep. Gamma aminobutyric acid (GABA)ergic hypnogenic neurons are thought to be critical for generating non-REM sleep through their inhibitory projections to wake-active regions of the brain. The postsynaptic GABA A receptor is a major molecular target of many anesthetics and thus may be a point of convergence between natural sleep and anesthesia. Furthermore, we also present growing evidence in this review that modulating wake-active neurotransmitter (e.g., acetylcholine, histamine) release can impact on anesthesia, supporting the idea that this point of convergence is at the level of the brain arousal systems. Conclusions While it is clear that general anesthetics can have effects at various points in the sleep-wake circuitry, it remains to be seen which points are true anesthetic targets. It will be challenging to separate nonspecific effects on baseline arousal from a causal mechanism. Sophisticated experimental approaches are necessary to address basic mechanisms of sleep and anesthesia and should advance our understanding in both of these fields. RésuméObjectif Les me´canismes par lesquels les anesthe´siques ge´ne´raux induisent une perte de conscience re´versible sont mal caracte´rise´s. Dans ce compte-rendu, nous examinons les donne´es probantes qui soutiennent que la perte de conscience induite par l'anesthe´sie pourrait eˆtre provoque´e par des actions sur les voies neuronales qui produisent le sommeil naturel. Constatations principales Il est clair que plusieurs anesthe´siques ge´ne´raux produisent des effets sur le cerveau (tels que de´tecte´s lors de l'enregistrement d'e´lectroence´phalogrammes) qui ressemblent a`ceux observe´s pendant le sommeil lent. On pense que les neurones hypnoge`nes GABAergiques sont des e´le´ments cruciaux pour la ge´ne´ration du sommeil lent en raison de leurs projections inhibitrices dans les re´gions du cerveau actives a`l'e´veil. Le re´cepteur GABA A post-synaptique est une importante cible mole´culaire de plusieurs anesthe´siques et pourrait par conse´quent constituer un point de convergence entre le sommeil naturel et l'anesthe´sie. De plus, nous pre´sentons aussi dans ce compte-rendu des donne´es probantes de plus en plus nombreuses qui sugge`rent que la modulation de la libe´ration des neurotransmetteurs actifs a`l'e´veil (par ex., acetylcholine, histamine) pourrait avoir un impact sur l'anesthe´sie, ce qui corrobore l'hypothe`se selon laquelle ce point de convergence se situe au niveau des syste`mes d'e´veil du cerveau.

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Section: Sleep and General Anesthesia 143mentioning

confidence: 98%

Sleep and general anesthesia

Franks

Zecharia

2010

Can J Anesth/J Can Anesth

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“…These findings fit well with the recent reconceptualization of sensory thalamus function: although sensory thalamic structures were previously considered as simple relay stations, they are now described as smart gatekeepers because they are tuned by cortical areas to the relevant properties of sensory input (reviewed in refs. 19,20).…”

mentioning

confidence: 99%

Dysfunction of the auditory thalamus in developmental dyslexia

Díaz¹,

Hintz²,

Kiebel

et al. 2012

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

154

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Developmental dyslexia, a severe and persistent reading and spelling impairment, is characterized by difficulties in processing speech sounds (i.e., phonemes). Here, we test the hypothesis that these phonological difficulties are associated with a dysfunction of the auditory sensory thalamus, the medial geniculate body (MGB). By using functional MRI, we found that, in dyslexic adults, the MGB responded abnormally when the task required attending to phonemes compared with other speech features. No other structure in the auditory pathway showed distinct functional neural patterns between the two tasks for dyslexic and control participants. Furthermore, MGB activity correlated with dyslexia diagnostic scores, indicating that the task modulation of the MGB is critical for performance in dyslexics. These results suggest that deficits in dyslexia are associated with a failure of the neural mechanism that dynamically tunes MGB according to predictions from cortical areas to optimize speech processing. This view on task-related MGB dysfunction in dyslexics has the potential to reconcile influential theories of dyslexia within a predictive coding framework of brain function.functional MRI | speech recognition | auditory processing | magnocellular

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“…However, it is now widely recognized that in addition to this, the brain has extensive reentrant connections between regions, implying that perception does not exclusively conform to a hierarchy of analysis (Bullier, 2001;Zeki, 1993). Instead, it has been suggested that conscious perception is achieved via reentrant processing (Cudeiro & Sillito, 2006;Lamme & Roelfsema, 2000;Pascual-Leone & Walsh, 2001;Zeki, 2001). In this section, we will discuss the reentrant processing account that was first offered to explain OSM , as well as other models of reentrant processing and their applicability to the phenomenon.…”

Section: Theories Of Osmmentioning

confidence: 99%

Substituting objects from consciousness: A review of object substitution masking

et al. 2013

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Object substitution masking (OSM) occurs when a sparse (e.g., four-dot), temporally trailing mask obscures the visibility of a briefly presented target. Here, we review theories of OSM: those that propose that OSM reflects the interplay between feedforward and feedback/reentrant neural processes, those that predict that feedforward processing alone gives rise to the phenomenon, and theories that focus on cognitive explanations, such as object updating. We discuss how each of these theories accommodates key findings from the OSM literature. In addition, we examine the relationship between OSM and other visual-cognitive phenomena, including object correspondence through occlusion, change blindness, metacontrast masking, backward masking, and visual short-term memory. Finally, we examine the level of processing at which OSM impairs target perception. Collectively, OSM appears to reflect the conditions under which the brain confuses two visual events for one when they are encoded with low spatiotemporal resolution, due to processing resources being otherwise occupied.Keywords Object substitution masking . Attention . Reentrant processing . Consciousness When observing a visual scene, at any point in time, we are conscious of only a small fraction of the available information. Given this limitation, it is important to understand the mechanisms that determine what stimuli we become conscious of, when we become conscious of them, and the nature of processing that occurs in the absence of explicit awareness. There exists a long and rich history in experimental psychology of using visual masking to explore such issues. Visual masking refers to conditions where the visibility of one to-be-reported visual stimulus (the target) is obscured by the presentation of another stimulus (the mask) that appears in close spatiotemporal proximity and does not require report. Object substitution masking (OSM) is a recent discovery in the field of visual masking and is an ideal tool for exploring questions about visual awareness because it selectively impairs the extent to which an individual becomes conscious of a visual stimulus without the extent of image-level degradation that other forms of visual masking induce. This review, therefore, focuses on the determinants and consequences of visual awareness in OSM.Here, we integrate a diverse range of literature to discern what OSM can tell us about perceptual consciousness and visual cognition in general. Specifically, we discuss the role of feedforward versus feedback processing in giving rise to OSM, whether the phenomenon is better characterized as reflecting object updating or object substitution, the similarities and differences between OSM and other forms of masking, and OSM's relationship to other visual-cognitive phenomena. In addition, we review evidence regarding the role of attention in masking. Our aim is to address controversies in the OSM literature in depth and offer insights into how some of them may already be resolved and how the field might go about resolving ...

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Looking back: corticothalamic feedback and early visual processing

Cited by 121 publications

References 90 publications

Sleep and general anesthesia

Sleep and general anesthesia

Dysfunction of the auditory thalamus in developmental dyslexia

Substituting objects from consciousness: A review of object substitution masking

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