GABAergic and cholinergic modulation of repetition suppression in inferior temporal cortex

Kuravi, Pradeep; Vogels, Rufin

doi:10.1038/s41598-018-31515-1

Cited by 8 publications

(4 citation statements)

References 36 publications

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“…Alteration in the excitation/inhibition balance of neural connectivity has been proposed as a mechanism underlying many of the manifestations occurring in ASD and ADHD, including atypical repetition suppression [ 50 , 55 , 81 ]. Since repetition suppression partly reflects GABAergic inhibition of glutaminergic pyramidal cells in the interneuronal network [ 54 , 55 ], reduced inhibition in the somatosensory cortex could underlie the atypical repetition suppression documented in our study. Additional perceptual phenomena that have been linked to alteration in the excitation/inhibition balance include binocular rivalry, spatial suppression/gain control and orientation discrimination (for reviews see, [ 22 , 82 ]).…”

Section: Discussionmentioning

confidence: 84%

Behavioural and neural markers of tactile sensory processing in infants at elevated likelihood of autism spectrum disorder and/or attention deficit hyperactivity disorder

Piccardi

Ali

Jones

et al. 2021

J Neurodevelop Disord

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Backgrounds Atypicalities in tactile processing are reported in autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) but it remains unknown if they precede and associate with the traits of these disorders emerging in childhood. We investigated behavioural and neural markers of tactile sensory processing in infants at elevated likelihood of ASD and/or ADHD compared to infants at typical likelihood of the disorders. Further, we assessed the specificity of associations between infant markers and later ASD or ADHD traits. Methods Ninety-one 10-month-old infants participated in the study (n = 44 infants at elevated likelihood of ASD; n = 20 infants at elevated likelihood of ADHD; n = 9 infants at elevated likelihood of ASD and ADHD; n = 18 infants at typical likelihood of the disorders). Behavioural and EEG responses to pairs of tactile stimuli were experimentally recorded and concurrent parental reports of tactile responsiveness were collected. ASD and ADHD traits were measured at 24 months through standardized assessment (ADOS-2) and parental report (ECBQ), respectively. Results There was no effect of infants’ likelihood status on behavioural markers of tactile sensory processing. Conversely, increased ASD likelihood associated with reduced neural repetition suppression to tactile input. Reduced neural repetition suppression at 10 months significantly predicted ASD (but not ADHD) traits at 24 months across the entire sample. Elevated tactile sensory seeking at 10 months moderated the relationship between early reduced neural repetition suppression and later ASD traits. Conclusions Reduced tactile neural repetition suppression is an early marker of later ASD traits in infants at elevated likelihood of ASD or ADHD, suggesting that a common pathway to later ASD traits exists despite different familial backgrounds. Elevated tactile sensory seeking may act as a protective factor, mitigating the relationship between early tactile neural repetition suppression and later ASD traits.

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Section: Discussionmentioning

confidence: 84%

Behavioural and neural markers of tactile sensory processing in infants at elevated likelihood of autism spectrum disorder and/or attention deficit hyperactivity disorder

Piccardi

Ali

Jones

et al. 2021

J Neurodevelop Disord

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“…As a whole, such adaptation may reflect neuronal fatigue potentially due to firing rate adaptation, synaptic depression, or afferent control 35 . Indeed, recent reports suggest that the cellular mechanism responsible for repetition-related adaptation arises from afferent input (in particular, GABAergic) to adapted cells 36 .…”

Section: Discussionmentioning

confidence: 99%

“…Alternatively, recent work has provided support for the causal involvement of somatostatin-positive (SOM+) neurons in MMN modulation 54 . Inspired by reports of inhibitory interneuron involvement in lateral inhibition and regulation of surround suppression 56 , 57 , one mechanistic explanation could be that these SOM+ neurons facilitating SSA by inhibiting pyramidal neurons during the standard condition 36 . Indeed, evidence shows that the suppression of activity may arise from SOM+ interneurons regulation of pyramidal neurons, as reversible inactivation of SOM+ neurons impair differentiation of stimulus presentation frequency in population activity 12 .…”

Section: Discussionmentioning

confidence: 99%

Stimulus-specific regulation of visual oddball differentiation in posterior parietal cortex

Zhou

Huang

Yu³

et al. 2020

Sci Rep

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The frequency at which a stimulus is presented determines how it is interpreted. For example, a repeated image may be of less interest than an image that violates the prior sequence. This process involves integration of sensory information and internal representations of stimulus history, functions carried out in higher-order sensory areas such as the posterior parietal cortex (PPC). Thus far, there are few detailed reports investigating the single-neuron mechanisms for processing of stimulus presentation frequency in PPC. To address this gap in knowledge, we recorded PPC activity using 2-photon calcium imaging and electrophysiology during a visual oddball paradigm. Calcium imaging results reveal differentiation at the level of single neurons for frequent versus rare conditions which varied depending on whether the stimulus was preferred or non-preferred by the recorded neural population. Such differentiation of oddball conditions was mediated primarily by stimulusindependent adaptation in the frequent condition. Behavioral flexibility requires the brain to generate distinct patterns of neural responses when a stimulus is observed frequently versus rarely. For example, a wild deer that encounters a car on a daily basis may perceive rare, intermittent encounters differently. The latter case is much more surprising since the stimulus (driving car) possesses substantially different features from the usual experienced environment. Accordingly, there must be circuitry in the brain that is able to differentiate such scenarios. The oddball paradigm is a classic sensory stimulus assay used to evaluate neural differentiation of stimulus presentation frequency 1,2. In this paradigm, the neural response to a rare, deviant stimulus is compared to the response to a frequently-presented standard stimulus; differentiation of the two conditions is quantified as the difference in responses between the standard and deviant (called mismatch negativity). Specifically, the mismatch negativity (MMN) is a neurophysiological difference waveform peaking in the 150-250 ms window after stimulus onset. The MMN refers to the difference in evoked response to the standard and deviant stimulus. Importantly, the MMN is distinct from the N100 (occurring between 50 and 150 ms post stimulus onset) and the P300 (occurring around 300-400 ms) components with respect to function and timing relative to stimulus onset 3,4. The MMN has been studied comprehensively in humans using EEG, MEG, and fMRI 5-10 , and to a lesser extent, in animal models with local field potential (LFP) and/or single units 11-16. Yet, few studies have extensively probed how individual neurons exhibit responses to oddball conditions as a function of stimulus properties. Stimulus preference and tuning in single neurons may influence MMN responses, highlighting the need for neural recordings at higher spatial granularity using methods such as 2-photon calcium imaging. It has been postulated that the MMN is a precursor to sensory discrimination 17,18. Within this framework, sensory ar...

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“…RS was first described in the inferior temporal cortex (IT) of macaque [29][30][31][32][33][34][35][36][37][38][39] and was also found in the rat primary visual cortex [40]. Another study conducted in the IT of macaques also revealed a modulation of the RS by GABA A -mediated inhibition [41].…”

Section: In Animalsmentioning

confidence: 95%

Habituation, Adaptation and Prediction Processes in Neurodevelopmental Disorders: A Comprehensive Review

Merchie

Gomot

2023

Brain Sciences

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Habituation, the simplest form of learning preserved across species and evolution, is characterized by a response decrease as a stimulus is repeated. This adaptive function has been shown to be altered in some psychiatric and neurodevelopmental disorders such as autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD) or schizophrenia. At the brain level, habituation is characterized by a decrease in neural activity as a stimulation is repeated, referred to as neural adaptation. This phenomenon influences the ability to make predictions and to detect change, two processes altered in some neurodevelopmental and psychiatric disorders. In this comprehensive review, the objectives are to characterize habituation, neural adaptation, and prediction throughout typical development and in neurodevelopmental disorders; and to evaluate their implication in symptomatology, specifically in sensitivity to change or need for sameness. A summary of the different approaches to investigate adaptation will be proposed, in which we report the contribution of animal studies as well as electrophysiological studies in humans to understanding of underlying neuronal mechanisms.

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GABAergic and cholinergic modulation of repetition suppression in inferior temporal cortex

Cited by 8 publications

References 36 publications

Behavioural and neural markers of tactile sensory processing in infants at elevated likelihood of autism spectrum disorder and/or attention deficit hyperactivity disorder

Behavioural and neural markers of tactile sensory processing in infants at elevated likelihood of autism spectrum disorder and/or attention deficit hyperactivity disorder

Stimulus-specific regulation of visual oddball differentiation in posterior parietal cortex

Habituation, Adaptation and Prediction Processes in Neurodevelopmental Disorders: A Comprehensive Review

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