Pub Date : 2023-02-22DOI: 10.1523/JNEUROSCI.twij.43.8.2023
{"title":"This Week in The Journal","authors":"","doi":"10.1523/JNEUROSCI.twij.43.8.2023","DOIUrl":"https://doi.org/10.1523/JNEUROSCI.twij.43.8.2023","url":null,"abstract":"","PeriodicalId":22786,"journal":{"name":"The Journal of Neuroscience","volume":"4 1","pages":"1280 - 1280"},"PeriodicalIF":0.0,"publicationDate":"2023-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73127434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-02-21DOI: 10.1101/2023.02.21.529373
Charly G. Lecomte, Stephen Mari, Johannie Audet, Sirine Yassine, Angèle N. Merlet, Caroline Morency, J. Harnie, Claudie Beaulieu, Louis Gendron, A. Frigon
Following incomplete spinal cord injury in animals, including humans, substantial locomotor recovery can occur. However, functional aspects of locomotion, such as negotiating obstacles, remains challenging. We collected kinematic and electromyography data in 10 adult cats (5 males, 5 females) before and at weeks 1-2 and 7-8 after a lateral mid-thoracic hemisection on the right side of the cord while they negotiated obstacles of three different heights. Intact cats always cleared obstacles without contact. At weeks 1-2 after hemisection, the ipsilesional right hindlimb contacted obstacles in ∼50% of trials, triggering a stumbling corrective reaction or absent responses, which we termed Other. When complete clearance occurred, we observed exaggerated ipsilesional hindlimb flexion when crossing the obstacle with contralesional Left limbs leading. At weeks 7-8 after hemisection, the proportion of complete clearance increased, Other responses decreased, and stumbling corrective reactions remained relatively unchanged. We found redistribution of weight support after hemisection, with reduced diagonal supports and increased homolateral supports, particularly on the left contralesional side. The main neural strategy for complete clearance in intact cats consisted of increased knee flexor activation. After hemisection, ipsilesional knee flexor activation remained, but it was insufficient or more variable as the limb approached the obstacle. Intact cats also increased their speed when stepping over an obstacle, an increase that disappeared after hemisection. The increase in complete clearance over time after hemisection paralleled the recovery of muscle activation patterns or new strategies. Our results suggest partial recovery of anticipatory control through neuroplastic changes in the locomotor control system. SIGNIFICANCE STATEMENT Most spinal cord injuries (SCIs) are incomplete and people can recover some walking functions. However, the main challenge for people with SCIs that do recover a high level of function is to produce a gait that can adjust to everyday occurrences, such as turning, stepping over an obstacle, etc. Here, we use the cat model to answer two basic questions: How does an animal negotiate an obstacle after an incomplete SCI and why does it fail to safely clear it? We show that the inability to clear an obstacle is because of improper activation of muscles that flex the knee. Animals recover a certain amount of function thanks to new strategies and changes within the nervous system.
{"title":"Neuromechanical Strategies for Obstacle Negotiation during Overground Locomotion following Incomplete Spinal Cord Injury in Adult Cats","authors":"Charly G. Lecomte, Stephen Mari, Johannie Audet, Sirine Yassine, Angèle N. Merlet, Caroline Morency, J. Harnie, Claudie Beaulieu, Louis Gendron, A. Frigon","doi":"10.1101/2023.02.21.529373","DOIUrl":"https://doi.org/10.1101/2023.02.21.529373","url":null,"abstract":"Following incomplete spinal cord injury in animals, including humans, substantial locomotor recovery can occur. However, functional aspects of locomotion, such as negotiating obstacles, remains challenging. We collected kinematic and electromyography data in 10 adult cats (5 males, 5 females) before and at weeks 1-2 and 7-8 after a lateral mid-thoracic hemisection on the right side of the cord while they negotiated obstacles of three different heights. Intact cats always cleared obstacles without contact. At weeks 1-2 after hemisection, the ipsilesional right hindlimb contacted obstacles in ∼50% of trials, triggering a stumbling corrective reaction or absent responses, which we termed Other. When complete clearance occurred, we observed exaggerated ipsilesional hindlimb flexion when crossing the obstacle with contralesional Left limbs leading. At weeks 7-8 after hemisection, the proportion of complete clearance increased, Other responses decreased, and stumbling corrective reactions remained relatively unchanged. We found redistribution of weight support after hemisection, with reduced diagonal supports and increased homolateral supports, particularly on the left contralesional side. The main neural strategy for complete clearance in intact cats consisted of increased knee flexor activation. After hemisection, ipsilesional knee flexor activation remained, but it was insufficient or more variable as the limb approached the obstacle. Intact cats also increased their speed when stepping over an obstacle, an increase that disappeared after hemisection. The increase in complete clearance over time after hemisection paralleled the recovery of muscle activation patterns or new strategies. Our results suggest partial recovery of anticipatory control through neuroplastic changes in the locomotor control system. SIGNIFICANCE STATEMENT Most spinal cord injuries (SCIs) are incomplete and people can recover some walking functions. However, the main challenge for people with SCIs that do recover a high level of function is to produce a gait that can adjust to everyday occurrences, such as turning, stepping over an obstacle, etc. Here, we use the cat model to answer two basic questions: How does an animal negotiate an obstacle after an incomplete SCI and why does it fail to safely clear it? We show that the inability to clear an obstacle is because of improper activation of muscles that flex the knee. Animals recover a certain amount of function thanks to new strategies and changes within the nervous system.","PeriodicalId":22786,"journal":{"name":"The Journal of Neuroscience","volume":"35 1","pages":"5623 - 5641"},"PeriodicalIF":0.0,"publicationDate":"2023-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87334821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-02-15DOI: 10.1523/JNEUROSCI.twij.43.7.2023
{"title":"This Week in The Journal","authors":"","doi":"10.1523/JNEUROSCI.twij.43.7.2023","DOIUrl":"https://doi.org/10.1523/JNEUROSCI.twij.43.7.2023","url":null,"abstract":"","PeriodicalId":22786,"journal":{"name":"The Journal of Neuroscience","volume":"23 1","pages":"1072 - 1073"},"PeriodicalIF":0.0,"publicationDate":"2023-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78162342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-02-14DOI: 10.1101/2023.02.13.528278
C. Peerboom, Sam de Kater, Nikki Jonker, Marijn P.J.M. Rieter, T. Wijne, C. Wierenga
During the first two postnatal weeks, intraneuronal chloride concentrations in rodents gradually decrease, causing a shift from depolarizing to hyperpolarizing GABA responses. The postnatal GABA shift is delayed in rodent models for neurodevelopmental disorders and in human patients, but the impact of a delayed GABA shift on the developing brain remains obscure. Here we examine the direct and indirect consequences of a delayed postnatal GABA shift on network development in organotypic hippocampal cultures made from 6- to 7-d-old mice by treating the cultures for 1 week with VU0463271, a specific inhibitor of the chloride exporter KCC2. We verified that VU treatment delayed the GABA shift and kept GABA signaling depolarizing until DIV9. We found that the structural and functional development of excitatory and inhibitory synapses at DIV9 was not affected after VU treatment. In line with previous studies, we observed that GABA signaling was already inhibitory in control and VU-treated postnatal slices. Surprisingly, 14 d after the VU treatment had ended (DIV21), we observed an increased frequency of spontaneous inhibitory postsynaptic currents in CA1 pyramidal cells, while excitatory currents were not changed. Synapse numbers and release probability were unaffected. We found that dendrite-targeting interneurons in the stratum radiatum had an elevated resting membrane potential, while pyramidal cells were less excitable compared with control slices. Our results show that depolarizing GABA signaling does not promote synapse formation after P7, and suggest that postnatal intracellular chloride levels indirectly affect membrane properties in a cell-specific manner. SIGNIFICANCE STATEMENT During brain development, the action of neurotransmitter GABA shifts from depolarizing to hyperpolarizing. This shift is a thought to play a critical role in synapse formation. A delayed shift is common in rodent models for neurodevelopmental disorders and in human patients, but its consequences for synaptic development remain obscure. Here, we delayed the GABA shift by 1 week in organotypic hippocampal cultures and carefully examined the consequences for circuit development. We find that delaying the shift has no direct effects on synaptic development, but instead leads to indirect, cell type-specific changes in membrane properties. Our data call for careful assessment of alterations in cellular excitability in neurodevelopmental disorders.
{"title":"Delaying the GABA Shift Indirectly Affects Membrane Properties in the Developing Hippocampus","authors":"C. Peerboom, Sam de Kater, Nikki Jonker, Marijn P.J.M. Rieter, T. Wijne, C. Wierenga","doi":"10.1101/2023.02.13.528278","DOIUrl":"https://doi.org/10.1101/2023.02.13.528278","url":null,"abstract":"During the first two postnatal weeks, intraneuronal chloride concentrations in rodents gradually decrease, causing a shift from depolarizing to hyperpolarizing GABA responses. The postnatal GABA shift is delayed in rodent models for neurodevelopmental disorders and in human patients, but the impact of a delayed GABA shift on the developing brain remains obscure. Here we examine the direct and indirect consequences of a delayed postnatal GABA shift on network development in organotypic hippocampal cultures made from 6- to 7-d-old mice by treating the cultures for 1 week with VU0463271, a specific inhibitor of the chloride exporter KCC2. We verified that VU treatment delayed the GABA shift and kept GABA signaling depolarizing until DIV9. We found that the structural and functional development of excitatory and inhibitory synapses at DIV9 was not affected after VU treatment. In line with previous studies, we observed that GABA signaling was already inhibitory in control and VU-treated postnatal slices. Surprisingly, 14 d after the VU treatment had ended (DIV21), we observed an increased frequency of spontaneous inhibitory postsynaptic currents in CA1 pyramidal cells, while excitatory currents were not changed. Synapse numbers and release probability were unaffected. We found that dendrite-targeting interneurons in the stratum radiatum had an elevated resting membrane potential, while pyramidal cells were less excitable compared with control slices. Our results show that depolarizing GABA signaling does not promote synapse formation after P7, and suggest that postnatal intracellular chloride levels indirectly affect membrane properties in a cell-specific manner. SIGNIFICANCE STATEMENT During brain development, the action of neurotransmitter GABA shifts from depolarizing to hyperpolarizing. This shift is a thought to play a critical role in synapse formation. A delayed shift is common in rodent models for neurodevelopmental disorders and in human patients, but its consequences for synaptic development remain obscure. Here, we delayed the GABA shift by 1 week in organotypic hippocampal cultures and carefully examined the consequences for circuit development. We find that delaying the shift has no direct effects on synaptic development, but instead leads to indirect, cell type-specific changes in membrane properties. Our data call for careful assessment of alterations in cellular excitability in neurodevelopmental disorders.","PeriodicalId":22786,"journal":{"name":"The Journal of Neuroscience","volume":"25 1","pages":"5483 - 5500"},"PeriodicalIF":0.0,"publicationDate":"2023-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78380494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-02-09DOI: 10.1101/2023.02.08.527708
M. Cui, Björn Herrmann
Hearing impairment affects many older adults but is often diagnosed decades after speech comprehension in noisy situations has become effortful. Accurate assessment of listening effort may thus help diagnose hearing impairment earlier. However, pupillometry—the most used approach to assess listening effort—has limitations that hinder its use in practice. The current study explores a novel way to assess listening effort through eye movements. Building on cognitive and neurophysiological work, we examine the hypothesis that eye movements decrease when speech listening becomes challenging. In three experiments with human participants from both sexes, we demonstrate, consistent with this hypothesis, that fixation duration increases and spatial gaze dispersion decreases with increasing speech masking. Eye movements decreased during effortful speech listening for different visual scenes (free viewing, object tracking) and speech materials (simple sentences, naturalistic stories). In contrast, pupillometry was less sensitive to speech masking during story listening, suggesting pupillometric measures may not be as effective for the assessments of listening effort in naturalistic speech-listening paradigms. Our results reveal a critical link between eye movements and cognitive load, suggesting that neural activity in the brain regions that support the regulation of eye movements, such as frontal eye field and superior colliculus, are modulated when listening is effortful. SIGNIFICANCE STATEMENT Assessment of listening effort is critical for early diagnosis of age-related hearing loss. Pupillometry is most used but has several disadvantages. The current study explores a novel way to assess listening effort through eye movements. We examine the hypothesis that eye movements decrease when speech listening becomes effortful. We demonstrate, consistent with this hypothesis, that fixation duration increases and gaze dispersion decreases with increasing speech masking. Eye movements decreased during effortful speech listening for different visual scenes (free viewing, object tracking) and speech materials (sentences, naturalistic stories). Our results reveal a critical link between eye movements and cognitive load, suggesting that neural activity in brain regions that support the regulation of eye movements are modulated when listening is effortful.
{"title":"Eye Movements Decrease during Effortful Speech Listening","authors":"M. Cui, Björn Herrmann","doi":"10.1101/2023.02.08.527708","DOIUrl":"https://doi.org/10.1101/2023.02.08.527708","url":null,"abstract":"Hearing impairment affects many older adults but is often diagnosed decades after speech comprehension in noisy situations has become effortful. Accurate assessment of listening effort may thus help diagnose hearing impairment earlier. However, pupillometry—the most used approach to assess listening effort—has limitations that hinder its use in practice. The current study explores a novel way to assess listening effort through eye movements. Building on cognitive and neurophysiological work, we examine the hypothesis that eye movements decrease when speech listening becomes challenging. In three experiments with human participants from both sexes, we demonstrate, consistent with this hypothesis, that fixation duration increases and spatial gaze dispersion decreases with increasing speech masking. Eye movements decreased during effortful speech listening for different visual scenes (free viewing, object tracking) and speech materials (simple sentences, naturalistic stories). In contrast, pupillometry was less sensitive to speech masking during story listening, suggesting pupillometric measures may not be as effective for the assessments of listening effort in naturalistic speech-listening paradigms. Our results reveal a critical link between eye movements and cognitive load, suggesting that neural activity in the brain regions that support the regulation of eye movements, such as frontal eye field and superior colliculus, are modulated when listening is effortful. SIGNIFICANCE STATEMENT Assessment of listening effort is critical for early diagnosis of age-related hearing loss. Pupillometry is most used but has several disadvantages. The current study explores a novel way to assess listening effort through eye movements. We examine the hypothesis that eye movements decrease when speech listening becomes effortful. We demonstrate, consistent with this hypothesis, that fixation duration increases and gaze dispersion decreases with increasing speech masking. Eye movements decreased during effortful speech listening for different visual scenes (free viewing, object tracking) and speech materials (sentences, naturalistic stories). Our results reveal a critical link between eye movements and cognitive load, suggesting that neural activity in brain regions that support the regulation of eye movements are modulated when listening is effortful.","PeriodicalId":22786,"journal":{"name":"The Journal of Neuroscience","volume":"120 1","pages":"5856 - 5869"},"PeriodicalIF":0.0,"publicationDate":"2023-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88476151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-02-08DOI: 10.1101/2023.02.07.527481
Yao Lu, Francesca Sciaccotta, Leah Kiely, Benjamin Bellanger, A. Erisir, Dan Meliza
The acoustic environment an animal experiences early in life shapes the structure and function of its auditory system. This process of experience-dependent development is thought to be primarily orchestrated by potentiation and depression of synapses, but plasticity of intrinsic voltage dynamics may also contribute. Here, we show that in juvenile male and female zebra finches, neurons in a cortical-level auditory area, the caudal mesopallium (CM), can rapidly change their firing dynamics. This plasticity was only observed in birds that were reared in a complex acoustic and social environment, which also caused increased expression of the low-threshold potassium channel Kv1.1 in the plasma membrane and endoplasmic reticulum (ER). Intrinsic plasticity depended on activity, was reversed by blocking low-threshold potassium currents, and was prevented by blocking intracellular calcium signaling. Taken together, these results suggest that Kv1.1 is rapidly mobilized to the plasma membrane by activity-dependent elevation of intracellular calcium. This produces a shift in the excitability and temporal integration of CM neurons that may be permissive for auditory learning in complex acoustic environments during a crucial period for the development of vocal perception and production. SIGNIFICANCE STATEMENT Neurons can change not only the strength of their connections to other neurons, but also how they integrate synaptic currents to produce patterns of action potentials. In contrast to synaptic plasticity, the mechanisms and functional roles of intrinisic plasticity remain poorly understood. We found that neurons in the zebra finch auditory cortex can rapidly shift their spiking dynamics within a few minutes in response to intracellular stimulation. This plasticity involves increased conductance of a low-threshold potassium current associated with the Kv1.1 channel, but it only occurs in birds reared in a rich acoustic environment. Thus, auditory experience regulates a mechanism of neural plasticity that allows neurons to rapidly adapt their firing dynamics to stimulation.
{"title":"Rapid, Activity-Dependent Intrinsic Plasticity in the Developing Zebra Finch Auditory Cortex","authors":"Yao Lu, Francesca Sciaccotta, Leah Kiely, Benjamin Bellanger, A. Erisir, Dan Meliza","doi":"10.1101/2023.02.07.527481","DOIUrl":"https://doi.org/10.1101/2023.02.07.527481","url":null,"abstract":"The acoustic environment an animal experiences early in life shapes the structure and function of its auditory system. This process of experience-dependent development is thought to be primarily orchestrated by potentiation and depression of synapses, but plasticity of intrinsic voltage dynamics may also contribute. Here, we show that in juvenile male and female zebra finches, neurons in a cortical-level auditory area, the caudal mesopallium (CM), can rapidly change their firing dynamics. This plasticity was only observed in birds that were reared in a complex acoustic and social environment, which also caused increased expression of the low-threshold potassium channel Kv1.1 in the plasma membrane and endoplasmic reticulum (ER). Intrinsic plasticity depended on activity, was reversed by blocking low-threshold potassium currents, and was prevented by blocking intracellular calcium signaling. Taken together, these results suggest that Kv1.1 is rapidly mobilized to the plasma membrane by activity-dependent elevation of intracellular calcium. This produces a shift in the excitability and temporal integration of CM neurons that may be permissive for auditory learning in complex acoustic environments during a crucial period for the development of vocal perception and production. SIGNIFICANCE STATEMENT Neurons can change not only the strength of their connections to other neurons, but also how they integrate synaptic currents to produce patterns of action potentials. In contrast to synaptic plasticity, the mechanisms and functional roles of intrinisic plasticity remain poorly understood. We found that neurons in the zebra finch auditory cortex can rapidly shift their spiking dynamics within a few minutes in response to intracellular stimulation. This plasticity involves increased conductance of a low-threshold potassium current associated with the Kv1.1 channel, but it only occurs in birds reared in a rich acoustic environment. Thus, auditory experience regulates a mechanism of neural plasticity that allows neurons to rapidly adapt their firing dynamics to stimulation.","PeriodicalId":22786,"journal":{"name":"The Journal of Neuroscience","volume":"2 1","pages":"6872 - 6883"},"PeriodicalIF":0.0,"publicationDate":"2023-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89961119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-02-08DOI: 10.1523/JNEUROSCI.twij.43.6.2023
{"title":"This Week in The Journal","authors":"","doi":"10.1523/JNEUROSCI.twij.43.6.2023","DOIUrl":"https://doi.org/10.1523/JNEUROSCI.twij.43.6.2023","url":null,"abstract":"","PeriodicalId":22786,"journal":{"name":"The Journal of Neuroscience","volume":"82 1","pages":"878 - 878"},"PeriodicalIF":0.0,"publicationDate":"2023-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90594337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-02-01DOI: 10.1101/2022.09.03.506453
Samson Chota, Rufin VanRullen, R. Gulbinaite
Both passive tactile stimulation and motor actions result in dynamic changes in beta band (15–30 Hz Hz) oscillations over somatosensory cortex. Similar to alpha band (8–12 Hz) power decrease in the visual system, beta band power also decreases following stimulation of the somatosensory system. This relative suppression of α and β oscillations is generally interpreted as an increase in cortical excitability. Here, next to traditional single-pulse stimuli, we used a random intensity continuous right index finger tactile stimulation (white noise), which enabled us to uncover an impulse response function of the somatosensory system. Contrary to previous findings, we demonstrate a burst-like initial increase rather than decrease of beta activity following white noise stimulation (human participants, N = 18, 8 female). These β bursts, on average, lasted for 3 cycles, and their frequency was correlated with resonant frequency of somatosensory cortex, as measured by a multifrequency steady-state somatosensory evoked potential paradigm. Furthermore, beta band bursts shared spectro-temporal characteristics with evoked and resting-state β oscillations. Together, our findings not only reveal a novel oscillatory signature of somatosensory processing that mimics the previously reported visual impulse response functions, but also point to a common oscillatory generator underlying spontaneous β bursts in the absence of tactile stimulation and phase-locked β bursts following stimulation, the frequency of which is determined by the resonance properties of the somatosensory system. SIGNIFICANCE STATEMENT The investigation of the transient nature of oscillations has gained great popularity in recent years. The findings of bursting activity, rather than sustained oscillations in the beta band, have provided important insights into its role in movement planning, working memory, inhibition, and reactivation of neural ensembles. In this study, we show that also in response to tactile stimulation the somatosensory system responds with ∼3 cycle oscillatory beta band bursts, whose spectro-temporal characteristics are shared with evoked and resting-state beta band oscillatory signatures of the somatosensory system. As similar bursts have been observed in the visual domain, these oscillatory signatures might reflect an important supramodal mechanism in sensory processing.
{"title":"Random Tactile Noise Stimulation Reveals Beta-Rhythmic Impulse Response Function of the Somatosensory System","authors":"Samson Chota, Rufin VanRullen, R. Gulbinaite","doi":"10.1101/2022.09.03.506453","DOIUrl":"https://doi.org/10.1101/2022.09.03.506453","url":null,"abstract":"Both passive tactile stimulation and motor actions result in dynamic changes in beta band (15–30 Hz Hz) oscillations over somatosensory cortex. Similar to alpha band (8–12 Hz) power decrease in the visual system, beta band power also decreases following stimulation of the somatosensory system. This relative suppression of α and β oscillations is generally interpreted as an increase in cortical excitability. Here, next to traditional single-pulse stimuli, we used a random intensity continuous right index finger tactile stimulation (white noise), which enabled us to uncover an impulse response function of the somatosensory system. Contrary to previous findings, we demonstrate a burst-like initial increase rather than decrease of beta activity following white noise stimulation (human participants, N = 18, 8 female). These β bursts, on average, lasted for 3 cycles, and their frequency was correlated with resonant frequency of somatosensory cortex, as measured by a multifrequency steady-state somatosensory evoked potential paradigm. Furthermore, beta band bursts shared spectro-temporal characteristics with evoked and resting-state β oscillations. Together, our findings not only reveal a novel oscillatory signature of somatosensory processing that mimics the previously reported visual impulse response functions, but also point to a common oscillatory generator underlying spontaneous β bursts in the absence of tactile stimulation and phase-locked β bursts following stimulation, the frequency of which is determined by the resonance properties of the somatosensory system. SIGNIFICANCE STATEMENT The investigation of the transient nature of oscillations has gained great popularity in recent years. The findings of bursting activity, rather than sustained oscillations in the beta band, have provided important insights into its role in movement planning, working memory, inhibition, and reactivation of neural ensembles. In this study, we show that also in response to tactile stimulation the somatosensory system responds with ∼3 cycle oscillatory beta band bursts, whose spectro-temporal characteristics are shared with evoked and resting-state beta band oscillatory signatures of the somatosensory system. As similar bursts have been observed in the visual domain, these oscillatory signatures might reflect an important supramodal mechanism in sensory processing.","PeriodicalId":22786,"journal":{"name":"The Journal of Neuroscience","volume":"23 1","pages":"3107 - 3119"},"PeriodicalIF":0.0,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85161240","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-02-01DOI: 10.1523/JNEUROSCI.twij.43.5.2023
{"title":"This Week in The Journal","authors":"","doi":"10.1523/JNEUROSCI.twij.43.5.2023","DOIUrl":"https://doi.org/10.1523/JNEUROSCI.twij.43.5.2023","url":null,"abstract":"","PeriodicalId":22786,"journal":{"name":"The Journal of Neuroscience","volume":"58 1","pages":"681 - 681"},"PeriodicalIF":0.0,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90559272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-25DOI: 10.1523/JNEUROSCI.twij.43.4.2023
{"title":"This Week in The Journal","authors":"","doi":"10.1523/JNEUROSCI.twij.43.4.2023","DOIUrl":"https://doi.org/10.1523/JNEUROSCI.twij.43.4.2023","url":null,"abstract":"","PeriodicalId":22786,"journal":{"name":"The Journal of Neuroscience","volume":"73 1","pages":"522 - 522"},"PeriodicalIF":0.0,"publicationDate":"2023-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90618950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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