Cortical Sensory Processing Research Articles

Lack of visual experience leads to severe distortions in the hand representation of the body model

This study investigates the impact of vision on the maintenance of hand representation in the implicit body model, particularly focusing on congenitally blind individuals. To address this, we performed a hand landmark localization task on blind individuals who lacked visual experience of their bodies and compared their performance to normally sighted and normally sighted but blindfolded participants. Through measurements of finger lengths, hand width, and shape index, we demonstrate that blind participants exhibit significantly greater distortions in their hand representation compared to sighted and blindfolded controls. Notably, blind individuals displayed a marked overestimation of hand width and an underestimation of finger lengths, particularly in digits D2, D3, and D4. Surprisingly, blind subjects with partial vision displayed more severe distortions than those with no residual vision. Furthermore, our findings reveal that late-blind participants exhibit similar levels of distortion as congenitally blind individuals, suggesting an extended period of susceptibility to the lack of visual input in shaping body representations. The Reverse Distortion (RD) hypothesis provides a plausible explanation for these distortions, suggesting that compensatory mechanisms occur within the body model to counteract the anisotropic cortical representations. Our results support this hypothesis: blind individuals have expanded cortical representations processing tactile information, so this could lead to more pronounced distortions in their hand representation of the body model. This underscores the importance of visual input in modulating body representations. Overall, our study highlights the malleability of body representations and the intricate interplay between sensory inputs and cortical processing in shaping the implicit body model.

Local field potential sharp waves with diversified impact on cortical neuronal encoding of haptic input

Cortical sensory processing is greatly impacted by internally generated activity. But controlling for that activity is difficult since the thalamocortical network is a high-dimensional system with rapid state changes. Therefore, to unwind the cortical computational architecture there is a need for physiological ‘landmarks’ that can be used as frames of reference for computational state. Here we use a waveshape transform method to identify conspicuous local field potential sharp waves (LFP-SPWs) in the somatosensory cortex (S1). LFP-SPW events triggered short-lasting but massive neuronal activation in all recorded neurons with a subset of neurons initiating their activation up to 20 ms before the LFP-SPW onset. In contrast, LFP-SPWs differentially impacted the neuronal spike responses to ensuing tactile inputs, depressing the tactile responses in some neurons and enhancing them in others. When LFP-SPWs coactivated with more distant cortical surface (ECoG)-SPWs, suggesting an involvement of these SPWs in global cortical signaling, the impact of the LFP-SPW on the neuronal tactile response could change substantially, including inverting its impact to the opposite. These cortical SPWs shared many signal fingerprint characteristics as reported for hippocampal SPWs and may be a biomarker for a particular type of state change that is possibly shared byboth hippocampus and neocortex.

At the onset of active whisking, the input layer of barrel cortex exhibits a 24 h window of increased excitability that depends on prior experience.

The development of motor control over sensory organs is a critical milestone in sensory processing, enabling active exploration and shaping of the sensory environment. However, whether the onset of sensory organ motor control directly influences the development of corresponding sensory cortices remains unknown. Here, we exploit the late onset of whisking behavior in mice to address this question in the somatosensory system. Using ex vivo electrophysiology, we discovered a transient increase in the intrinsic excitability of excitatory neurons in layer IV of the barrel cortex, which processes whisker input, precisely coinciding with the onset of active whisking at postnatal day 14 (P14). This increase in neuronal gain was specific to layer IV, independent of changes in synaptic strength, and required prior sensory experience. Strikingly, the effect was not observed in layer II/III of the barrel cortex or in the visual cortex upon eye opening, suggesting a unique interaction between the development of active sensing and the thalamocortical input layer in the somatosensory system. Predictive modeling indicated that changes in active membrane conductances alone could reliably distinguish P14 neurons in control but not whisker-deprived hemispheres. Our findings demonstrate an experience-dependent, lamina-specific refinement of neuronal excitability tightly linked to the emergence of active whisking. This transient increase in the gain of the thalamic input layer coincides with a critical period for synaptic plasticity in downstream layers, suggesting a role in facilitating cortical maturation and sensory processing. Together, our results provide evidence for a direct interaction between the development of motor control and sensory cortex, offering new insights into the experience-dependent development and refinement of sensory systems. These findings have broad implications for understanding the interplay between motor and sensory development, and how the mechanisms of perception cooperate with behavior.

Changes in visually and auditory attended audiovisual speech processing in cochlear implant users: A longitudinal ERP study

Limited auditory input, whether caused by hearing loss or by electrical stimulation through a cochlear implant (CI), can be compensated by the remaining senses. Specifically for CI users, previous studies reported not only improved visual skills, but also altered cortical processing of unisensory visual and auditory stimuli. However, in multisensory scenarios, it is still unclear how auditory deprivation (before implantation) and electrical hearing experience (after implantation) affect cortical audiovisual speech processing.Here, we present a prospective longitudinal electroencephalography (EEG) study which systematically examined the deprivation- and CI-induced alterations of cortical processing of audiovisual words by comparing event-related potentials (ERPs) in postlingually deafened CI users before and after implantation (five weeks and six months of CI use). A group of matched normal-hearing (NH) listeners served as controls. The participants performed a word-identification task with congruent and incongruent audiovisual words, focusing their attention on either the visual (lip movement) or the auditory speech signal. This allowed us to study the (top-down) attention effect on the (bottom-up) sensory cortical processing of audiovisual speech.When compared to the NH listeners, the CI candidates (before implantation) and the CI users (after implantation) exhibited enhanced lipreading abilities and an altered cortical response at the N1 latency range (90–150 ms) that was characterized by a decreased theta oscillation power (4–8 Hz) and a smaller amplitude in the auditory cortex. After implantation, however, the auditory-cortex response gradually increased and developed a stronger intra-modal connectivity. Nevertheless, task efficiency and activation in the visual cortex was significantly modulated in both groups by focusing attention on the visual as compared to the auditory speech signal, with the NH listeners additionally showing an attention-dependent decrease in beta oscillation power (13–30 Hz).In sum, these results suggest remarkable deprivation effects on audiovisual speech processing in the auditory cortex, which partially reverse after implantation. Although even experienced CI users still show distinct audiovisual speech processing compared to NH listeners, pronounced effects of (top-down) direction of attention on (bottom-up) audiovisual processing can be observed in both groups. However, NH listeners but not CI users appear to show enhanced allocation of cognitive resources in visually as compared to auditory attended audiovisual speech conditions, which supports our behavioural observations of poorer lipreading abilities and reduced visual influence on audition in NH listeners as compared to CI users.

Diabetic ketoacidosis with central nervous system involvement: Conventional and advanced magnetic resonance neuroimaging findings.

Diabetic ketoacidosis (DKA) is a serious complication in children with diabetes mellitus type 1 (DM1). In rare and severe cases DKA may be complicated by cerebral edema, central brain herniation and cerebral infarctions. We present the magnetic resonance imaging findings in a child with DKA and central nervous system involvement; diffusion tensor imaging (DTI) and functional MRI (fMRI) were performed to assess the white matter integrity of sensory pathways and cortical sensory processing. Conventional imaging showed bilateral uncal herniation, effacement of the perimesencephalic cisterns, wide ischemic lesions in the posterior cerebral artery (PCA) territories, sagging brainstem and Duret's hemorrhage consistent with signs of central brain herniation and intracranial hypertension. Advanced MRI showed a possible left-sided cortical reorganization for sensory function, with underlying left cortico-talamic and cortico-spinal pathways less severely impaired. Knowledge of the full framework in these conditions is of vital importance for timely patient management; advanced neuroimaging techniques may be considered as prognostic indicators in those cases with extensive involvement of eloquent brain areas.

Vasotocin receptor gene genotypes moderate the relationship between cortical thickness and sensory processing

Sensory processing is the process by which the central nervous system gathers, interprets, and regulates sensory stimuli in response to environmental cues. However, our understanding of the genetic factors and neuroanatomical correlations that influence sensory processing is limited. The vasotocin system modulates sensory input responsiveness, making it a potential candidate for further investigation. Additionally, human neuroimaging studies have demonstrated that the ability to modulate sensory stimuli is related to neuroanatomical features such as cortical thickness. Therefore, this study aimed to examine the relationship between functional polymorphisms in vasotocin receptor (VTR) genes, sensory profiles, and neuroanatomical correlations. We used structural magnetic resonance imaging (MRI) and the Adolescent/Adult Sensory Profile (AASP) questionnaire in 98 healthy adult participants to assess sensory processing and identified seven single nucleotide polymorphisms. We found that A-allele carriers of rs1042615 in VTR had higher scores for “sensory sensitivity” and “sensation avoiding”. Moreover, higher scores for three AASP subscales were associated with decreased cortical thickness in various regions, including the right precentral, paracentral, and fusiform gyri, as well as bilateral inferior temporal gyri. This study sheds light on the potential role of genetic variations in the VTR in modulating sensory processing and correlation with cortical thickness which has future implications for better understanding sensory abnormalities in neurodevelopmental disorders.

Laminar neural dynamics of auditory evoked responses: Computational modeling of local field potentials in auditory cortex of non-human primates

Evoked neural responses to sensory stimuli have been extensively investigated in humans and animal models both to enhance our understanding of brain function and to aid in clinical diagnosis of neurological and neuropsychiatric conditions. Recording and imaging techniques such as electroencephalography (EEG), magnetoencephalography (MEG), local field potentials (LFPs), and calcium imaging provide complementary information about different aspects of brain activity at different spatial and temporal scales. Modeling and simulations provide a way to integrate these different types of information to clarify underlying neural mechanisms.In this study, we aimed to shed light on the neural dynamics underlying auditory evoked responses by fitting a rate-based model to LFPs recorded via multi-contact electrodes which simultaneously sampled neural activity across cortical laminae. Recordings included neural population responses to best-frequency (BF) and non-BF tones at four representative sites in primary auditory cortex (A1) of awake monkeys. The model considered major neural populations of excitatory, parvalbumin-expressing (PV), and somatostatin-expressing (SOM) neurons across layers 2/3, 4, and 5/6. Unknown parameters, including the connection strength between the populations, were fitted to the data. Our results revealed similar population dynamics, fitted model parameters, predicted equivalent current dipoles (ECD), tuning curves, and lateral inhibition profiles across recording sites and animals, in spite of quite different extracellular current distributions. We found that PV firing rates were higher in BF than in non-BF responses, mainly due to different strengths of tonotopic thalamic input, whereas SOM firing rates were higher in non-BF than in BF responses due to lateral inhibition.In conclusion, we demonstrate the feasibility of the model-fitting approach in identifying the contributions of cell-type specific population activity to stimulus-evoked LFPs across cortical laminae, providing a foundation for further investigations into the dynamics of neural circuits underlying cortical sensory processing.

Reduced somatosensory evoked potentials and paired-pulse inhibition in the primary somatosensory cortex of athletes with chronic pain.

Chronic pain impedes athletic training and performance. However, it is challenging to identify the precise causes of chronic pain for effective treatment. To examine possible neuroplastic changes in sensory transmission and cortical processing, we compared somatosensory evoked potentials (SEPs) and paired-pulse inhibition (PPI) in primary sensory cortex (S1) between athletes with chronic pain and control athletes. Sixty-six intercollegiate athletes (39 males and 27 females) were recruited for this study, 45 control athletes and 21 reporting persistent pain for > 3months. Sensory-evoked potentials were induced in S1 by constant-current square-wave pulses (0.2-ms duration) delivered to the right median nerve, while PPI was induced by paired stimulation at interstimulus intervals of 30 and 100ms (PPI-30 and PPI-100ms, respectively). All participants were randomly presented with total 1,500 (each 500 stimuli) single stimuli and stimulus pairs at 2Hz. Both N20 amplitude and PPI-30ms were significantly lower in athletes with chronic pain compared to control athletes, while P25 amplitude and PPI-100ms did not differ significantly between groups. Chronic pain in athletes is associated with substantially altered excitatory-inhibitory balance within the primary somatosensory cortex, possibly due to reduced thalamocortical excitatory transmission and suppressed cortical inhibitory transmission.

Principles of nociceptive coding in the anterior cingulate cortex

The perception of pain is a multidimensional sensory and emotional/affective experience arising from distributed brain activity. However, the involved brain regions are not specific for pain. Thus, how the cortex distinguishes nociception from other aversive and salient sensory stimuli remains elusive. Additionally, the resulting consequences of chronic neuropathic pain on sensory processing have not been characterized. Using invivo miniscope calcium imaging with cellular resolution in freely moving mice, we elucidated the principles of nociceptive and sensory coding in the anterior cingulate cortex, a region essential for pain processing. We found that population activity, not single-cell responses, allowed discriminating noxious from other sensory stimuli, ruling out the existence of nociception-specific neurons. Additionally, single-cell stimulus selectivity was highly dynamic over time, but stimulus representation at the population level remained stable. Peripheral nerve injury-induced chronic neuropathic pain led to dysfunctional encoding of sensory events by exacerbation of responses to innocuous stimuli and impairment of pattern separation and stimulus classification, which were restored by analgesic treatment. These findings provide a novel interpretation for altered cortical sensory processing in chronic neuropathic pain and give insights into the effects of systemic analgesic treatment in the cortex.

Oxytocin promotes prefrontal population activity via the PVN-PFC pathway to regulate pain

Neurons in the prefrontal cortex (PFC) can provide top-down regulation of sensory-affective experiences such as pain. Bottom-up modulation of sensory coding in the PFC, however, remains poorly understood. Here, we examined how oxytocin (OT) signaling from the hypothalamus regulates nociceptive coding in the PFC. Invivo time-lapse endoscopic calcium imaging in freely behaving rats showed that OT selectively enhanced population activity in the prelimbic PFC in response to nociceptive inputs. This population response resulted from the reduction of evoked GABAergic inhibition and manifested as elevated functional connectivity involving pain-responsive neurons. Direct inputs from OT-releasing neurons in the paraventricular nucleus (PVN) of the hypothalamus are crucial to maintaining this prefrontal nociceptive response. Activation of the prelimbic PFC by OT or direct optogenetic stimulation of oxytocinergic PVN projections reduced acute and chronic pain. These results suggest that oxytocinergic signaling in the PVN-PFC circuit constitutes a key mechanism to regulate cortical sensory processing.

Normal connectivity of thalamorecipient networks in barrel equivalents of the reeler cortex.

The reeler mouse mutant has long served as a primary model to study the development of cortical layers, which is governed by the extracellular glycoprotein reelin secreted by Cajal-Retzius cells. Because layers organize local and long-range circuits for sensory processing, we investigated whether intracortical connectivity is compromised by reelin deficiency in this model. We generated a transgenic reeler mutant (we used both sexes), in which layer 4-fated spiny stellate neurons are labeled with tdTomato and applied slice electrophysiology and immunohistochemistry with synaptotagmin-2 to study the circuitry between the major thalamorecipient cell types, namely excitatory spiny stellate and inhibitory fast-spiking (putative basket) cells. In the reeler mouse, spiny stellate cells are clustered into barrel equivalents. In these clusters, we found that intrinsic physiology, connectivity, and morphology of spiny stellate and fast-spiking, putative basket cells does not significantly differ between reeler and controls. Properties of unitary connections, including connection probability, were very comparable in excitatory cell pairs and spiny stellate/fast-spiking cell pairs, suggesting an intact excitation-inhibition balance at the first stage of cortical sensory information processing. Together with previous findings, this suggests that thalamorecipient circuitry in the barrel cortex develops and functions independently of proper cortical lamination and postnatal reelin signaling.

Cortical sensory processing across motivational states during goal-directed behavior

Behavioral states can influence performance of goal-directed sensorimotor tasks. Yet, it is unclear how altered neuronal sensory representations in these states relate to task performance and learning. We trained water-restricted mice in a two-whisker discrimination task to study cortical circuits underlying perceptual decision-making under different levels of thirst. We identified somatosensory cortices as well as the premotor cortex as part of the circuit necessary for task execution. Two-photon calcium imaging in these areas identified populations selective to sensory or motor events. Analysis of task performance during individual sessions revealed distinct behavioral states induced by decreasing levels of thirst-related motivation. Learning was better explained by improvements in motivational state control rather than sensorimotor association. Whisker sensory representations in the cortex were altered across behavioral states. In particular, whisker stimuli could be better decoded from neuronal activity during high task performance states, suggesting that state-dependent changes of sensory processing influence decision-making.

A preliminary trial of botulinum toxin type A in patients with vestibular migraine: A longitudinal fMRI study.

ObjectiveThis study aims to investigate the efficacy of botulinum toxin type A (BTX-A) in the prophylactic management of vestibular migraine (VM) and to determine whether this treatment modulates intrinsic functional brain network.MethodsVestibular migraine patients (n = 20, mean age 45.4 years) who were resistant to conventional prophylactic therapies had BTX-A injection and rs-fMRI before and 2 months after the injection. We also measured the changes in the frequency of vertigo and migraine attacks, symptomatic functional disability scores, and neuropsychiatric inventories.ResultsAfter BTX-A injection, the mean monthly frequencies of migraine and vertigo episodes decreased significantly compared with the baseline (p < 0.01, paired t-test). The Headache Impact Test-6 score and the Migraine Disability Assessment, and the vertigo parameters, measured by the Dizziness Handicap Inventory and the Vertigo Symptom Scale, showed an improvement, as did the anxiety and depression scores 2 months after BTX-A treatment. The low-frequency fluctuation analysis of the rs-fMRI data found significant changes in the functional connectivity of the right superior temporal gyrus. Adoption of this cluster as the seed region increased the functional connectivity with the left post-central gyrus, right supramarginal gyrus, and right middle temporal gyrus after BTX-A treatment.ConclusionThis prospective study suggests that BTX-A treatment is effective at ameliorating migraine and vertigo symptoms in VM patients who were resistant to conventional therapies. Along with symptomatic improvements, changes in the functional connectivity within the multisensory vestibular and pain networks suggest a dysmodulation of multimodal sensory integration and abnormal cortical processing of the vestibular and pain signals in VM patients.

P601. Kalrn Mutation Identified in Individuals With Schizophrenia Recapitulates Disease-Relevant Neuro-oscillatory Aberrations in the Mouse Visual and Prefrontal Cortices

Aberrations in basic sensory cortical processing are present in several neuropsychiatric disorders. Electrophysiological biomarkers of sensory processing dysfunction can be reliably measured in both human patients and animal models, providing a translational strategy for linking molecular, circuit, and cognitive aspects of the disease. We recently developed a mouse model with a mutation in the Kalrn gene observed in a cohort of individuals with schizophrenia. These Kalrn-PT mice recapitulate structural changes in patients with schizophrenia, including adolescent-onset dendritic changes in the neocortex. Here we sought to understand how these structural changes may affect neural synchrony in local and interregional cortical circuits, focusing on a sensory processing paradigm with established disease relevance.

Spatiotemporal patterns of population response in the visual cortex under isoflurane: from wakefulness to loss of consciousness.

Anesthetic drugs are widely used in medicine and research to mediate loss of consciousness (LOC). Isoflurane is a commonly used anesthetic drug; however, its effects on cortical sensory processing, in particular around LOC, are not well understood. Using voltage-sensitive dye imaging, we measured visually evoked neuronal population response from the visual cortex in awake and anesthetized mice at 3 increasing concentrations of isoflurane, thus controlling the level of anesthesia from wakefulness to deep anesthesia. At low concentration of isoflurane, the effects on neuronal measures were minor relative to the awake condition. These effects augmented with increasing isoflurane concentration, while around LOC point, they showed abrupt and nonlinear changes. At the network level, we found that isoflurane decreased the stimulus-evoked intra-areal spatial spread of local neural activation, previously reported to be mediated by horizontal connections, and also reduced intra-areal synchronization of neuronal population. The synchronization between different visual areas decreased with higher isoflurane levels. Isoflurane reduced the population response amplitude and prolonged their latencies while higher visual areas showed increased vulnerability to isoflurane concentration. Our results uncover the changes in neural activity and synchronization at isoflurane concentrations leading to LOC and suggest reverse hierarchical shutdown of cortical areas.

Cerebral cortical processing time is elongated in human brain evolution

An increase in number of neurons is presumed to underlie the enhancement of cognitive abilities in brain evolution. The evolution of human cognition is then expected to have accompanied a prolongation of net neural-processing time due to the accumulation of processing time of individual neurons over an expanded number of neurons. Here, we confirmed this prediction and quantified the amount of prolongation in vivo, using noninvasive measurements of brain responses to sounds in unanesthetized human and nonhuman primates. Latencies of the N1 component of auditory-evoked potentials recorded from the scalp were approximately 40, 50, 60, and 100 ms for the common marmoset, rhesus monkey, chimpanzee, and human, respectively. Importantly, the prominent increase in human N1 latency could not be explained by the physical lengthening of the auditory pathway, and therefore reflected an extended dwell time for auditory cortical processing. A longer time window for auditory cortical processing is advantageous for analyzing time-varying acoustic stimuli, such as those important for speech perception. A novel hypothesis concerning human brain evolution then emerges: the increase in cortical neuronal number widened the timescale of sensory cortical processing, the benefits of which outweighed the disadvantage of slow cognition and reaction.

Hyperexcitability of Sensory Neurons in Fragile X Mouse Model.

Sensory hypersensitivity and somatosensory deficits represent the core symptoms of Fragile X syndrome (FXS). These alterations are believed to arise from changes in cortical sensory processing, while potential deficits in the function of peripheral sensory neurons residing in dorsal root ganglia remain unexplored. We found that peripheral sensory neurons exhibit pronounced hyperexcitability in Fmr1 KO mice, manifested by markedly increased action potential (AP) firing rate and decreased threshold. Unlike excitability changes found in many central neurons, no significant changes were observed in AP rising and falling time, peak potential, amplitude, or duration. Sensory neuron hyperexcitability was caused primarily by increased input resistance, without changes in cell capacitance or resting membrane potential. Analyses of the underlying mechanisms revealed reduced activity of HCN channels and reduced expression of HCN1 and HCN4 in Fmr1 KO compared to WT. A selective HCN channel blocker abolished differences in all measures of sensory neuron excitability between WT and Fmr1 KO neurons. These results reveal a hyperexcitable state of peripheral sensory neurons in Fmr1 KO mice caused by dysfunction of HCN channels. In addition to the intrinsic neuronal dysfunction, the accompanying paper examines deficits in sensory neuron association/communication with their enveloping satellite glial cells, suggesting contributions from both neuronal intrinsic and extrinsic mechanisms to sensory dysfunction in the FXS mouse model.

Perinatal Penicillin Exposure Affects Cortical Development and Sensory Processing

The prevalent use of antibiotics in pregnant women and neonates raises concerns about long-term risks for children’s health, but their effects on the central nervous system is not well understood. We studied the effects of perinatal penicillin exposure (PPE) on brain structure and function in mice with a therapeutically relevant regimen. We used a battery of behavioral tests to evaluate anxiety, working memory, and sensory processing, and immunohistochemistry to quantify changes in parvalbumin-expressing inhibitory interneurons (PV+ INs), perineuronal nets (PNNs), as well as microglia density and morphology. In addition, we performed mesoscale calcium imaging to study neural activity and functional connectivity across cortical regions, and two-photon imaging to monitor dendritic spine and microglial dynamics. We found that adolescent PPE mice have abnormal sensory processing, including impaired texture discrimination and altered prepulse inhibition. Such behavioral changes are associated with increased spontaneous neural activities in various cortical regions, and delayed maturation of PV+ INs in the somatosensory cortex. Furthermore, adolescent PPE mice have elevated elimination of dendritic spines on the apical dendrites of layer 5 pyramidal neurons, as well as increased ramifications and spatial coverage of cortical microglia. Finally, while synaptic defects are transient during adolescence, behavioral abnormalities persist into adulthood. Our study demonstrates that early-life exposure to antibiotics affects cortical development, leaving a lasting effect on brain functions.

Greater Neural Differentiation in the Ventral Visual Cortex Is Associated with Youthful Memory in Superaging.

Superagers are older adults who maintain youthful memory despite advanced age. Previous studies showed that superagers exhibit greater structural and intrinsic functional brain integrity, which contribute to their youthful memory. However, no studies, to date, have examined brain activity as superagers learn and remember novel information. Here, we analyzed functional magnetic resonance imaging data collected from 41 young and 40 older adults while they performed a paired associate visual recognition memory task. Superaging was defined as youthful performance on the long delay free recall of the California Verbal Learning Test. We assessed the fidelity of neural representations as participants encoded and later retrieved a series of word stimuli paired with a face or a scene image. Superagers, like young adults, exhibited more distinct neural representations in the fusiform gyrus and parahippocampal gyrus while viewing visual stimuli belonging to different categories (greater neural differentiation) and more similar category representations between encoding and retrieval (greater neural reinstatement), compared with typical older adults. Greater neural differentiation and reinstatement were associated with superior memory performance in all older adults. Given that the fidelity of cortical sensory processing depends on neural plasticity and is trainable, these mechanisms may be potential biomarkers for future interventions to promote successful aging.

Motor and sensory cortical processing of neural oscillatory activities revealed by human swallowing using intracranial electrodes

SummarySwallowing is attributed to the orchestration of motor output and sensory input. We hypothesized that swallowing can illustrate differences between motor and sensory neural processing. Eight epileptic participants fitted with intracranial electrodes over the orofacial cortex were asked to swallow a water bolus. Mouth opening and swallowing were treated as motor tasks, whereas water injection was treated as a sensory task. Phase-amplitude coupling between lower-frequency and high γ (HG) bands (75–150 Hz) was investigated. An α (10–16 Hz)-HG coupling appeared before motor-related HG power increases (burst), and a θ (5–9 Hz)-HG coupling appeared during sensory-related HG bursts. The peaks of motor-related coupling were 0.6–0.7 s earlier than that of HG power. The motor-related HG was modulated at the trough of the α oscillation, and the sensory-related HG amplitude was modulated at the peak of the θ oscillation. These contrasting results can help to elucidate the brain's sensory motor functions.