scholarly journals The Orofacial Somatosensory System Is Modulated During Speech Planning and Production

2020 ◽  
Vol 63 (8) ◽  
pp. 2637-2648
Author(s):  
Brianna J. McGuffin ◽  
Julie M. Liss ◽  
Ayoub Daliri

Purpose In our previous studies, we showed that the brain modulates the auditory system, and the modulation starts during speech planning. However, it remained unknown whether the brain uses similar mechanisms to modulate the orofacial somatosensory system. Here, we developed a novel behavioral paradigm to (a) examine whether the somatosensory system is modulated during speech planning and (b) determine the somatosensory modulation's time course during planning and production. Method Participants ( N = 20) completed two experiments in which we applied electrical current stimulation to the lower lip to induce somatosensory sensation. In the first experiment, we used a staircase method (one-up, four-down) to determine each participant's perceptual threshold at rest (i.e., the stimulus that the participant detected on 85% of trials). In the second experiment, we estimated each participant's detection ratio of electrical stimuli (with a magnitude equivalent of their perceptual threshold) delivered at various time points before speaking and during a control condition (silent reading). Results We found that the overall detection ratio in the silent reading condition remained unchanged relative to the detection ratio at rest. Approximately 536 ms before speech onset, the detection ratio in the speaking condition was similar to that in the silent reading condition; however, the detection ratio in the speaking condition gradually started to decrease and reached its lowest level at 58 ms before speech onset. Conclusions Overall, we provided compelling behavioral evidence that, as the speech motor system prepares speech movements, it also modulates the orofacial somatosensory system in a temporally specific manner.

PLoS Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
pp. e3001038
Author(s):  
Sebastian Sauppe ◽  
Kamal K. Choudhary ◽  
Nathalie Giroud ◽  
Damián E. Blasi ◽  
Elisabeth Norcliffe ◽  
...  

Planning to speak is a challenge for the brain, and the challenge varies between and within languages. Yet, little is known about how neural processes react to these variable challenges beyond the planning of individual words. Here, we examine how fundamental differences in syntax shape the time course of sentence planning. Most languages treat alike (i.e., align with each other) the 2 uses of a word like “gardener” in “the gardener crouched” and in “the gardener planted trees.” A minority keeps these formally distinct by adding special marking in 1 case, and some languages display both aligned and nonaligned expressions. Exploiting such a contrast in Hindi, we used electroencephalography (EEG) and eye tracking to suggest that this difference is associated with distinct patterns of neural processing and gaze behavior during early planning stages, preceding phonological word form preparation. Planning sentences with aligned expressions induces larger synchronization in the theta frequency band, suggesting higher working memory engagement, and more visual attention to agents than planning nonaligned sentences, suggesting delayed commitment to the relational details of the event. Furthermore, plain, unmarked expressions are associated with larger desynchronization in the alpha band than expressions with special markers, suggesting more engagement in information processing to keep overlapping structures distinct during planning. Our findings contrast with the observation that the form of aligned expressions is simpler, and they suggest that the global preference for alignment is driven not by its neurophysiological effect on sentence planning but by other sources, possibly by aspects of production flexibility and fluency or by sentence comprehension. This challenges current theories on how production and comprehension may affect the evolution and distribution of syntactic variants in the world’s languages.


Author(s):  
Jochen Seitz ◽  
Katharina Bühren ◽  
Georg G. von Polier ◽  
Nicole Heussen ◽  
Beate Herpertz-Dahlmann ◽  
...  

Objective: Acute anorexia nervosa (AN) leads to reduced gray (GM) and white matter (WM) volume in the brain, which however improves again upon restoration of weight. Yet little is known about the extent and clinical correlates of these brain changes, nor do we know much about the time-course and completeness of their recovery. Methods: We conducted a meta-analysis and a qualitative review of all magnetic resonance imaging studies involving volume analyses of the brain in both acute and recovered AN. Results: We identified structural neuroimaging studies with a total of 214 acute AN patients and 177 weight-recovered AN patients. In acute AN, GM was reduced by 5.6% and WM by 3.8% compared to healthy controls (HC). Short-term weight recovery 2–5 months after admission resulted in restitution of about half of the GM aberrations and almost full WM recovery. After 2–8 years of remission GM and WM were nearly normalized, and differences to HC (GM: –1.0%, WM: –0.7%) were no longer significant, although small residual changes could not be ruled out. In the qualitative review some studies found GM volume loss to be associated with cognitive deficits and clinical prognosis. Conclusions: GM and WM were strongly reduced in acute AN. The completeness of brain volume rehabilitation remained equivocal.


1993 ◽  
Vol 4 (3) ◽  
pp. 227-237 ◽  
Author(s):  
Donald G. Stein ◽  
Marylou M. Glasier ◽  
Stuart W. Hoffman

It is only within the last ten years that research on treatment for central nervous system (CNS) recovery after injury has become more focused on the complexities involved in promoting recovery from brain injury when the CNS is viewed as an integrated and dynamic system. There have been major advances in research in recovery over the last decade, including new information on the mechanics and genetics of metabolism and chemical activity, the definition of excitotoxic effects and the discovery that the brain itself secretes complex proteins, peptides and hormones which are capable of directly stimulating the repair of damaged neurons or blocking some of the degenerative processes caused by the injury cascade. Many of these agents, plus other nontoxic naturally occurring substances, are being tested as treatment for brain injury. Further work is needed to determine appropriate combinations of treatments and optimum times of administration with respect to the time course of the CNS disorder. In order to understand the mechanisms that mediate traumatic brain injury and repair, there must be a merging of findings from neurochemical studies with data from intensive behavioral testing.


2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Laurence Barrier ◽  
Bernard Fauconneau ◽  
Anastasia Noël ◽  
Sabrina Ingrand

There is evidence linking sphingolipid abnormalities, APP processing, and neuronal death in Alzheimer's disease (AD). We previously reported a strong elevation of ceramide levels in the brain of the APPSL/PS1Ki mouse model of AD, preceding the neuronal death. To extend these findings, we analyzed ceramide and related-sphingolipid contents in brain from two other mouse models (i.e., APPSLand APPSL/PS1M146L) in which the time-course of pathology is closer to that seen in most currently available models. Conversely to our previous work, ceramides did not accumulate in disease-associated brain regions (cortex and hippocampus) from both models. However, the APPSL/PS1Ki model is unique for its drastic neuronal loss coinciding with strong accumulation of neurotoxic Aβisoforms, not observed in other animal models of AD. Since there are neither neuronal loss nor toxic Aβspecies accumulation in APPSLmice, we hypothesized that it might explain the lack of ceramide accumulation, at least in this model.


2016 ◽  
Vol 91 (4) ◽  
Author(s):  
Luiza A. Castro-Jorge ◽  
Carla D. Pretto ◽  
Asa B. Smith ◽  
Oded Foreman ◽  
Kelly E. Carnahan ◽  
...  

ABSTRACT Interleukin-1β (IL-1β), an inflammatory cytokine and IL-1 receptor ligand, has diverse activities in the brain. We examined whether IL-1 signaling contributes to the encephalitis observed in mouse adenovirus type 1 (MAV-1) infection, using mice lacking the IL-1 receptor (Il1r1 −/− mice). Il1r1 −/− mice demonstrated reduced survival, greater disruption of the blood-brain barrier (BBB), higher brain viral loads, and higher brain inflammatory cytokine and chemokine levels than control C57BL/6J mice. We also examined infections of mice defective in IL-1β production (Pycard −/− mice) and mice defective in trafficking of Toll-like receptors to the endosome (Unc93b1 −/− mice). Pycard −/− and Unc93b1 −/− mice showed lower survival (similar to Il1r1 −/− mice) than control mice but, unlike Il1r1 −/− mice, did not have increased brain viral loads or BBB disruption. Based on the brain cytokine levels, MAV-1-infected Unc93b1 −/− mice had a very different inflammatory profile from infected Il1r1 −/− and Pycard −/− mice. Histological examination demonstrated pathological findings consistent with encephalitis in control and knockout mice; however, intranuclear viral inclusions were seen only in Il1r1 −/− mice. A time course of infection of control and Il1r1 −/− mice evaluating the kinetics of viral replication and cytokine production revealed differences between the mouse strains primarily at 7 to 8 days after infection, when mice began succumbing to MAV-1 infection. In the absence of IL-1 signaling, we noted an increase in the transcription of type I interferon (IFN)-stimulated genes. Together, these results indicate that IL-1 signaling is important during MAV-1 infection and suggest that, in its absence, increased IFN-β signaling may result in increased neuroinflammation. IMPORTANCE The investigation of encephalitis pathogenesis produced by different viruses is needed to characterize virus and host-specific factors that contribute to disease. MAV-1 produces viral encephalitis in its natural host, providing a good model for studying factors involved in encephalitis development. We investigated the role of IL-1 signaling during MAV-1-induced encephalitis. Unexpectedly, the lack of IL-1 signaling increased the mortality and inflammation in mice infected with MAV-1. Also, there was an increase in the transcription of type I IFN-stimulated genes that correlated with the observed increased mortality and inflammation. The findings highlight the complex nature of encephalitis and suggests that IL-1 has a protective effect for the development of MAV-1-induced encephalitis.


2006 ◽  
Vol 290 (6) ◽  
pp. R1565-R1569 ◽  
Author(s):  
Kimberly P. Kinzig ◽  
Karen A. Scott ◽  
Jayson Hyun ◽  
Sheng Bi ◽  
Timothy H. Moran

The gut peptide ghrelin has been shown to stimulate food intake after both peripheral and central administration, and the hypothalamic arcuate nucleus has been proposed to be the major site for mediating this feeding stimulatory action. Ghrelin receptors are widely distributed in the brain, and hindbrain ghrelin administration has been shown to potently stimulate feeding, suggesting that there may be other sites for ghrelin action. In the present study, we have further assessed potential sites for ghrelin action by comparing the ability of lateral and fourth ventricular ghrelin administration to stimulate food intake and alter patterns of hypothalamic gene expression. Ghrelin (0.32, 1, or 3.2 nmol) in the lateral or fourth ventricle significantly increased food intake in the first 4 h after injection, with no ventricle-dependent differences in degree or time course of hyperphagia. One nanomole of ghrelin into either the lateral or fourth ventricle resulted in similar increases in arcuate nucleus neuropeptide Y mRNA expression. Expression levels of agouti-related peptide or proopiomelanocortin mRNA were not affected by ghrelin administration. These data demonstrate that ghrelin can affect food intake and hypothalamic gene expression through interactions at multiple brain sites.


2021 ◽  
Vol 33 (1) ◽  
pp. 146-157
Author(s):  
Chong Zhao ◽  
Geoffrey F. Woodman

It is not definitely known how direct-current stimulation causes its long-lasting effects. Here, we tested the hypothesis that the long time course of transcranial direct-current stimulation (tDCS) is because of the electrical field increasing the plasticity of the brain tissue. If this is the case, then we should see tDCS effects when humans need to encode information into long-term memory, but not at other times. We tested this hypothesis by delivering tDCS to the ventral visual stream of human participants during different tasks (i.e., recognition memory vs. visual search) and at different times during a memory task. We found that tDCS improved memory encoding, and the neural correlates thereof, but not retrieval. We also found that tDCS did not change the efficiency of information processing during visual search for a certain target object, a task that does not require the formation of new connections in the brain but instead relies on attention and object recognition mechanisms. Thus, our findings support the hypothesis that direct-current stimulation modulates brain activity by changing the underlying plasticity of the tissue.


1998 ◽  
Vol 119 (1) ◽  
pp. 27-33 ◽  
Author(s):  
Norbert Dieringer ◽  
Hans Straka

Removal of the labyrinthine organs on one side results in a number of severe postural and dynamic reflex deficits. Over time some of these behavioral deficits normalize again. At a chronic stage the brain of frogs exhibits a number of changes in vestibular and propriospinal circuits on the operated side that were studied in vitro. The onset of changes in the vestibular nuclear complex was delayed, became evident only after head posture had recovered by more than 50%, and was independent of the presence or absence of a degeneration of vestibular nerve afferent fibers. The time course of changes measured in the isolated spinal cord paralleled the time course of normalization of head and body posture. Results obtained after selective lesions of individual labyrinthine nerve branches show that unilateral inactivation of utricular afferent inputs is a necessary and sufficient condition to provoke postural deficits and propriospinal changes similar to those after the removal of all labyrinthine organs. The presence of multiple synaptic changes at distributed anatomic sites over different periods of time suggests that different parts of the central nervous system are involved in the normalization of different manifestations of the vestibular lesion syndrome. (Otolaryngol Head Neck Surg 1998;119:27–33.)


2019 ◽  
Author(s):  
Alan Taitz ◽  
Diego E Shalom ◽  
Marcos A Trevisan

Silent reading is a cognitive operation that produces verbal content with no vocal output. One relevant question is the extent to which this verbal content is processed as overt speech in the brain. To address this, we investigated the signatures of articulatory processing during reading. We acquired sound, eye trajectories and vocal gestures during the reading of consonant-consonant-vowel (CCV) pseudowords. We found that the duration of the first fixations on the CCVs during silent reading are correlated to the duration of the transitions between consonants when the CCVs are actually uttered. An articulatory model of the vocal system was implemented to show that consonantal transitions measure the articulatory effort required to produce the CCVs. These results demonstrate that silent reading is modulated by slight articulatory features such as the laryngeal abduction needed to devoice a single consonant or the reshaping of the vocal tract between successive consonants.


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