scholarly journals Respiration competes with theta for modulating parietal cortex neurons

2019 ◽  
Author(s):  
Felix Jung ◽  
Yevgenij Yanovsky ◽  
Jurij Brankačk ◽  
Adriano BL Tort ◽  
Andreas Draguhn

AbstractRecent work has shown that nasal respiration entrains local field potential (LFP) and neuronal activity in widespread regions of the brain. This includes non-olfactory regions where respiration-coupled oscillations have been described in different mammals, such as rodents, cats and humans. They may, thus, constitute a global signal aiding interregional communication. Nevertheless, the brain produces other widespread slow rhythms, such as theta oscillations, which also mediate long-range synchronization of neuronal activity. It is completely unknown how these different signals interact to control neuronal network activity. In this work, we characterized respiration- and theta-coupled activity in the posterior parietal cortex of mice. Our results show that respiration-coupled and theta oscillations have different laminar profiles, in which respiration preferentially entrains LFPs and units in more superficial layers, whereas theta modulation does not differ across the parietal cortex. Interestingly, we find that the percentage of theta-modulated units increases in the absence of respiration-coupled oscillations, suggesting that both rhythms compete for modulating parietal cortex neurons. We further show through intracellular recordings that synaptic inhibition is likely to play a role in generating respiration-coupled oscillations at the membrane potential level. Finally, we provide anatomical and electrophysiological evidence of reciprocal monosynaptic connections between the anterior cingulate and posterior parietal cortices, suggesting a possible source of respiration-coupled activity in the parietal cortex.

Author(s):  
Marion R Van Horn ◽  
Nicholas J Benfey ◽  
Colleen Ann Shikany ◽  
Liza J Severs ◽  
Tara Deemyad

Astrocytes are known to play many important roles in brain function. However, research underscoring the extent to which astrocytes modulate neuronal activity is still underway. Here we review the latest evidence regarding the contribution of astrocytes to neuronal oscillations across the brain, with a specific focus on how astrocytes respond to changes in brain state (e.g., sleep, arousal, stress). We then discuss the general mechanisms by which astrocytes signal to neurons to modulate neuronal activity, ultimately driving changes in behavior, followed by a discussion of how astrocytes contribute to respiratory rhythms in the medulla. Lastly, we contemplate the possibility that brainstem astrocytes could modulate brain-wide oscillations by communicating the status of oxygenation to higher cortical areas.


2020 ◽  
Author(s):  
Joshua M. Carlson ◽  
Lin Fang

AbstractIn a sample of highly anxious individuals, the relationship between gray matter volume brain morphology and attentional bias to threat was assessed. Participants performed a dot-probe task of attentional bias to threat and gray matter volume was acquired from whole brain structural T1-weighted MRI scans. The results replicate previous findings in unselected samples that elevated attentional bias to threat is linked to greater gray matter volume in the anterior cingulate cortex, middle frontal gyrus, and striatum. In addition, we provide novel evidence that elevated attentional bias to threat is associated with greater gray matter volume in the right posterior parietal cortex, cerebellum, and other distributed regions. Lastly, exploratory analyses provide initial evidence that distinct sub-regions of the right posterior parietal cortex may contribute to attentional bias in a sex-specific manner. Our results illuminate how differences in gray matter volume morphology relate to attentional bias to threat in anxious individuals. This knowledge could inform neurocognitive models of anxiety-related attentional bias to threat and targets of neuroplasticity in anxiety interventions such as attention bias modification.


2004 ◽  
Vol 92 (3) ◽  
pp. 1892-1903 ◽  
Author(s):  
Dana M. Small ◽  
Joel Voss ◽  
Y. Erica Mak ◽  
Katharine B. Simmons ◽  
Todd Parrish ◽  
...  

Flavor perception arises from the central integration of peripherally distinct sensory inputs (taste, smell, texture, temperature, sight, and even sound of foods). The results from psychophysical and neuroimaging studies in humans are converging with electrophysiological findings in animals and a picture of the neural correlates of flavor processing is beginning to emerge. Here we used event-related fMRI to evaluate brain response during perception of flavors (i.e., taste/odor liquid mixtures not differing in temperature or texture) compared with the sum of the independent presentation of their constituents (taste and/or odor). All stimuli were presented in liquid form so that olfactory stimulation was by the retronasal route. Mode of olfactory delivery is important because neural suppression has been observed in chemosensory regions during congruent taste–odor pairs when the odors are delivered by the orthonasal route and require subjects to sniff. There were 2 flavors. One contained a familiar/congruent taste–odor pair (vanilla/sweet) and the other an unfamiliar/incongruent taste–odor pair (vanilla/salty). Three unimodal stimuli, including 2 tastes (sweet and salty) and one odor (vanilla), as well as a tasteless/odorless liquid (baseline) were presented. Superadditive responses during the perception of the congruent flavor compared with the sum of its constituents were observed in the anterior cingulate cortex (ACC), dorsal insula, anterior ventral insula extending into the caudal orbitofrontal cortex (OFC), frontal operculum, ventral lateral prefrontal cortex, and posterior parietal cortex. These regions were not present in a similar analysis of the incongruent flavor compared with the sum of its constituents. All of these regions except the ventrolateral prefrontal cortex were also isolated in a direct contrast of congruent − incongruent. Additionally, the anterior cingulate, posterior parietal cortex, frontal operculum, and ventral insula/caudal OFC were also more active in vanilla + salty minus incongruent, suggesting that delivery of an unfamiliar taste–odor combination may lead to suppressed neural responses. Taken together with previous findings in the literature, these results suggest that the insula, OFC, and ACC are key components of the network underlying flavor perception and that taste–smell integration within these and other regions is dependent on 1) mode of olfactory delivery and 2) previous experience with taste/smell combinations.


2021 ◽  
Author(s):  
Megan Allen ◽  
Ben S. Huang ◽  
Michael J. Notaras ◽  
Aiman Lodhi ◽  
Estibaliz Barrio Alonso ◽  
...  

AbstractThe cellular mechanisms of Autism Spectrum Disorder (ASD) are poorly understood. Cumulative evidence suggests that abnormal synapse function underlies many features of this disease. Astrocytes play in several key neuronal processes, including the formation of synapses and the modulation of synaptic plasticity. Astrocyte abnormalities have also been identified in the postmortem brain tissue of ASD patients. However, it remains unclear whether astrocyte pathology plays a mechanistic role in ASD, as opposed to a compensatory response. To address this, we strategically combined stem cell culturing with transplantation techniques to determine disease specific properties inherent to patient derived astrocytes. We demonstrate that ASD astrocytes induce repetitive behavior as well as impair memory and long-term potentiation when transplanted into the healthy mouse brain. These in vivo phenotypes were accompanied by reduced neuronal network activity and spine density caused by ASD astrocytes in hippocampal neurons in vitro. Transplanted ASD astrocytes also exhibit exaggerated Ca2+ fluctuations in chimeric brains. Genetic modulation of evoked Ca2+ responses in ASD astrocytes modulates behavior and neuronal activity deficits. Thus, we determine that ASD patient astrocytes are sufficient to induce repetitive behavior as well as cognitive deficit, suggesting a previously unrecognized primary role for astrocytes in ASD.


2021 ◽  
Vol 15 ◽  
Author(s):  
Tamás Földi ◽  
Magor L. Lőrincz ◽  
Antal Berényi

Self-organized neuronal oscillations rely on precisely orchestrated ensemble activity in reverberating neuronal networks. Chronic, non-malignant disorders of the brain are often coupled to pathological neuronal activity patterns. In addition to the characteristic behavioral symptoms, these disturbances are giving rise to both transient and persistent changes of various brain rhythms. Increasing evidence support the causal role of these “oscillopathies” in the phenotypic emergence of the disease symptoms, identifying neuronal network oscillations as potential therapeutic targets. While the kinetics of pharmacological therapy is not suitable to compensate the disease related fine-scale disturbances of network oscillations, external biophysical modalities (e.g., electrical stimulation) can alter spike timing in a temporally precise manner. These perturbations can warp rhythmic oscillatory patterns via resonance or entrainment. Properly timed phasic stimuli can even switch between the stable states of networks acting as multistable oscillators, substantially changing the emergent oscillatory patterns. Novel transcranial electric stimulation (TES) approaches offer more reliable neuronal control by allowing higher intensities with tolerable side-effect profiles. This precise temporal steerability combined with the non- or minimally invasive nature of these novel TES interventions make them promising therapeutic candidates for functional disorders of the brain. Here we review the key experimental findings and theoretical background concerning various pathological aspects of neuronal network activity leading to the generation of epileptic seizures. The conceptual and practical state of the art of temporally targeted brain stimulation is discussed focusing on the prevention and early termination of epileptic seizures.


2007 ◽  
Vol 97 (5) ◽  
pp. 3684-3695 ◽  
Author(s):  
Itay Asher ◽  
Eran Stark ◽  
Moshe Abeles ◽  
Yifat Prut

Recent studies have shown that the local field potential (LFP) can provide a simple method for obtaining an accurate measure of reaching and saccade behaviors. However, it is not clear whether this signal is equally informative with respect to more complex movements. Here we recorded LFPs and single units (SUs) from different areas in the posterior parietal cortex of macaques during a prehension task and compared LFP selectivity with SU selectivity. We found that parietal LFPs were often selective to target direction or object and that percentages of selective LFPs were similar to percentages of selective SUs. Nevertheless, SUs were more informative than LFPs in several respects. Preferred directions and objects of LFPs usually deviated from a uniform distribution, unlike preferences of SUs. Furthermore, preferences of LFPs did not reflect preferences of SUs even when the two signals were recorded simultaneously via the same electrode. Additionally, selectivity of movement-evoked LFPs appeared only after movement onset, whereas SUs frequently showed premovement selectivity. Spectral analysis revealed a lower signal-to-noise ratio of the LFP signal. Different frequency bands derived from a single LFP site showed inconsistent preferences. Significant relations with target parameters were found for all tested bands of LFP, but effects in the fast (gamma) band exhibited properties that were consistent with contamination of the LFP by residual spiking activity. Taken together, our results suggest that the LFP provides a simple method for extracting ample movement-related information. However, some of its properties make it less adequate for predicting rapidly changing movements.


2019 ◽  
Vol 116 (52) ◽  
pp. 26274-26279 ◽  
Author(s):  
Richard A. Andersen ◽  
Tyson Aflalo ◽  
Spencer Kellis

A dramatic example of translational monkey research is the development of neural prosthetics for assisting paralyzed patients. A neuroprosthesis consists of implanted electrodes that can record the intended movement of a paralyzed part of the body, a computer algorithm that decodes the intended movement, and an assistive device such as a robot limb or computer that is controlled by these intended movement signals. This type of neuroprosthetic system is also referred to as a brain–machine interface (BMI) since it interfaces the brain with an external machine. In this review, we will concentrate on BMIs in which microelectrode recording arrays are implanted in the posterior parietal cortex (PPC), a high-level cortical area in both humans and monkeys that represents intentions to move. This review will first discuss the basic science research performed in healthy monkeys that established PPC as a good source of intention signals. Next, it will describe the first PPC implants in human patients with tetraplegia from spinal cord injury. From these patients the goals of movements could be quickly decoded, and the rich number of action variables found in PPC indicates that it is an appropriate BMI site for a very wide range of neuroprosthetic applications. We will discuss research on learning to use BMIs in monkeys and humans and the advances that are still needed, requiring both monkey and human research to enable BMIs to be readily available in the clinic.


2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
I Leonova ◽  
N Burova ◽  
S Boldueva ◽  
M Demidova ◽  
A Khomulo ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: None. In patients with microvascular angina (MVA) besides of chest pain, a high neuronal activity of certain parts of the head (right anterior insula cortex) was revealed, which is not observed in the control in patients with coronary heart disease with coronary atherosclerosis. There is an opinion that the abnormal sensation of pain is caused not by myocardial ischemia, but by a violation of neuronal regulation. Functional MRI (fMRI) is currently a widely used method of functional mapping of the brain. The principle of the method is to register a BOLD signal (blood oxygen level-depended) from voxels (volumetric points) when examining the brain in response to the fulfillment of a task (paradigm). In response to the activation of a particular region of the brain, hemodynamic parameters change in it, which leads to a decrease in the level of deoxyhemoglobin and an increase in the level of oxyhemoglobin. With neuroimaging, this phenomenon is characterized by an increase in signal intensity in a series of T2 * images, the quantitative assessment of which allows indirectly determining the degree of neuronal activation. The study included 11 patients with MVA (3 men, 8 women). The average age of the patients was 61.45 ± 7.80 years. MVA was proved classic criteria and microvascular disorders (perfusion abnormalities) by cardiac PET. Neuroimaging examination included positron emission tomography scanning using 18-fluoro deoxyglucose (18F-FDG PET) and functional magnetic resonance imaging (fMRI) scanning using the GO / NOGO two-stimulus experimental paradigm. Throughout the study, fMRI and PET data were obtained for 11 patients with MVA and 20 healthy volunteers (control group). Results In patients with MVA, a decrease in neuronal activity was detected during the execution of actions ("GO" tests) compared with the norm in some brain structures: bilateral anterior and middle cingulate gyrus, additional motor region, postcentral gyrus, left in the islet cortex, on the right in the supramarginal gyrus. When ignoring the second stimulus ("P-P ignore."). A decrease compared with the norm was found bilaterally in the anterior and posterior cingulate cortex, the wedge, on the right in the cortex of the rolandic operculum and supramarginal gyrus. The detected clusters of decreased neuronal activity when performing actions and ignoring the second stimulus intersect bilaterally in the middle and anterior cingulate cortex, in the left paracentral lobe, and the right supramarginal gyrus. When suppressing actions ("NOGO samples"), no significant differences were found. According to PET, no significant changes in the level of glucose metabolism in patients with MVA compared with the control group were found. Conclusion In patients with MVA, a decrease in neuronal activity was found when performing actions compared to the norm in some brain structures.


2005 ◽  
Vol 94 (6) ◽  
pp. 3951-3960 ◽  
Author(s):  
Nataliya A. Tsvyetlynska ◽  
Russell H. Hill ◽  
Sten Grillner

Activation of the vertebrate locomotor network is mediated by glutamatergic synaptic drive, normally initiated by the brain stem. Previous investigations have studied the role of glutamate receptors, especially NMDA receptors, in generating and regulating locomotor pattern generation. Few studies, however, have focused on the role of AMPA receptors in shaping network activity, especially with regard to their rapid desensitization. It is important to determine whether AMPA receptor desensitization plays a role in regulating neuronal network activity. We examined this question on both the network and synaptic levels in the lamprey ( Lampetra fluviatilis) spinal cord using a selective and potent inhibitor of AMPA receptor desensitization, cyclothiazide (CTZ). The solvent dimethyl sulfoxide (DMSO) is commonly used to dissolve this drug, as well as many others. Unexpectedly, the vehicle alone already at 0.02%, but not at 0.01%, caused significant increases in excitatory postsynaptic potential (EPSP) amplitudes and NMDA-induced locomotor frequency. The results indicate that DMSO may have a profound influence when used ≥0.02%, a concentration 10–50 times less than that most commonly used. Subsequently we applied CTZ concentrations ≤10 μM (DMSO ≤0.01%). CTZ (1.25–5 μM) caused an appreciable and significant increase in EPSPs mediated by non-NMDA receptors and in both AMPA- and NMDA-induced locomotor frequency, but no effects on EPSPs mediated by NMDA receptors. From the effects of CTZ it is apparent that AMPA receptor desensitization plays an important role in determining locomotor frequency and that this is likely a result of its limiting function on AMPA receptor–mediated EPSPs.


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