scholarly journals Collective excitability in a mesoscopic neuronal model of epileptic activity

2017 ◽  
Author(s):  
Maciej Jedynak ◽  
Antonio J. Pons ◽  
Jordi Garcia-Ojalvo
Keyword(s):  
Neuronal Model ◽  
Epileptic Activity ◽  
Brain Areas ◽  
Sustained Activity ◽  
Collective Activity ◽  
Neural Mass ◽  
Joint Dynamics ◽  
Coupling Strengths ◽  
Neuronal Oscillators ◽  
The Brain

The brain can be understood as a collection of interacting neuronal oscillators, but the extent to which its sustained activity is due to coupling among brain areas is still unclear. Here we study the joint dynamics of two cortical columns described by Jansen-Rit neural mass models, and show that coupling between the columns gives rise to stochastic initiations of sustained collective activity, which can be interpreted as epileptic events. For large enough coupling strengths, termination of these events results mainly from the emergence of synchronization between the columns, and thus is controlled by coupling instead of noise. Stochastic triggering and noise-independent durations are characteristic of excitable dynamics, and thus we interpret our results in terms of collective excitability.

scholarly journals Comparative Analysis of Methods for Estimation of Undirected Coupling from Time Series of Intracranial Eegs of Cortex of Rats-Genetic Models of Absence Epilepsy

2017 ◽  
Vol 12 (2) ◽  
pp. 317-326
Author(s):  
А.А. Грищенко ◽  
A.A. Grishchenko
Keyword(s):  
Time Window ◽  
Surrogate Data ◽  
Epileptic Activity ◽  
Absence Epilepsy ◽  
Information Function ◽  
Brain Areas ◽  
To Receive ◽  
Intracranial Recordings ◽  
The Brain ◽  
Mutual Information Function

Studying coupling between brain areas from its electromagnetic activity is one of the key approaches in epilepsy research now, since epileptic activity has been considered to be a result of pathological synchronization in the brain. Often, research is conducted on animal models, because this allows to perform intracranial measurement, and to get rid of interference caused by the skull and to receive signals from deeper regions of the brain such as thalamus or hippocampus. In this study, the intracranial recordings from the frontal and parietal areas of cortex are investigated with a nonlinear correlation coefficient and a mutual information function in a sliding time window. The coupling estimates obtained were subjected for statistical analysis for significance using surrogate data. The dynamics of connectivity between the frontal cortex and the parietal cortex was shown to vary from seizure to seizure and from animal to animal. Therefore, estimates of the significant change in connectivity associated with initiation of the absense seizure, found previously based on averaging over a large number of animals and a large number of seizures for an each animal, can be a result of contribution of a relatively small number of seizures (less than a half of considered), for which the changes are significant.

Controllability Analysis of the Neural Mass Model with Dynamic Parameters

2017 ◽  
Vol 29 (2) ◽  
pp. 485-501 ◽  
Author(s):  
Xian Liu ◽  
Jing Gao ◽  
Guan Wang ◽  
Zhi-Wang Chen
Keyword(s):  
Neuronal Model ◽  
Condition Numbers ◽  
Neural Mass Model ◽  
Potential Significance ◽  
Mass Model ◽  
Neural Mass ◽  
Nervous Disorder ◽  
Dynamical Parameters ◽  
Quantitative Indicators ◽  
The Brain

The development of control technology for the brain is of potential significance to the prevention and treatment of neuropsychiatric disorders and the improvement of humans’ mental health. A controllability analysis of the brain is necessary to ensure the feasibility of the brain control. In this letter, we investigate the influences of dynamical parameters on the controllability in the neural mass model by using controllability indices as quantitative indicators. The indices are obtained by computing Lie brackets and condition numbers of the system model. We show how controllability changes with important parameters of our dynamical (neuronal) model. Our results suggest that the underlying dynamical parameters have certain ranges with better controllability. We hope it can play potential roles in therapy for brain nervous disorder disease.

scholarly journals Synchronization in the connectome: Metastable oscillatory modes emerge from interactions in the brain spacetime network

2022 ◽  
Author(s):  
Joana Cabral ◽  
Francesca Castaldo ◽  
Jakub Vohryzek ◽  
Vladimir Litvak ◽  
Christian Bick ◽  
...  
Keyword(s):  
Coupled Oscillators ◽  
Brain Activity ◽  
Power Spectra ◽  
Brain Areas ◽  
Neural Mass ◽  
Spatially Distributed ◽  
Weakly Stable ◽  
Human Brains ◽  
The Brain

A rich repertoire of oscillatory signals is detected from human brains with electro- and magnetoencephalography (EEG/MEG). However, the principles underwriting coherent oscillations and their link with neural activity remain unclear. Here, we hypothesise that the emergence of transient brain rhythms is a signature of weakly stable synchronization between spatially distributed brain areas, occurring at network-specific collective frequencies due to non-negligible conduction times. We test this hypothesis using a phenomenological network model to simulate interactions between neural mass potentials (resonating at 40Hz) in the structural connectome. Crucially, we identify a critical regime where metastable oscillatory modes emerge spontaneously in the delta (0.5-4Hz), theta (4-8Hz), alpha (8-13Hz) and beta (13-30Hz) frequency bands from weak synchronization of subsystems, closely approximating the MEG power spectra from 89 healthy individuals. Grounded in the physics of delay-coupled oscillators, these numerical analyses demonstrate the role of the spatiotemporal connectome in structuring brain activity in the frequency domain.

Aetiologies and anatomy of confabulation

2017 ◽  
Author(s):  
Armin Schnider
Keyword(s):  
Brain Damage ◽  
Limbic Encephalitis ◽  
Artery Aneurysm ◽  
Anterior Communicating Artery ◽  
Brain Areas ◽  
Anatomical Basis ◽  
Korsakoff Syndrome ◽  
Hypoxic Brain ◽  
Degenerative Dementia ◽  
The Brain

What diseases cause confabulations and which are the brain areas whose damage is responsible? This chapter reviews the causes, both historic and present, of confabulations and deduces the anatomo-clinical relationships for the four forms of confabulation in the following disorders: alcoholic Korsakoff syndrome, traumatic brain injury, rupture of an anterior communicating artery aneurysm, posterior circulation stroke, herpes and limbic encephalitis, hypoxic brain damage, degenerative dementia, tumours, schizophrenia, and syphilis. Overall, clinically relevant confabulation is rare. Some aetiologies have become more important over time, others have virtually disappeared. While confabulations seem to be more frequent after anterior brain damage, only one form has a distinct anatomical basis.

scholarly journals Limbic Expression of mRNA Coding for Chemoreceptors in Human Brain—Lessons from Brain Atlases

2021 ◽  
Vol 22 (13) ◽  
pp. 6858
Author(s):  
Fanny Gaudel ◽  
Gaëlle Guiraudie-Capraz ◽  
François Féron
Keyword(s):  
G Proteins ◽  
The Body ◽  
Trace Amines ◽  
Chemical Senses ◽  
Brain Areas ◽  
Genes Encoding ◽  
The Central Nervous System ◽  
Human Brains ◽  
The Brain ◽  
Brain Atlases

Animals strongly rely on chemical senses to uncover the outside world and adjust their behaviour. Chemical signals are perceived by facial sensitive chemosensors that can be clustered into three families, namely the gustatory (TASR), olfactory (OR, TAAR) and pheromonal (VNR, FPR) receptors. Over recent decades, chemoreceptors were identified in non-facial parts of the body, including the brain. In order to map chemoreceptors within the encephalon, we performed a study based on four brain atlases. The transcript expression of selected members of the three chemoreceptor families and their canonical partners was analysed in major areas of healthy and demented human brains. Genes encoding all studied chemoreceptors are transcribed in the central nervous system, particularly in the limbic system. RNA of their canonical transduction partners (G proteins, ion channels) are also observed in all studied brain areas, reinforcing the suggestion that cerebral chemoreceptors are functional. In addition, we noticed that: (i) bitterness-associated receptors display an enriched expression, (ii) the brain is equipped to sense trace amines and pheromonal cues and (iii) chemoreceptor RNA expression varies with age, but not dementia or brain trauma. Extensive studies are now required to further understand how the brain makes sense of endogenous chemicals.

scholarly journals Initiators of Classical and Lectin Complement Pathways Are Differently Engaged after Traumatic Brain Injury—Time-Dependent Changes in the Cortex, Striatum, Thalamus and Hippocampus in a Mouse Model

2020 ◽  
Vol 22 (1) ◽  
pp. 45
Author(s):  
Agata Ciechanowska ◽  
Katarzyna Ciapała ◽  
Katarzyna Pawlik ◽  
Marco Oggioni ◽  
Domenico Mercurio ◽  
...  
Keyword(s):  
Brain Injury ◽  
Microglial Cell ◽  
Lectin Pathway ◽  
Brain Areas ◽  
Mannose Binding ◽  
Primary Microglial Cell ◽  
Cellular Markers ◽  
The Brain ◽  
Binding Lectin ◽  
Complement Pathways

The complement system is involved in promoting secondary injury after traumatic brain injury (TBI), but the roles of the classical and lectin pathways leading to complement activation need to be clarified. To this end, we aimed to determine the ability of the brain to activate the synthesis of classical and lectin pathway initiators in response to TBI and to examine their expression in primary microglial cell cultures. We have modeled TBI in mice by controlled cortical impact (CCI), a clinically relevant experimental model. Using Real-time quantitative polymerase chain reaction (RT-qPCR) we analyzed the expression of initiators of classical the complement component 1q, 1r and 1s (C1q, C1r, and C1s) and lectin (mannose binding lectin A, mannose binding lectin C, collectin 11, ficolin A, and ficolin B) complement pathways and other cellular markers in four brain areas (cortex, striatum, thalamus and hippocampus) of mice exposed to CCI from 24 h and up to 5 weeks. In all murine ipsilateral brain structures assessed, we detected long-lasting, time- and area-dependent significant increases in the mRNA levels of all classical (C1q, C1s, C1r) and some lectin (collectin 11, ficolin A, ficolin B) initiator molecules after TBI. In parallel, we observed significantly enhanced expression of cellular markers for neutrophils (Cd177), T cells (Cd8), astrocytes (glial fibrillary acidic protein—GFAP), microglia/macrophages (allograft inflammatory factor 1—IBA-1), and microglia (transmembrane protein 119—TMEM119); moreover, we detected astrocytes (GFAP) and microglia/macrophages (IBA-1) protein level strong upregulation in all analyzed brain areas. Further, the results obtained in primary microglial cell cultures suggested that these cells may be largely responsible for the biosynthesis of classical pathway initiators. However, microglia are unlikely to be responsible for the production of the lectin pathway initiators. Immunofluorescence analysis confirmed that at the site of brain injury, the C1q is localized in microglia/macrophages and neurons but not in astroglial cells. In sum, the brain strongly reacts to TBI by activating the local synthesis of classical and lectin complement pathway activators. Thus, the brain responds to TBI with a strong, widespread and persistent upregulation of complement components, the targeting of which may provide protection in TBI.

Comparing the brain areas supporting nondeclarative categorization and recognition memory

2002 ◽  
Vol 14 (2) ◽  
pp. 245-257 ◽  
Author(s):  
Paul J Reber ◽  
Eric C Wong ◽  
Richard B Buxton
Keyword(s):  
Recognition Memory ◽  
Brain Areas ◽  
The Brain

Cannabidiol Has a Unique Effect on Global Brain Activity: A Pharmacological, Functional MRI Study in Awake Mice 

2021 ◽  
Author(s):  
Aymen Sadaka ◽  
Ana Ozuna ◽  
Richard Ortiz ◽  
Praveen Kulkarni ◽  
Clare Johnson ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Brain Activity ◽  
Stress Disorders ◽  
Functional Coupling ◽  
Specific Information ◽  
Imaging Data ◽  
Post Traumatic Stress ◽  
Brain Areas ◽  
Dose Dependent ◽  
The Brain

Abstract Background: The phytocannabinoid cannabidiol (CBD) is a potential treatment for post-traumatic stress disorders. How does CBD interact with the brain to alter behavior? We hypothesized that CBD would produce a dose-dependent reduction in brain activity and functional coupling in neural circuitry associated with fear and defense. Methods: During the scanning session awake mice were given vehicle or CBD (3, 10, or 30 mg/kg I.P.) and imaged for 10 min post treatment. Mice were also treated with the 10 mg/kg dose of CBD and imaged one hr later for resting state BOLD functional connectivity (rsFC). Imaging data were registered to a 3D MRI mouse atlas providing site-specific information on 138 different brain areas. Blood samples were collected for CBD measurements.Results: CBD produced a dose-dependent polarization of activation along the rostral-caudal axis of the brain. The olfactory bulb and prefrontal cortex showed an increase in positive BOLD whereas the brainstem and cerebellum showed a decrease in BOLD signal. This negative BOLD affected many areas connected to the ascending reticular activating system (ARAS). The ARAS was decoupled to much of the brain but was hyperconnected to the olfactory system and prefrontal cortex. The pattern of ARAS connectivity closely overlapped with brain areas showing high levels N-acyl-phosphatidylethanolamines-specific phospholipase D (NAPE-PLD) messenger RNA.Conclusion: The CBD-induced decrease in ARAS activity is consistent with an emerging literature suggesting that CBD reduces autonomic arousal under conditions of emotional and physical stress. The putative target and mechanism of action is NAPE-PLD the enzyme responsible for the biosynthesis of lipid signaling molecules like anandamide.

scholarly journals Social instigation and repeated aggressive confrontations in male Swiss mice: analysis of plasma corticosterone, CRF and BDNF levels in limbic brain areas

2017 ◽  
Vol 39 (2) ◽  
pp. 98-105 ◽  
Author(s):  
Paula Madeira Fortes ◽  
Lucas Albrechet-Souza ◽  
Mailton Vasconcelos ◽  
Bruna Maria Ascoli ◽  
Ana Paula Menegolla ◽  
...  
Keyword(s):  
Aggressive Behavior ◽  
Physiological Responses ◽  
Plasma Corticosterone ◽  
Corticotropin Releasing Factor ◽  
Brain Areas ◽  
Social Stressors ◽  
Swiss Mice ◽  
The Brain ◽  
Over Time ◽  
Resident Intruder

Abstract Introduction: Agonistic behaviors help to ensure survival, provide advantage in competition, and communicate social status. The resident-intruder paradigm, an animal model based on male intraspecific confrontations, can be an ethologically relevant tool to investigate the neurobiology of aggressive behavior. Objectives: To examine behavioral and neurobiological mechanisms of aggressive behavior in male Swiss mice exposed to repeated confrontations in the resident intruder paradigm. Methods: Behavioral analysis was performed in association with measurements of plasma corticosterone of mice repeatedly exposed to a potential rival nearby, but inaccessible (social instigation), or to 10 sessions of social instigation followed by direct aggressive encounters. Moreover, corticotropin-releasing factor (CRF) and brain-derived neurotrophic factor (BNDF) were measured in the brain of these animals. Control mice were exposed to neither social instigation nor aggressive confrontations. Results: Mice exposed to aggressive confrontations exhibited a similar pattern of species-typical aggressive and non-aggressive behaviors on the first and the last session. Moreover, in contrast to social instigation only, repeated aggressive confrontations promoted an increase in plasma corticosterone. After 10 aggressive confrontation sessions, mice presented a non-significant trend toward reducing hippocampal levels of CRF, which inversely correlated with plasma corticosterone levels. Conversely, repeated sessions of social instigation or aggressive confrontation did not alter BDNF concentrations at the prefrontal cortex and hippocampus. Conclusion: Exposure to repeated episodes of aggressive encounters did not promote habituation over time. Additionally, CRF seems to be involved in physiological responses to social stressors.

scholarly journals Contribution of Neuroinflammation to the Pathogenesis of Cancer Cachexia

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Alessio Molfino ◽  
Gianfranco Gioia ◽  
Filippo Rossi Fanelli ◽  
Alessandro Laviano
Keyword(s):  
Adipose Tissue ◽  
Food Intake ◽  
Proinflammatory Cytokines ◽  
Adaptive Response ◽  
Energy Homeostasis ◽  
Cancer Cachexia ◽  
Behavioral Changes ◽  
Brain Areas ◽  
Functional Changes ◽  
The Brain

Inflammation characterizes the course of acute and chronic diseases and is largely responsible for the metabolic and behavioral changes occurring during the clinical journey of patients. Robust data indicate that, during cancer, functional modifications within brain areas regulating energy homeostasis contribute to the onset of anorexia, reduced food intake, and increased catabolism of muscle mass and adipose tissue. In particular, functional changes are associated with increased hypothalamic concentration of proinflammatory cytokines, which suggests that neuroinflammation may represent the adaptive response of the brain to peripheral challenges, including tumor growth. Within this conceptual framework, the vagus nerve appears to be involved in conveying alert signals to the hypothalamus, whereas hypothalamic serotonin appears to contribute to triggering catabolic signals.

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