Role of network connectivity in intercellular calcium signaling

2008 ◽  
Vol 237 (6) ◽  
pp. 745-754 ◽  
Author(s):  
I.V. Dokukina ◽  
M.E. Gracheva ◽  
E.A. Grachev ◽  
J.D. Gunton
2021 ◽  
pp. 216770262095934
Author(s):  
Julia M. Sheffield ◽  
Holger Mohr ◽  
Hannes Ruge ◽  
Deanna M. Barch

Rapid instructed task learning (RITL) is the uniquely human ability to transform task information into goal-directed behavior without relying on trial-and-error learning. RITL is a core cognitive process supported by functional brain networks. In patients with schizophrenia, RITL ability is impaired, but the role of functional network connectivity in these RITL deficits is unknown. We investigated task-based connectivity of eight a priori network pairs in participants with schizophrenia ( n = 29) and control participants ( n = 31) during the performance of an RITL task. Multivariate pattern analysis was used to determine which network connectivity patterns predicted diagnostic group. Of all network pairs, only the connectivity between the cingulo-opercular network (CON) and salience network (SAN) during learning classified patients and control participants with significant accuracy (80%). CON-SAN connectivity during learning was significantly associated with task performance in participants with schizophrenia. These findings suggest that impaired interactions between identification of salient stimuli and maintenance of task goals contributes to RITL deficits in participants with schizophrenia.


Author(s):  
Lisa Bartha-Doering ◽  
Ernst Schwartz ◽  
Kathrin Kollndorfer ◽  
Florian Ph. S. Fischmeister ◽  
Astrid Novak ◽  
...  

AbstractThe present study is interested in the role of the corpus callosum in the development of the language network. We, therefore, investigated language abilities and the language network using task-based fMRI in three cases of complete agenesis of the corpus callosum (ACC), three cases of partial ACC and six controls. Although the children with complete ACC revealed impaired functions in specific language domains, no child with partial ACC showed a test score below average. As a group, ACC children performed significantly worse than healthy controls in verbal fluency and naming. Furthermore, whole-brain ROI-to-ROI connectivity analyses revealed reduced intrahemispheric and right intrahemispheric functional connectivity in ACC patients as compared to controls. In addition, stronger functional connectivity between left and right temporal areas was associated with better language abilities in the ACC group. In healthy controls, no association between language abilities and connectivity was found. Our results show that ACC is associated not only with less interhemispheric, but also with less right intrahemispheric language network connectivity in line with reduced verbal abilities. The present study, thus, supports the excitatory role of the corpus callosum in functional language network connectivity and language abilities.


2003 ◽  
Vol 278 (47) ◽  
pp. 46270-46277 ◽  
Author(s):  
Mu-Lan He ◽  
Arturo E. Gonzalez-Iglesias ◽  
Stanko S. Stojilkovic

2018 ◽  
Vol 19 (11) ◽  
pp. 3390 ◽  
Author(s):  
Sudip Paudel ◽  
Regan Sindelar ◽  
Margaret Saha

Accumulating evidence over the past three decades suggests that altered calcium signaling during development may be a major driving force for adult pathophysiological events. Well over a hundred human genes encode proteins that are specifically dedicated to calcium homeostasis and calcium signaling, and the majority of these are expressed during embryonic development. Recent advances in molecular techniques have identified impaired calcium signaling during development due to either mutations or dysregulation of these proteins. This impaired signaling has been implicated in various human diseases ranging from cardiac malformations to epilepsy. Although the molecular basis of these and other diseases have been well studied in adult systems, the potential developmental origins of such diseases are less well characterized. In this review, we will discuss the recent evidence that examines different patterns of calcium activity during early development, as well as potential medical conditions associated with its dysregulation. Studies performed using various model organisms, including zebrafish, Xenopus, and mouse, have underscored the critical role of calcium activity in infertility, abortive pregnancy, developmental defects, and a range of diseases which manifest later in life. Understanding the underlying mechanisms by which calcium regulates these diverse developmental processes remains a challenge; however, this knowledge will potentially enable calcium signaling to be used as a therapeutic target in regenerative and personalized medicine.


2021 ◽  
Author(s):  
Alejandra J.H. Cabrera ◽  
Barry M Gumbiner ◽  
Young V Kwon

Given the role of E-cadherin (E-cad) in holding epithelial cells together, the inverse relationship between E-cad levels and cell invasion has been perceived as a principle underlying the invasiveness of tumor cells. In contrast, our study employing the Drosophila model of cell dissemination demonstrates that E-cad is necessary for the invasiveness of RasV12-transformed cells in vivo. Drosophila E-cad/β-catenin disassembles at adherens junctions and assembles at invasive protrusions—the actin- and cortactin-rich invadopodia-like protrusions associated with breach of the extracellular matrix (ECM)—during cell dissemination. Loss of E-cad attenuates dissemination of RasV12-transformed cells by impairing their ability to compromise the ECM. Strikingly, the remodeling of E-cad/β-catenin subcellular distribution is controlled by two discrete intracellular calcium signaling pathways: Ca2+ release from endoplasmic reticulum via the inositol triphosphate receptor (IP3R) disassembles E-cad at adherens junctions while Ca2+ entry via the mechanosensitive channel Piezo assembles E-cad at invasive protrusions. Thus, our study provides molecular insights into the unconventional role of E-cad in cell invasion during cell dissemination in vivo and describes the discrete roles of intracellular calcium signaling in the remodeling of E-cad/β-catenin subcellular localization.


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