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Astrocytes are sensitive to ongoing neuronal/network activities and, accordingly, regulate neuronal functions (synaptic transmission, synaptic plasticity, behavior, etc.) by the context-dependent release of several gliotransmitters (e.g., glutamate, glycine, D -serine, ATP). To sense diverse input, astrocytes express a plethora of G-protein coupled receptors, which couple, via G i/o and G q , to the intracellular Ca 2+ release channel IP 3 -receptor (IP 3 R). Indeed, manipulating astrocytic IP 3 R-Ca 2+ signaling is highly consequential at the network and behavioral level: Depleting IP 3 R subtype 2 (IP 3 R2) results in reduced GPCR-Ca 2+ signaling and impaired synaptic plasticity; enhancing IP 3 R-Ca 2+ signaling affects cognitive functions such as learning and memory, sleep, and mood. However, as a result of discrepancies in the literature, the role of GPCR-IP 3 R-Ca 2+ signaling, especially under physiological conditions, remains inconclusive. One primary reason for this could be that IP 3 R2 has been used to represent all astrocytic IP 3 Rs, including IP 3 R1 and IP 3 R3. Indeed, IP 3 R1 and IP 3 R3 are unique Ca 2+ channels in their own right; they have unique biophysical properties, often display distinct distribution, and are differentially regulated. As a result, they mediate different physiological roles to IP 3 R2. Thus, these additional channels promise to enrich the diversity of spatiotemporal Ca 2+ dynamics and provide unique opportunities for integrating neuronal input and modulating astrocyte–neuron communication. The current review weighs evidence supporting the existence of multiple astrocytic-IP 3 R isoforms, summarizes distinct sub-type specific properties that shape spatiotemporal Ca 2+ dynamics. We also discuss existing experimental tools and future refinements to better recapitulate the endogenous activities of each IP 3 R isoform.

[This retracts the article DOI: 10.3389/fncel.2014.00382.].

[This retracts the article DOI: 10.3389/fncel.2019.00061.].

Multiple independent genomic profiling efforts have recently identified clinically and molecularly distinct subgroups of ependymoma arising from all three anatomic compartments of the central nervous system (supratentorial brain, posterior fossa, and spinal cord). These advances motivated a consensus meeting to discuss: (1) the utility of current histologic grading criteria, (2) the integration of molecular-based stratification schemes in future clinical trials for patients with ependymoma and (3) current therapy in the context of molecular subgroups. Discussion at the meeting generated a series of consensus statements and recommendations from the attendees, which comment on the prognostic evaluation and treatment decisions of patients with intracranial ependymoma (WHO Grade II/III) based on the knowledge of its molecular subgroups. The major consensus among attendees was reached that treatment decisions for ependymoma (outside of clinical trials) should not be based on grading (II vs III). Supratentorial and posterior fossa ependymomas are distinct diseases, although the impact on therapy is still evolving. Molecular subgrouping should be part of all clinical trials henceforth.

[This retracts the article DOI: 10.3389/fncel.2018.00480.].[This retracts the article DOI: 10.3389/fncel.2018.00480.].

Anxiety disorders (ADs), namely generalized AD, panic disorder and phobias, are common, etiologically complex conditions with a partially genetic basis. Despite differing on diagnostic definitions based on clinical presentation, ADs likely represent various expressions of an underlying common diathesis of abnormal regulation of basic threat–response systems. We conducted genome-wide association analyses in nine samples of European ancestry from seven large, independent studies. To identify genetic variants contributing to genetic susceptibility shared across interview-generated DSM-based ADs, we applied two phenotypic approaches: (1) comparisons between categorical AD cases and supernormal controls, and (2) quantitative phenotypic factor scores (FS) derived from a multivariate analysis combining information across the clinical phenotypes. We used logistic and linear regression, respectively, to analyze the association between these phenotypes and genome-wide single nucleotide polymorphisms. Meta-analysis for each phenotype combined results across the nine samples for over 18 000 unrelated individuals. Each meta-analysis identified a different genome-wide significant region, with the following markers showing the strongest association: for case–control contrasts, rs1709393 located in an uncharacterized non-coding RNA locus on chromosomal band 3q12.3 ( P =1.65 × 10 −8 ); for FS, rs1067327 within CAMKMT encoding the calmodulin-lysine N -methyltransferase on chromosomal band 2p21 ( P =2.86 × 10 −9 ). Independent replication and further exploration of these findings are needed to more fully understand the role of these variants in risk and expression of ADs.

Objective: To compare the safety and effectiveness of transplanted cells from different sources for spinal cord injury (SCI). Design: A systematic review and Bayesian network meta-analysis. Data sources: Medline, Embase, and the Cochrane Central Register of Controlled Trials. Study selection: We included randomized controlled trials, case-control studies, and case series related to cell transplantation for SCI patients, that included at least 1 of the following outcome measures: American Spinal Cord Injury Association (ASIA) Impairment Scale (AIS grade), ASIA motor score, ASIA sensory score, the Functional Independence Measure score (FIM), International Association of Neurorestoratology Spinal Cord Injury Functional Rating Scale (IANR-SCIFRS), or adverse events. Follow-up data were analysed at 6 and 12 months. Results: Forty-four eligible trials, involving 1266 patients, investigated 6 treatments: olfactory ensheathing cells (OECs), neural stem cells/ neural progenitor cells (NSCs), mesenchymal stem cells (MSCs), Schwann cells, macrophages, and combinations of cells (MSCs plus Schwann cells). Macrophages improved the AIS grade at 12 months (mean 0.42, 95% confidence interval: 0‒0.91, low certainty), MSCs improved the AIS grade at 6 months (0.42, 0.15‒0.73, moderate certainty) and FIM score at 12 months (42.83, 36.33‒49.18, very low certainty), the motor score at 6 months (4.43, 0.91‒7.78, moderate certainty), light touch at 6 (10.01, 5.81‒13.88, moderate certainty) and at 12 months (11.48, 6.31‒16.64, moderate certainty), pinprick score at 6 (14.54, 9.76‒19.46, moderate certainty) and at 12 months (12.48, 7.09‒18.12, moderate certainty), and the IANR-SCIFRS at 6 (3.96, 0.62‒6.97, moderate certainty) and at 12 months (5.54, 2.45‒8.42, moderate certainty). OECs improved the FIM score at 6 months (-9.35, -17.00 to -1.71, moderate certainty). No intervention improved the motor score significantly at 12 months. The certainty of other interventions was low or very low. Overall, the number of adverse events associated with transplanted cells was low. Conclusions: Patients with SCI who receive transplantation of macrophages, MSCs, NSCs, or OECs may have improved disease prognosis. MSCs are the primary recommendations. Further exploration of the mechanism of cell transplantation in the treatment of SCI, transplantation time window, transplantation methods, and monitoring of the number of transplanted cells and cell survival is needed.

[This retracts the article DOI: 10.3389/fncel.2015.00087.].[This retracts the article DOI: 10.3389/fncel.2015.00087.].

[This retracts the article DOI: 10.3389/fncel.2019.00233.].[This retracts the article DOI: 10.3389/fncel.2019.00233.].

[This retracts the article DOI: 10.3389/fncel.2013.00043.].[This retracts the article DOI: 10.3389/fncel.2013.00043.].