scholarly journals Cell-type specific burst firing interacts with theta and beta activity in prefrontal cortex during attention states

2017 ◽  
Author(s):  
B. Voloh ◽  
T. Womelsdorf
Keyword(s):  
Prefrontal Cortex ◽  
Population Level ◽  
Burst Firing ◽  
Anterior Cingulate ◽  
Beta Activity ◽  
Cell Type ◽  
Beta Band ◽  
Beta Power ◽  
A Cell ◽  
Cell Type Specific

AbstractPopulation-level theta and beta band activity in anterior cingulate and prefrontal cortex (ACC/PFC) are prominent signatures of endogenously controlled, adaptive behaviors. But how these rhythmic activities are linked to cell-type specific activity has remained unclear. Here, we suggest such a cell-to-systems level linkage. We found that the rate of burst spiking events is enhanced particularly during attention states and that attention-specific burst spikes have a unique temporal relationship to local theta and beta band population level activities. For the 5-10Hz theta frequency range, bursts coincided with transient increases of local theta power relative to non-bursts, particularly for bursts of putative interneurons. For the 16-30Hz beta frequency, bursts of putative interneurons phase synchronized stronger than nonbursts, and were associated with larger beta power modulation. In contrast, burst of putative pyramidal cells were overall similarly beta-synchronized than nonbursts, but were linked with stronger beta power only when they occurred early in the beta cycle. These findings suggests that in the ACC/PFC during attention states, mechanisms underlying burst firing are intimately linked to narrow band population level activities, providing a cell-type specific window into the emergence, resetting, or termination of oscillatory activities.

scholarly journals Cell-Type Specific Burst Firing Interacts with Theta and Beta Activity in Prefrontal Cortex During Attention States

2017 ◽  
Vol 28 (12) ◽  
pp. 4348-4364 ◽  
Author(s):  
B Voloh ◽  
T Womelsdorf
Keyword(s):  
Prefrontal Cortex ◽  
Burst Firing ◽  
Beta Activity ◽  
Cell Type ◽  
Cell Type Specific

scholarly journals Fragile X Mental Retardation Protein Bidirectionally Controls Dendritic Ih in a Cell Type-Specific Manner between Mouse Hippocampus and Prefrontal Cortex

2020 ◽  
Vol 40 (27) ◽  
pp. 5327-5340 ◽  
Author(s):  
Federico Brandalise ◽  
Brian E. Kalmbach ◽  
Preeti Mehta ◽  
Olivia Thornton ◽  
Daniel Johnston ◽  
...  
Keyword(s):  
Mental Retardation ◽  
Prefrontal Cortex ◽  
Fragile X ◽  
Cell Type ◽  
Fragile X Mental Retardation ◽  
Mental Retardation Protein ◽  
Specific Manner ◽  
Mouse Hippocampus ◽  
A Cell ◽  
Cell Type Specific

IFIH1-deficiency results in a cell-type specific alteration of autophagic activity in response to S. typhimurium

2017 ◽  
Vol 55 (05) ◽  
pp. e28-e56
Author(s):  
S Macheiner ◽  
R Gerner ◽  
A Pfister ◽  
A Moschen ◽  
H Tilg
Keyword(s):  
Cell Type ◽  
A Cell ◽  
Cell Type Specific ◽  
Autophagic Activity ◽  
Specific Alteration

scholarly journals A cell type‐specific expression map of NCoR1 and SMRT transcriptional co‐repressors in the mouse brain

2020 ◽  
Vol 528 (13) ◽  
pp. 2218-2238 ◽  
Author(s):  
Attilio Iemolo ◽  
Patricia Montilla‐Perez ◽  
I‐Chi Lai ◽  
Yinuo Meng ◽  
Syreeta Nolan ◽  
...  
Keyword(s):  
Mouse Brain ◽  
Cell Type ◽  
Specific Expression ◽  
Cell Type Specific Expression ◽  
A Cell ◽  
Cell Type Specific

scholarly journals Cell type‐specific DNA methylation analysis of the prefrontal cortex of patients with schizophrenia

2021 ◽  
Author(s):  
Junko Ueda ◽  
Miki Bundo ◽  
Yutaka Nakachi ◽  
Kiyoto Kasai ◽  
Tadafumi Kato ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Prefrontal Cortex ◽  
Cell Type ◽  
Methylation Analysis ◽  
Cell Type Specific ◽  
Dna Methylation Analysis

Gene therapy can target mutations such as BRAF, which have been shown to make tumors more susceptible to autophagy suppression

2021 ◽  
Author(s):  
Moataz Dowaidar
Keyword(s):  
Signaling Pathways ◽  
Chemotherapy Resistance ◽  
Effective Strategy ◽  
Cell Type ◽  
Normal Cells ◽  
A Cell ◽  
Cell Type Specific ◽  
Catabolic Process ◽  
Specific Impact

Autophagy is a double-edged sword in cancer, and numerous aspects should be taken into account before deciding on the most effective strategy to target the process. The fact that several clinical studies are now ongoing does not mean that the patient group that may benefit from autophagy-targeting medicines has been identified. Autophagy inhibitors that are more potent and specialized, as well as autophagy indicators, are also desperately required. The fact that these inhibitors only work against tumors that rely on autophagy for survival (RAS mutants) makes it difficult to distinguish them from tumors that continue to develop even when autophagy is absent. Furthermore, mutations such as BRAF have been shown to make tumors more susceptible to autophagy suppression, suggesting that targeting such tumours may be a viable strategy for overcoming their chemotherapy resistance. In the meantime, we are unable to identify if autophagy regulation works in vivo or whether it selectively targets a disease while inflicting injury to other healthy organs and tissues. A cell-type-specific impact appears to be observed with such therapy. As a result, it is just as important to consider the differences between tumors that originate in different organs as it is to consider the signaling pathways that are similar across them. For a therapy or cure to be effective, the proposed intervention must be tailored to the specific needs of each patient.Over the last several years, a growing amount of data has implicated autophagy in a variety of disorders, including cancer. In normal cells, this catabolic process is also required for cell survival and homeostasis. Despite the fact that medications targeting intermediates in the autophagy signaling pathway are being created and evaluated at both the preclinical and clinical levels, given the complicated function of autophagy in cancer, we still have a long way to go in terms of establishing an effective therapeutic approach. This article discusses current tactics for exploiting cancer cells' autophagy dependency, as well as obstacles in the area. We believe that the unanswered concerns raised in this work will stimulate researchers to investigate previously unknown connections between autophagy and other signaling pathways, which might lead to the development of novel, highly specialized autophagy therapies.

Elements regulating an alternatively spliced exon of the rat fibronectin gene

1993 ◽  
Vol 13 (9) ◽  
pp. 5301-5314 ◽  
Author(s):  
G S Huh ◽  
R O Hynes
Keyword(s):  
Splice Sites ◽  
Cell Type ◽  
Long Distance ◽  
Sequence Elements ◽  
Alternatively Spliced ◽  
A Cell ◽  
Cell Type Specific ◽  
Alternatively Spliced Exons

We have investigated the regulation of splicing of one of the alternatively spliced exons in the rat fibronectin gene, the EIIIB exon. This 273-nucleotide exon is excluded by some cells and included to various degrees by others. We find that EIIIB is intrinsically poorly spliced and that both its exon sequences and its splice sites contribute to its poor recognition. Therefore, cells which recognize the EIIIB exon must have mechanisms for improving its splicing. Furthermore, in order for EIIB to be regulated, a balance must exist between the EIIIB splice sites and those of its flanking exons. Although the intron upstream of EIIIB does not appear to play a role in the recognition of EIIIB for splicing, the intron downstream contains sequence elements which can promote EIIIB recognition in a cell-type-specific fashion. These elements are located an unusually long distance from the exon that they regulate, more than 518 nucleotides downstream from EIIIB, and may represent a novel mode of exon regulation.

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