scholarly journals Metabolic efficiency with fast spiking in the squid axon

Author(s):  
Abdelmalik Moujahid ◽  
Alicia d'Anjou
Author(s):  
Grażyna Mazurkiewicz-Boroń ◽  
Teresa Bednarz ◽  
Elżbieta Wilk-Woźniak

Microbial efficiency in a meromictic reservoirIndices of microbial efficiency (expressed as oxygen consumption and carbon dioxide release) were determined in the water column of the meromictic Piaseczno Reservoir (in an opencast sulphur mine), which is rich in sulphur compounds. Phytoplankton abundances were low in both the mixolimnion (up to 15 m depth) and monimolimnion (below 15 m depth). In summer and winter, carbon dioxide release was 3-fold and 5-fold higher, respectively, in the monimolimnion than in the mixolimnion. Laboratory enrichments of the sulphur substrate of the water resulted in a decrease in oxygen consumption rate of by about 42% in mixolimnion samples, and in the carbon dioxide release rate by about 69% in monimolimnion samples. Water temperature, pH and bivalent ion contents were of major importance in shaping the microbial metabolic efficiency in the mixolimnion, whilst in the monimolimnion these relationships were not evident.


Author(s):  
Luis Enrique Arroyo-García ◽  
Arturo G. Isla ◽  
Yuniesky Andrade-Talavera ◽  
Hugo Balleza-Tapia ◽  
Raúl Loera-Valencia ◽  
...  

AbstractIn Alzheimer’s disease (AD) the accumulation of amyloid-β (Aβ) correlates with degradation of cognition-relevant gamma oscillations. The gamma rhythm relies on proper neuronal spike-gamma coupling, specifically of fast-spiking interneurons (FSN). Here we tested the hypothesis that decrease in gamma power and FSN synchrony precede amyloid plaque deposition and cognitive impairment in AppNL-G-F knock-in mice (AppNL-G-F). The aim of the study was to evaluate the amyloidogenic pathology progression in the novel AppNL-G-F mouse model using in vitro electrophysiological network analysis. Using patch clamp of FSNs and pyramidal cells (PCs) with simultaneous gamma oscillation recordings, we compared the activity of the hippocampal network of wild-type mice (WT) and the AppNL-G-F mice at four disease stages (1, 2, 4, and 6 months of age). We found a severe degradation of gamma oscillation power that is independent of, and precedes Aβ plaque formation, and the cognitive impairment reported previously in this animal model. The degradation correlates with increased Aβ1-42 concentration in the brain. Analysis on the cellular level showed an impaired spike-gamma coupling of FSN from 2 months of age that correlates with the degradation of gamma oscillations. From 6 months of age PC firing becomes desynchronized also, correlating with reports in the literature of robust Aβ plaque pathology and cognitive impairment in the AppNL-G-F mice. This study provides evidence that impaired FSN spike-gamma coupling is one of the earliest functional impairment caused by the amyloidogenic pathology progression likely is the main cause for the degradation of gamma oscillations and consequent cognitive impairment. Our data suggests that therapeutic approaches should be aimed at restoring normal FSN spike-gamma coupling and not just removal of Aβ.


2021 ◽  
Vol 108 (Supplement_2) ◽  
Author(s):  
A Vassiliou ◽  
K Alavian ◽  
M Tsujishita ◽  
H Bae

Abstract Introduction Primary brain tumours originate from cells within the brain. The commonest malignant types are gliomas which are graded from I-IV. Emerging evidence has elucidated the function of the mitochondrially localised B-cell lymphoma-extra-large (Bcl-xL) protein, and its promotion of tumour progression-associated properties. Our lab has previously established that Bcl-xL-overexpressing neurons increase metabolic efficiency by producing more adenosine triphosphate and consuming less oxygen, which we assumed, fuels cancer cells to proliferate. Method We quantified the subcellular expression patterns of Bcl-xL in primary brain tumour samples through immunohistochemistry on a brain tissue microarray containing 16 glioma cases from Grades II-IV. We used antibodies against Bcl-xL, heat shock protein 60 for mitochondrial detection and proliferating cell nuclear antigen for cancerous cell detection. Results Bcl-xL is overexpressed in cancerous cells of Grade IV gliomas and is significantly greater than cancerous cells of Grade III and Grade II gliomas. Cancerous cells express higher levels of Bcl-xL than non-cancerous cells in all grades of glioma. Conclusions Bcl-xL-overexpressing neurons exhibit enhanced metabolic efficiency, contributing to increased proliferation rates. Future research should focus on the characterisation of ATP levels and oxygen consumption in glioma cells. Conclusively, pharmacological inhibition of Bcl-xL will suppress the proliferation rate in gliomas and cease cancer cell growth.


1993 ◽  
Vol 38 (11) ◽  
pp. 2001-2009 ◽  
Author(s):  
Manfred J. Müller ◽  
Lars U. Schmidt ◽  
Jürgen Körber ◽  
Alexander von Zur Mühlen ◽  
Helmuth Canzler ◽  
...  

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