scholarly journals Fast-spiking interneurons have an initial orientation bias that is lost with vision

2011 ◽  
Vol 14 (9) ◽  
pp. 1121-1123 ◽  
Author(s):  
Sandra J Kuhlman ◽  
Elaine Tring ◽  
Joshua T Trachtenberg
1999 ◽  
Vol 16 (2) ◽  
pp. 303-318 ◽  
Author(s):  
P. ADORJÁN ◽  
J. B. LEVITT ◽  
J. S. LUND ◽  
K. OBERMAYER

We report results of numerical simulations for a model of generation of orientation selectivity in macaque striate cortex. In contrast to previous models, where the initial orientation bias is generated by convergent geniculate input to simple cells and subsequently sharpened by lateral circuits, our approach is based on anisotropic intracortical excitatory connections which provide both the initial orientation bias and its subsequent amplification. Our study shows that the emerging response properties are similar to the response properties that are observed experimentally, hence the hypothesis of an intracortical generation of orientation bias is a sensible alternative to the notion of an afferent bias by convergent geniculocortical projection patterns. In contrast to models based on an afferent orientation bias, however, the “intracortical hypothesis” predicts that orientation tuning gradually evolves from an initially nonoriented response and a complete loss of orientation tuning when the recurrent excitation is blocked, but new experiments must be designed to unambiguously decide between both hypotheses.


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.


Genetics ◽  
1996 ◽  
Vol 142 (3) ◽  
pp. 761-776 ◽  
Author(s):  
Lori A Rinckel ◽  
David J Garfinkel

Abstract In Saccharomyces cerevisiae, the target site specificity of the retrotransposon Ty1 appears to involve the Ty integration complex recognizing chromatin structures. To determine whether changes in chromatin structure affect Ty1 and Ty2 target site preference, we analyzed Ty transposition at the CAN1 locus in mutants containing altered levels of histone proteins. A Δhta1-htb1 mutant with decreased levels of H2A and H2B histone proteins showed a pattern of Ty1 and Ty2 insertions at CAN1 that was significantly different from that of both the wild-type and a Δhta2-htb2 mutant, which does not have altered histone protein levels. Altered levels of H2A and H2B proteins disrupted a dramatic orientation bias in the CAN1 promoter region. In the wild-type strains, few Ty1 and Ty2 insertions in the promoter region were oriented opposite to the direction of CAN1 transcription. In the Δhta1-htb1 background, however, numerous Ty1 and Ty2 insertions were in the opposite orientation clustered within the TATA region. This altered insertion pattern does not appear to be due to a bias caused by selecting canavanine resistant isolates in the different HTA1-HTB1 backgrounds. Our results suggest that reduced levels of histone proteins alter Ty target site preference and disrupt an asymmetric Ty insertion pattern.


PLoS ONE ◽  
2012 ◽  
Vol 7 (8) ◽  
pp. e41215 ◽  
Author(s):  
Michael J. Gandal ◽  
Addie May Nesbitt ◽  
Richard M. McCurdy ◽  
Mark D. Alter

1983 ◽  
Vol 14 (1) ◽  
pp. 77-79 ◽  
Author(s):  
R. Ranvaud ◽  
K. Schmidt-Koenig ◽  
J. Kiepenheuer ◽  
O. C. Gasparotto

Gene ◽  
2000 ◽  
Vol 259 (1-2) ◽  
pp. 207-215 ◽  
Author(s):  
Reina Uno ◽  
Yoichi Nakayama ◽  
Kazuharu Arakawa ◽  
Masaru Tomita

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