Representation of Rigid Stimulus Transformations by Cortical Activity Patterns

2008 ◽  
Vol 11 (5) ◽  
pp. 603-608 ◽  
Author(s):  
Crystal T Engineer ◽  
Claudia A Perez ◽  
YeTing H Chen ◽  
Ryan S Carraway ◽  
Amanda C Reed ◽  
...  

1977 ◽  
Vol 15 (6) ◽  
pp. 793-798 ◽  
Author(s):  
Jarl Risberg ◽  
Alexander V. Maximilian ◽  
Isak Prohovnik

2011 ◽  
Vol 34 (11) ◽  
pp. 1823-1838 ◽  
Author(s):  
Jai A. Shetake ◽  
Jordan T. Wolf ◽  
Ryan J. Cheung ◽  
Crystal T. Engineer ◽  
Satyananda K. Ram ◽  
...  

2017 ◽  
Vol 24 (2) ◽  
pp. 130-141 ◽  
Author(s):  
Nailya Lotfullina ◽  
Roustem Khazipov

Ethanol induces massive neuroapoptosis in the developing brain. One of the main hypotheses that has been put forward to explain the deleterious actions of ethanol in the immature brain involves an inhibition of neuronal activity. Here, we review recent evidence for this hypothesis obtained in the somatosensory cortex and hippocampus of neonatal rodents. In both structures, ethanol strongly inhibits brain activity. At the doses inducing massive neuroapoptosis, ethanol completely suppresses the early activity patterns of spindle-bursts and gamma oscillations in the neocortex and the early sharp-waves in the hippocampus. The inhibitory effects of ethanol decrease with age and in adult animals, ethanol only mildly depresses neuronal firing and induces delta-wave activity. Suppression of cortical activity in neonatal animals likely involves inhibition of the myoclonic twitches, an important physiological trigger for the early activity bursts, and inhibition of the thalamocortical and intracortical circuits through a potentiation of GABAergic transmission and an inhibition of N-methyl-d-aspartate (NMDA) receptors, that is in keeping with the neuroapoptotic effects of other agents acting on GABA and NMDA receptors. These findings provide support for the hypothesis that the ethanol-induced inhibition of cortical activity is an important pathophysiological mechanism underlying massive neuroapoptosis induced by ethanol in the developing brain.


2020 ◽  
Vol 14 ◽  
Author(s):  
Sang-Yeon Lee ◽  
Byung Yoon Choi ◽  
Ja-Won Koo ◽  
Dirk De Ridder ◽  
Jae-Jin Song

Just as the human brain works in a Bayesian manner to minimize uncertainty regarding external stimuli, a deafferented brain due to hearing loss attempts to obtain or “fill in” the missing auditory information, resulting in auditory phantom percepts (i.e., tinnitus). Among various types of hearing loss, sudden sensorineural hearing loss (SSNHL) has been extensively reported to be associated with tinnitus. However, the reason that tinnitus develops selectively in some patients with SSNHL remains elusive, which led us to hypothesize that patients with SSNHL with tinnitus (SSNHL-T) and those without tinnitus (SSNHL-NT) may exhibit different cortical activity patterns. In the current study, we compared resting-state quantitative electroencephalography findings between 13 SSNHL-T and 13 SSNHL-NT subjects strictly matched for demographic characteristics and hearing thresholds. By performing whole-brain source localization analysis complemented by functional connectivity analysis, we aimed to determine the as-yet-unidentified cortical oscillatory signatures that may reveal potential prerequisites for the perception of tinnitus in patients with SSNHL. Compared with the SSNHL-NT group, the SSNHL-T group showed significantly higher cortical activity in Bayesian inferential network areas such as the frontopolar cortex, orbitofrontal cortex (OFC), and pregenual anterior cingulate cortex (pgACC) for the beta 3 and gamma frequency bands. This suggests that tinnitus develops in a brain with sudden auditory deafferentation only if the Bayesian inferential network updates the missing auditory information and the pgACC-based top-down gatekeeper system is actively involved. Additionally, significantly increased connectivity between the OFC and precuneus for the gamma frequency band was observed in the SSNHL-T group, further suggesting that tinnitus derived from Bayesian inference may be linked to the default mode network so that tinnitus is regarded as normal. Taken together, our preliminary results suggest a possible mechanism for the selective development of tinnitus in patients with SSNHL. Also, these areas could serve as the potential targets of neuromodulatory approaches to preventing the development or prolonged perception of tinnitus in subjects with SSNHL.


Neuroscience ◽  
2014 ◽  
Vol 258 ◽  
pp. 292-306 ◽  
Author(s):  
T.M. Centanni ◽  
A.M. Sloan ◽  
A.C. Reed ◽  
C.T. Engineer ◽  
R.L. Rennaker ◽  
...  

2019 ◽  
Vol 29 (11) ◽  
pp. 4662-4678 ◽  
Author(s):  
Jason P Gallivan ◽  
Craig S Chapman ◽  
Daniel J Gale ◽  
J Randall Flanagan ◽  
Jody C Culham

Abstract The primate visual system contains myriad feedback projections from higher- to lower-order cortical areas, an architecture that has been implicated in the top-down modulation of early visual areas during working memory and attention. Here we tested the hypothesis that these feedback projections also modulate early visual cortical activity during the planning of visually guided actions. We show, across three separate human functional magnetic resonance imaging (fMRI) studies involving object-directed movements, that information related to the motor effector to be used (i.e., limb, eye) and action goal to be performed (i.e., grasp, reach) can be selectively decoded—prior to movement—from the retinotopic representation of the target object(s) in early visual cortex. We also find that during the planning of sequential actions involving objects in two different spatial locations, that motor-related information can be decoded from both locations in retinotopic cortex. Together, these findings indicate that movement planning selectively modulates early visual cortical activity patterns in an effector-specific, target-centric, and task-dependent manner. These findings offer a neural account of how motor-relevant target features are enhanced during action planning and suggest a possible role for early visual cortex in instituting a sensorimotor estimate of the visual consequences of movement.


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