learning deficits
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2022 ◽  
Author(s):  
Benjamin M Seitz ◽  
Ivy B Hoang ◽  
Aaron P Blaisdell ◽  
Melissa J Sharpe

For over two decades, midbrain dopamine was considered synonymous with the prediction error in temporal-difference reinforcement learning. Central to this proposal is the notion that reward-predictive stimuli become endowed with the scalar value of predicted rewards. When these cues are subsequently encountered, their predictive value is compared to the value of the actual reward received allowing for the calculation of prediction errors. Phasic firing of dopamine neurons was proposed to reflect this computation, facilitating the backpropagation of value from the predicted reward to the reward-predictive stimulus, thus reducing future prediction errors. There are two critical assumptions of this proposal: 1) that dopamine errors can only facilitate learning about scalar value and not more complex features of predicted rewards, and 2) that the dopamine signal can only be involved in anticipatory learning in which cues or actions precede rewards. Recent work has challenged the first assumption, demonstrating that phasic dopamine signals across species are involved in learning about more complex features of the predicted outcomes, in a manner that transcends this value computation. Here, we tested the validity of the second assumption. Specifically, we examined whether phasic midbrain dopamine activity would be necessary for backward conditioning- when a neutral cue reliably follows a rewarding outcome. Using a specific Pavlovian-to-Instrumental Transfer (PIT) procedure, we show rats learn both excitatory and inhibitory components of a backward association, and that this association entails knowledge of the specific identity of the reward and cue. We demonstrate that brief optogenetic inhibition of ventral tegmental area dopamine (VTA DA) neurons timed to the transition between the reward and cue, reduces both of these components of backward conditioning. These findings suggest VTA DA neurons are capable of facilitating associations between contiguously occurring events, regardless of the content of those events. We conclude that these data are in line with suggestions that the VTA DA error acts as a universal teaching signal. This may provide insight into why dopamine function has been implicated in a myriad of psychological disorders that are characterized by very distinct reinforcement-learning deficits.


2022 ◽  
Author(s):  
Jonathan S Tsay ◽  
Steven Tan ◽  
Marlena Chu ◽  
Richard B Ivry ◽  
Emily A Cooper

Successful goal-directed actions require constant fine-tuning in response to errors introduced by changes in the body and environment. This implicit adaptive process has been assumed to operate in a statistically optimal fashion, reducing its sensitivity to errors when sensory uncertainty is high. However, recent work has shown that visual uncertainty attenuates implicit adaptation for small errors, but not large errors, a result that is at odds with an optimal integration hypothesis. This error size interaction has motivated a new hypothesis that sensory uncertainty impacts the distribution of the perceived error locations but not the system's sensitivity to errors. To examine these competing hypotheses, previous studies have experimentally manipulated uncertainty. But it is unknown which hypothesis best describes motor adaptation to sensory uncertainty experienced during daily life. To address this question, we recruited individuals with low vision due to diverse clinical conditions impacting visual uncertainty and matched controls. The groups were tested on visuomotor tasks designed to isolate implicit adaptation and maintain tight control over the error size. In two experiments, low vision was associated with attenuated implicit adaptation only for small errors, but not for large errors. Taken together with prior work in which visual uncertainty was experimentally manipulated, these results support the notion that increasing sensory uncertainty increases the likelihood that errors are mis-localized but does not affect error sensitivity, offering a novel account for the motor learning deficits seen in low vision.


2021 ◽  
Vol 125 ◽  
pp. 108415
Author(s):  
Rita Asdikian ◽  
Helene Hajjar ◽  
Sana Alturk ◽  
Jean-Pierre Asdikian ◽  
Fatima Jaafar ◽  
...  

2021 ◽  
Vol 17 (S12) ◽  
Author(s):  
Jiaqi Sun ◽  
John CL Mamo ◽  
Ryu Takechi ◽  
Yuji Owada ◽  
Joseph Nicolazzo ◽  
...  

2021 ◽  
Vol 9 (5) ◽  
pp. 01-07
Author(s):  
Theofilidis Antonis

Μemory by itself as a function, loses its capabilities with a normal deterioration. However, there are acquired conditions that negatively affect the functions of memory, resulting in dysfunction of its stages. Thus possible damage to the structures of the hemisphere that controls these processes disrupts the comprehension, organization and categorization of the material to be memorized. Patients with damage to these systems will have difficulty remembering because they have not adequately coded the material. Patients with Multiple Sclerosis report short-term memory difficulties in the sense that they have difficulty remembering details of recent conversations and events. Aim: To investigate the memory storage difficulties in Multiple Sclerosis. Materials and Methods: An international literature review was performed on Memory Disorders in Multiple Sclerosis. Conclusion: In patients with Multiple Sclerosis learning deficits are greatly aided by processing speed and working memory. It has been observed that slow mental processing makes it difficult for many patients with Multiple Sclerosis to capture an entire verbal message, especially if it is large, complex, delivered quickly and with external stimuli, such as a noisy environment


2021 ◽  
Vol 15 ◽  
Author(s):  
Siavash Fazel Darbandi ◽  
Crystal Esau ◽  
Cindy Lesage-Pelletier ◽  
Simon Monis ◽  
Luc Poitras ◽  
...  

The Dlx homeodomain transcription factors play important roles in the differentiation and migration of GABAergic interneuron precursors. The mouse and human genomes each have six Dlx genes organized into three convergently transcribed bigene clusters (Dlx1/2, Dlx3/4, and Dlx5/6) with cis-regulatory elements (CREs) located in the intergenic region of each cluster. Amongst these, the I56i and I12b enhancers from the Dlx1/2 and Dlx5/6 locus, respectively, are active in the developing forebrain. I56i is also a binding site for GTF2I, a transcription factor whose function is associated with increased sociability and Williams–Beuren syndrome. In determining the regulatory roles of these CREs on forebrain development, we have generated mutant mouse-lines where Dlx forebrain intergenic enhancers have been deleted (I56i(–/–), I12b(–/–)). Loss of Dlx intergenic enhancers impairs expression of Dlx genes as well as some of their downstream targets or associated genes including Gad2 and Evf2. The loss of the I56i enhancer resulted in a transient decrease in GABA+ cells in the developing forebrain. The intergenic enhancer mutants also demonstrate increased sociability and learning deficits in a fear conditioning test. Characterizing mice with mutated Dlx intergenic enhancers will help us to further enhance our understanding of the role of these Dlx genes in forebrain development.


Life Sciences ◽  
2021 ◽  
pp. 120094
Author(s):  
Elena V. Kozlova ◽  
Bruno Carabelli ◽  
Anthony E. Bishay ◽  
Maximilian E. Denys ◽  
Devi B. Chinthirla ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Dorothee Pöhlchen ◽  
Marthe Priouret ◽  
Miriam S. Kraft ◽  
Florian P. Binder ◽  
Deniz A. Gürsel ◽  
...  

Obsessive-compulsive disorder (OCD) is characterized by recurrent, persistent thoughts and repetitive behaviors causing stress and anxiety. In the associative learning model of OCD, mechanisms of fear extinction are supposed to partly underlie symptom development, maintenance and treatment of OCD, proposing that OCD patients suffer from rigid memory associations and inhibitory learning deficits. To test these assumptions, previous studies have used skin conductance and subjective ratings as readouts in fear conditioning paradigms, finding impaired fear extinction learning, impaired fear extinction recall or no differences between individuals with OCD and healthy controls. Against this heterogeneous background, we tested fear acquisition and extinction in 37 OCD patients and 56 healthy controls, employing skin conductance as well as pupillometry and startle electromyography. Extinction recall was also included in a subsample. We did not observe differences between groups in any of the task phases, except a trend toward higher startle amplitudes during extinction for OCD. Overall, sensitive readouts such as pupillometry and startle responses did not provide evidence for moderate-to-large inhibitory learning deficits using classical fear conditioning, challenging the assumption of generically impaired extinction learning and memory in OCD.


PLoS Biology ◽  
2021 ◽  
Vol 19 (9) ◽  
pp. e3001407
Author(s):  
Ulrike Kuhl ◽  
Sarah Sobotta ◽  
Michael A. Skeide ◽  

Mathematical learning deficits are defined as a neurodevelopmental disorder (dyscalculia) in the International Classification of Diseases. It is not known, however, how such deficits emerge in the course of early brain development. Here, we conducted functional and structural magnetic resonance imaging (MRI) experiments in 3- to 6-year-old children without formal mathematical learning experience. We followed this sample until the age of 7 to 9 years, identified individuals who developed deficits, and matched them to a typically developing control group using comprehensive behavioral assessments. Multivariate pattern classification distinguished future cases from controls with up to 87% accuracy based on the regional functional activity of the right posterior parietal cortex (PPC), the network-level functional activity of the right dorsolateral prefrontal cortex (DLPFC), and the effective functional and structural connectivity of these regions. Our results indicate that mathematical learning deficits originate from atypical development of a frontoparietal network that is already detectable in early childhood.


2021 ◽  
Vol 118 (39) ◽  
pp. e2109040118
Author(s):  
Yu-Ju Chen ◽  
Shin-Meng Deng ◽  
Hui-Wen Chen ◽  
Chi-Hui Tsao ◽  
Wei-Ting Chen ◽  
...  

The biological mechanisms underpinning learning are unclear. Mounting evidence has suggested that adult hippocampal neurogenesis is involved although a causal relationship has not been well defined. Here, using high-resolution genetic mapping of adult neurogenesis, combined with sequencing information, we identify follistatin (Fst) and demonstrate its involvement in learning and adult neurogenesis. We confirmed that brain-specific Fst knockout (KO) mice exhibited decreased hippocampal neurogenesis and demonstrated that FST is critical for learning. Fst KO mice exhibit deficits in spatial learning, working memory, and long-term potentiation (LTP). In contrast, hippocampal overexpression of Fst in KO mice reversed these impairments. By utilizing RNA sequencing and chromatin immunoprecipitation, we identified Asic4 as a target gene regulated by FST and show that Asic4 plays a critical role in learning deficits caused by Fst deletion. Long-term overexpression of hippocampal Fst in C57BL/6 wild-type mice alleviates age-related decline in cognition, neurogenesis, and LTP. Collectively, our study reveals the functions for FST in adult neurogenesis and learning behaviors.


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