scholarly journals Cognitive control links alcohol use, trait disinhibition, and reduced cognitive capacity: Evidence for medial prefrontal cortex dysregulation during reward-seeking behavior

2012 ◽  
Vol 122 (1-2) ◽  
pp. 112-118 ◽  
Author(s):  
Tim Bogg ◽  
Rena Fukunaga ◽  
Peter R. Finn ◽  
Joshua W. Brown
2014 ◽  
Vol 26 (4) ◽  
pp. 683-698 ◽  
Author(s):  
Charlotte E. Hartwright ◽  
Ian A. Apperly ◽  
Peter C. Hansen

The medial pFC (mPFC) is frequently reported to play a central role in Theory of Mind (ToM). However, the contribution of this large cortical region in ToM is not well understood. Combining a novel behavioral task with fMRI, we sought to demonstrate functional divisions between dorsal and rostral mPFC. All conditions of the task required the representation of mental states (beliefs and desires). The level of demands on cognitive control (high vs. low) and the nature of the demands on reasoning (deductive vs. abductive) were varied orthogonally between conditions. Activation in dorsal mPFC was modulated by the need for control, whereas rostral mPFC was modulated by reasoning demands. These findings fit with previously suggested domain-general functions for different parts of mPFC and suggest that these functions are recruited selectively in the service of ToM.


2020 ◽  
Author(s):  
Lailun Nahar ◽  
Caleb A. Grant ◽  
Cameron Hewett ◽  
Diego Cortes ◽  
Ashlie N. Reker ◽  
...  

2017 ◽  
Vol 81 (10) ◽  
pp. S215-S216
Author(s):  
Arron W.S. Metcalfe ◽  
Bradley J. MacIntosh ◽  
Alvi H. Islam ◽  
Henri J.M.M. Mutsaerts ◽  
Daphne Korczak ◽  
...  

2018 ◽  
Vol 1678 ◽  
pp. 419-431 ◽  
Author(s):  
Huijun Zhong ◽  
Jie Dang ◽  
Zhenghao Huo ◽  
Zhanbing Ma ◽  
Jing Chen ◽  
...  

Author(s):  
Simon J. Durrant ◽  
Jennifer M. Johnson

Abstract Purpose of Review A recent resurgence of interest in schema theory has influenced research on sleep-dependent memory consolidation and led to a new understanding of how schemata might be activated during sleep and play a role in the reorganisation of memories. This review is aimed at synthesising recent findings into a coherent narrative and draw overall conclusions. Recent Findings Rapid consolidation of schematic memories has been shown to benefit from an interval containing sleep. These memories have shown reduced reliance on the hippocampus following consolidation in both humans and rodents. Using a variety of methodologies, notably including the DRM paradigm, it has been shown that activation of a schema can increase the rate of false memory as a result of activation of semantic associates during slow wave sleep (SWS). Memories making use of a schema have shown increased activity in the medial prefrontal cortex, which may reflect both the schematic activation itself and a cognitive control component selecting an appropriate schema to use. SWS seems to be involved in assimilation of new memories within existing semantic frameworks and in making memories more explicit, while REM sleep may be more associated with creating entirely novel associations while keeping memories implicit. Summary Sleep plays an important role in schematic memory consolidation, with more rapid consolidation, reduced hippocampal involvement, and increased prefrontal involvement as the key characteristics. Both SWS and REM sleep may have a role to play.


2020 ◽  
Author(s):  
Judit Cabana-Domínguez ◽  
Elena Martín-García ◽  
Ana Gallego-Roman ◽  
Rafael Maldonado ◽  
Noèlia Fernàndez-Castillo ◽  
...  

ABSTRACTBackground and PurposeCocaine addiction causes serious health problems and no effective treatment is available yet. We previously identified a genetic risk variant for cocaine addiction in the PLCB1 gene and found this gene upregulated in postmortem brains of cocaine abusers and in human dopaminergic neuron-like cells after an acute cocaine exposure. Here, we functionally tested the contribution of PLCB1 gene to cocaine addictive properties in mice.Experimental approachWe used heterozygous Plcb1 knockout mice (Plcb1+/-) and characterized their behavioral phenotype. Subsequently, mice were trained for operant conditioning and self-administered cocaine for 10 days. Plcb1+/- mice were assessed for cocaine motivation, followed by 26 days of extinction and finally evaluated for cue-induced reinstatement of cocaine seeking. Gene expression alterations after reinstatement were assessed in medial prefrontal cortex (mPFC) and hippocampus (HPC) by RNAseq.Key ResultsPlcb1+/- mice showed normal behavior, although they had increased anxiety and impaired short-term memory. Importantly, after cocaine self-administration and extinction, we found a reduction in the cue-induced reinstatement of cocaine-seeking behavior in Plcb1+/- mice. After reinstatement, we identified transcriptomic alterations in the medial prefrontal cortex of Plcb1+/- mice, mostly related to pathways relevant to addiction like the dopaminergic synapse and long-term potentiation.Conclusions and ImplicationsTo conclude, we found that heterozygous deletion of the Plcb1 gene decreases cue-induced reinstatement of cocaine seeking, pointing at PLCB1 as a possible therapeutic target for preventing relapse and treating cocaine addiction.


2021 ◽  
Author(s):  
Tatiana D. Viena ◽  
Gabriela E. Rasch ◽  
Timothy A. Allen

AbstractThe paraventricular nucleus (PVT) of the midline thalamus is a critical higher-order cortico-thalamo-cortical integration site that plays a critical role in various behaviors including reward seeking, cue saliency, and emotional memory. Anatomical studies have shown that PVT projects to both medial prefrontal cortex (mPFC) and hippocampus (HC). However, dual mPFC-HC projecting neurons which could serve a role in synchronizing mPFC and HC activity during PVT-dependent behaviors, have not been explored. Here we used a dual retrograde adenoassociated virus (AAV) tracing approach to characterize the location and proportion of different projection populations that send collaterals to mPFC and/or ventral hippocampus (vHC). Additionally, we examined the distribution of calcium binding proteins calretinin (CR) and calbindin (CB) with respect to these projection populations PVT. We found that PVT contains separate populations of cells that project to mPFC, vHC, and those that innervate both regions. Interestingly, dual mPFC-HC projecting cells expressed neither CR or CB. Topographically, mPFC- and vHC-projecting CB+ and CR+ cells clustered around dual projecting neurons in PVT. These results are consistent with the features of dual mPFC-vHC projecting cells in the nucleus reuniens (RE) and suggestive of a functional mPFC-PVT-vHC system that may support mPFC-vHC interactions in PVT-dependent behaviors.


2019 ◽  
Vol 31 (5) ◽  
pp. 1661-1674 ◽  
Author(s):  
Jungmeen Kim-Spoon ◽  
Kirby Deater-Deckard ◽  
Alexis Brieant ◽  
Nina Lauharatanahirun ◽  
Jacob Lee ◽  
...  

AbstractAdolescence is a period of heightened susceptibility to peer influences, and deviant peer affiliation has well-established implications for the development of psychopathology. However, little is known about the role of brain functions in pathways connecting peer contexts and health risk behaviors. We tested developmental cascade models to evaluate contributions of adolescent risk taking, peer influences, and neurobehavioral variables of risk processing and cognitive control to substance use among 167 adolescents who were assessed annually for four years. Risk taking at Time 1 was related to substance use at Time 4 indirectly through peer substance use at Time 2 and insular activation during risk processing at Time 3. Furthermore, neural cognitive control moderated these effects. Greater insular activation during risk processing was related to higher substance use for those with greater medial prefrontal cortex activation during cognitive control, but it was related to lower substance use among those with lower medial prefrontal cortex activation during cognitive control. Neural processes related to risk processing and cognitive control play a crucial role in the processes linking risk taking, peer substance use, and adolescents’ own substance use.


Brain ◽  
2018 ◽  
Vol 141 (12) ◽  
pp. 3361-3376 ◽  
Author(s):  
Baltazar Zavala ◽  
Anthony Jang ◽  
Michael Trotta ◽  
Codrin I Lungu ◽  
Peter Brown ◽  
...  

Abstract There is increasing evidence that the medial prefrontal cortex participates in conflict and feedback monitoring while the subthalamic nucleus adjusts actions. Yet how these two structures coordinate their activity during cognitive control remains poorly understood. We recorded from the human prefrontal cortex and the subthalamic nucleus simultaneously while participants (n = 22) performed a novel task involving high conflict trials, complete response inhibition trials, and trial-to-trial behavioural adaptations to conflict and errors. Overall, we found that within-trial adaptions to both conflict and complete response inhibition involved changes in the theta band while across-trial behavioural adaptations to both conflict and errors involved changes in the beta band (P < 0.05). Yet the role each region’s theta and beta oscillations played during the task differed significantly between the two sites. Trials that involved either within-trial conflict or complete response inhibition were associated with increased theta phase synchrony between the medial prefrontal cortex and the subthalamic nucleus (P < 0.05). Despite increased synchrony, however, increases in prefrontal theta power were associated with response inhibition, while increases in subthalamic theta power were associated with response execution (P < 0.05). In the beta band, post-response increases in prefrontal beta power were suppressed when the completed trial contained either conflict or an erroneous response (P < 0.05). Subthalamic beta power, on the other hand, was only modified during the subsequent trial that followed a conflict or error trial. Notably, these adaptation trials exhibited slower response times (P < 0.05), suggesting that both brain regions contribute to across-trial adaptations but do so at different stages of the adaptation process. Taken together, our data shed light on the mechanisms underlying within-trial and across-trial cognitive control and how disruption of this network can negatively impact cognition. More broadly, however, our data also demonstrate that the specific role of a brain region, rather than the frequency being utilized, governs the behavioural correlates of oscillatory activity.


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