Dorsolateral Prefrontal Cortical Parallel Circuit in Schizophrenia: Postmortem Abnormalities

2002 ◽  
pp. 235-251
Author(s):  
Blynn G. Bunney ◽  
William E. Bunney ◽  
Richard Stein ◽  
Steven G. Potkin
Keyword(s):  
Prefrontal Cortical ◽  
Dorsolateral Prefrontal ◽  
Parallel Circuit

scholarly journals The Role of Primate Prefrontal Cortex in Bias and Shift Between Visual Dimensions

2019 ◽  
Vol 30 (1) ◽  
pp. 85-99 ◽  
Author(s):  
Farshad A Mansouri ◽  
Mark J Buckley ◽  
Daniel J Fehring ◽  
Keiji Tanaka
Keyword(s):  
Prefrontal Cortex ◽  
Anterior Cingulate ◽  
Top Down ◽  
Attentional Processes ◽  
Prefrontal Cortical ◽  
Frontopolar Cortex ◽  
Dorsolateral Prefrontal ◽  
Cortical Regions ◽  
Visual Cortical ◽  
Bilateral Lesions

Abstract Imaging and neural activity recording studies have shown activation in the primate prefrontal cortex when shifting attention between visual dimensions is necessary to achieve goals. A fundamental unanswered question is whether representations of these dimensions emerge from top-down attentional processes mediated by prefrontal regions or from bottom-up processes within visual cortical regions. We hypothesized a causative link between prefrontal cortical regions and dimension-based behavior. In large cohorts of humans and macaque monkeys, performing the same attention shifting task, we found that both species successfully shifted between visual dimensions, but both species also showed a significant behavioral advantage/bias to a particular dimension; however, these biases were in opposite directions in humans (bias to color) versus monkeys (bias to shape). Monkeys’ bias remained after selective bilateral lesions within the anterior cingulate cortex (ACC), frontopolar cortex, dorsolateral prefrontal cortex (DLPFC), orbitofrontal cortex (OFC), or superior, lateral prefrontal cortex. However, lesions within certain regions (ACC, DLPFC, or OFC) impaired monkeys’ ability to shift between these dimensions. We conclude that goal-directed processing of a particular dimension for the executive control of behavior depends on the integrity of prefrontal cortex; however, representation of competing dimensions and bias toward them does not depend on top-down prefrontal-mediated processes.

Dysregulated Prefrontal Cortical RhoA Signal Transduction in Bipolar Disorder with Psychosis: New Implications for Disease Pathophysiology

2019 ◽  
Vol 30 (1) ◽  
pp. 59-71
Author(s):  
Bailey A Kermath ◽  
Amanda M Vanderplow ◽  
Michael E Cahill
Keyword(s):  
Signal Transduction ◽  
Bipolar Disorder ◽  
Signal Transduction Pathway ◽  
Signal Transduction Pathways ◽  
Cellular Functions ◽  
Protein Activity ◽  
Cortical Function ◽  
Prefrontal Cortical ◽  
Dorsolateral Prefrontal ◽  
Key Factor

Abstract While research has identified alterations in dorsolateral prefrontal cortical function as a key factor to the etiology of bipolar disorder, few studies have uncovered robust changes in protein signal transduction pathways in this disorder. Given the direct relevance of protein-based expressional alterations to cellular functions and because many of the key regulatory mechanisms for the disease pathogenesis likely include alterations in protein activity rather than changes in expression alone, the identification of alterations in discrete signal transduction pathways in bipolar disorder would have broad implications for understanding the disease pathophysiology. As prior microarray data point to a previously unrecognized involvement of the RhoA network in bipolar disorder, here we investigate the protein expression and activity of key components of a RhoA signal transduction pathway in dorsolateral prefrontal cortical homogenates from subjects with bipolar disorder. The results of this investigation implicate overactivation of prefrontal cortical RhoA signaling in specific subtypes of bipolar disorder. The specificity of these findings is demonstrated by a lack of comparable changes in schizophrenia; however, our findings do identify convergence between both disorders at the level of activity-mediated actin cytoskeletal regulation. These findings have implications for understanding the altered cortical synaptic connectivity of bipolar disorder.

scholarly journals Mechanistic link between right prefrontal cortical activity and anxious arousal revealed using transcranial magnetic stimulation in healthy subjects

2019 ◽  
Vol 45 (4) ◽  
pp. 694-702 ◽  
Author(s):  
Nicholas L. Balderston ◽  
Emily M. Beydler ◽  
Camille Roberts ◽  
Zhi-De Deng ◽  
Thomas Radman ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Transcranial Magnetic Stimulation ◽  
Healthy Subjects ◽  
Magnetic Stimulation ◽  
Dorsolateral Prefrontal Cortex ◽  
Subcortical Structures ◽  
Prefrontal Cortical ◽  
Dorsolateral Prefrontal ◽  
Before And After ◽  
The Right

AbstractMuch of the mechanistic research on anxiety focuses on subcortical structures such as the amygdala; however, less is known about the distributed cortical circuit that also contributes to anxiety expression. One way to learn about this circuit is to probe candidate regions using transcranial magnetic stimulation (TMS). In this study, we tested the involvement of the dorsolateral prefrontal cortex (dlPFC), in anxiety expression using 10 Hz repetitive TMS (rTMS). In a within-subject, crossover experiment, the study measured anxiety in healthy subjects before and after a session of 10 Hz rTMS to the right dorsolateral prefrontal cortex (dlPFC). It used threat of predictable and unpredictable shock to induce anxiety and anxiety potentiated startle to assess anxiety. Counter to our hypotheses, results showed an increase in anxiety-potentiated startle following active but not sham rTMS. These results suggest a mechanistic link between right dlPFC activity and physiological anxiety expression. This result supports current models of prefrontal asymmetry in affect, and lays the groundwork for further exploration into the cortical mechanisms mediating anxiety, which may lead to novel anxiety treatments.

scholarly journals Convergence of case-specific epigenetic alterations identify a confluence of genetic vulnerabilities tied to opioid dependence

2021 ◽  
Author(s):  
Olivia Corradin ◽  
Richard Sallari ◽  
An T. Hoang ◽  
Bibi S Kassim ◽  
Gabriella Ben Hutta ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Opioid Dependence ◽  
Opioid Use Disorder ◽  
Opioid Overdose ◽  
Opioid Use ◽  
Prefrontal Cortical ◽  
Patient Heterogeneity ◽  
Dorsolateral Prefrontal ◽  
Number Of Sexual Partners ◽  
Genetic And Environmental Factors

Opioid dependence is a highly heterogeneous disease driven by a variety of genetic and environmental risk factors which have yet to be fully elucidated. We interrogated the effects of opioid dependence on the brain using ChIP-seq to quantify patterns of H3K27 acetylation in dorsolateral prefrontal cortical neurons isolated from 51 opioid-overdose cases and 51 accidental death controls. Among opioid cases, we observed global hypoacetylation and identified 388 putative enhancers consistently depleted for H3K27ac. Machine learning on H3K27ac patterns predicts case-control status with high accuracy. We focus on case-specific regulatory alterations, revealing 81,399 hypoacetylation events, uncovering vast inter-patient heterogeneity. We developed a strategy to decode this heterogeneity based on convergence analysis, which leveraged promoter-capture Hi-C to identify five genes over-burdened by alterations in their regulatory network or "plexus": ASTN2, KCNMA1, DUSP4, GABBR2, ENOX1. These convergent loci are enriched for opioid use disorder risk genes and heritability for generalized anxiety, number of sexual partners, and years of education. Overall, our multi-pronged approach uncovers neurobiological aspects of opioid dependence and captures genetic and environmental factors perpetuating the opioid epidemic.

Differential Expression Patterns of the TNF Pathway in Dorsolateral Prefrontal Cortical Regions (BA9/BA46) in Schizophrenia and Mood Disorder

2020 ◽  
Vol 87 (9) ◽  
pp. S271-S272
Author(s):  
Tharini Ketharanathan ◽  
Avril Pereira ◽  
Andrew Lawrence ◽  
Ian Everall ◽  
Suresh Sundram
Keyword(s):  
Mood Disorder ◽  
Differential Expression ◽  
Expression Patterns ◽  
Prefrontal Cortical ◽  
Dorsolateral Prefrontal ◽  
Cortical Regions
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