Neurocircuitry of Affective, Cognitive, and Regulatory Systems

2018 ◽  
Author(s):  
Annmarie MacNamara ◽  
K. Luan Phan
Keyword(s):  
Cognitive Processes ◽  
Brain Regions ◽  
Cognition And Emotion ◽  
Functional Perspective ◽  
Regulatory Systems ◽  
Affect And Cognition ◽  
Subcortical Regions ◽  
Response Output ◽  
And Function ◽  
Regulatory Functions

This chapter provides a review and synthesis of the neurocircuitry involved in affect and cognition and their interactions as it relates to regulatory functions. Cognition and emotion are considered together taking a more integrated, functional perspective. The chapter first gives an overview regarding structure and function of key brain regions, that is, prefrontal and cingulate regions, insula, and subcortical regions, as well as other temporal-parietal-occipital regions. Following this overview, the chapter proceeds with summarizing key neuroscientific findings as organized by cognitive processes and their relevance for emotion. The choice of processes reflects the key stages involved in responding to a stimulus, from the time of sensory input to behavioral response/output, namely perception, learning and memory central executive functions, cognitive appraisal, and reappraisal. The overall aim of the chapter is to provide a better understanding of cognitive-emotional interactions at the neurocircuit level.

scholarly journals Silence, Solitude, and Serotonin: Neural Mechanisms Linking Hearing Loss and Social Isolation

2020 ◽  
Vol 10 (6) ◽  
pp. 367
Author(s):  
Sarah M. Keesom ◽  
Laura M. Hurley
Keyword(s):  
Hearing Loss ◽  
Social Isolation ◽  
Human Subjects ◽  
Brain Regions ◽  
Neural Systems ◽  
Depression And Anxiety ◽  
Auditory Cognition ◽  
Regulatory Systems ◽  
Two Factors ◽  
And Function

For social animals that communicate acoustically, hearing loss and social isolation are factors that independently influence social behavior. In human subjects, hearing loss may also contribute to objective and subjective measures of social isolation. Although the behavioral relationship between hearing loss and social isolation is evident, there is little understanding of their interdependence at the level of neural systems. Separate lines of research have shown that social isolation and hearing loss independently target the serotonergic system in the rodent brain. These two factors affect both presynaptic and postsynaptic measures of serotonergic anatomy and function, highlighting the sensitivity of serotonergic pathways to both types of insult. The effects of deficits in both acoustic and social inputs are seen not only within the auditory system, but also in other brain regions, suggesting relatively extensive effects of these deficits on serotonergic regulatory systems. Serotonin plays a much-studied role in depression and anxiety, and may also influence several aspects of auditory cognition, including auditory attention and understanding speech in challenging listening conditions. These commonalities suggest that serotonergic pathways are worthy of further exploration as potential intervening mechanisms between the related conditions of hearing loss and social isolation, and the affective and cognitive dysfunctions that follow.

scholarly journals Desikan-Killiany-Tourville Atlas Compatible Version of M-CRIB Neonatal Parcellated Whole Brain Atlas: The M-CRIB 2.0

2018 ◽  
Author(s):  
Bonnie Alexander ◽  
Wai Yen Loh ◽  
Lillian G. Matthews ◽  
Andrea L. Murray ◽  
Chris Adamson ◽  
...  
Keyword(s):  
Brain Regions ◽  
Brain Atlas ◽  
Whole Brain ◽  
Brain Structure And Function ◽  
Postmenstrual Age ◽  
Mri Scans ◽  
Subcortical Regions ◽  
Cortical Regions ◽  
And Function ◽  
Ventral Diencephalon

AbstractOur recently published M-CRIB atlas comprises 100 neonatal brain regions including 68 compatible with the widely-used Desikan-Killiany adult cortical atlas. A successor to the Desikan-Killiany atlas is the Desikan-Killiany-Tourville atlas, in which some regions with unclear boundaries were removed, and many existing boundaries were revised to conform to clearer landmarks in sulcal fundi. Our first aim here was to modify cortical M-CRIB regions to comply with the Desikan-Killiany-Tourville protocol, in order to offer: a) compatibility with this adult cortical atlas, b) greater labelling accuracy due to clearer landmarks, and c) optimisation of cortical regions for integration with surface-based infant parcellation pipelines. Secondly, we aimed to update subcortical regions in order to offer greater compatibility with subcortical segmentations produced in FreeSurfer. Data utilized were the T2-weighted MRI scans in our M-CRIB atlas, for ten healthy neonates (postmenstrual age at MRI 40-43 weeks, 4 female), and corresponding parcellated images. Edits were performed on the parcellated images in volume space using ITK-SNAP. Cortical updates included deletion of frontal and temporal poles and ‘Banks STS’, and modification of boundaries of many other regions. Changes to subcortical regions included the addition of ‘ventral diencephalon’, and deletion of ‘subcortical matter’ labels. A detailed updated parcellation protocol was produced. The resulting whole-brain M-CRIB 2.0 atlas comprises 94 regions altogether. This atlas provides comparability with adult Desikan-Killiany-Tourville-labelled cortical data and FreeSurfer-labelled subcortical data, and is more readily adaptable for incorporation into surface-based neonatal parcellation pipelines. As such, it offers the ability to help facilitate a broad range of investigations into brain structure and function both at the neonatal time point and developmentally across the lifespan.

Inefficient Encoding as an Explanation for Age-Related Deficits in Recollection-Based Processing

2014 ◽  
Vol 28 (3) ◽  
pp. 148-161 ◽  
Author(s):  
David Friedman ◽  
Ray Johnson
Keyword(s):  
Older Adults ◽  
Young Adults ◽  
Cognitive Processes ◽  
Brain Activity ◽  
Memory Performance ◽  
Brain Regions ◽  
Semantic Retrieval ◽  
Age Related ◽  
The Face ◽  
Episodic Memories

A cardinal feature of aging is a decline in episodic memory (EM). Nevertheless, there is evidence that some older adults may be able to “compensate” for failures in recollection-based processing by recruiting brain regions and cognitive processes not normally recruited by the young. We review the evidence suggesting that age-related declines in EM performance and recollection-related brain activity (left-parietal EM effect; LPEM) are due to altered processing at encoding. We describe results from our laboratory on differences in encoding- and retrieval-related activity between young and older adults. We then show that, relative to the young, in older adults brain activity at encoding is reduced over a brain region believed to be crucial for successful semantic elaboration in a 400–1,400-ms interval (left inferior prefrontal cortex, LIPFC; Johnson, Nessler, & Friedman, 2013 ; Nessler, Friedman, Johnson, & Bersick, 2007 ; Nessler, Johnson, Bersick, & Friedman, 2006 ). This reduced brain activity is associated with diminished subsequent recognition-memory performance and the LPEM at retrieval. We provide evidence for this premise by demonstrating that disrupting encoding-related processes during this 400–1,400-ms interval in young adults affords causal support for the hypothesis that the reduction over LIPFC during encoding produces the hallmarks of an age-related EM deficit: normal semantic retrieval at encoding, reduced subsequent episodic recognition accuracy, free recall, and the LPEM. Finally, we show that the reduced LPEM in young adults is associated with “additional” brain activity over similar brain areas as those activated when older adults show deficient retrieval. Hence, rather than supporting the compensation hypothesis, these data are more consistent with the scaffolding hypothesis, in which the recruitment of additional cognitive processes is an adaptive response across the life span in the face of momentary increases in task demand due to poorly-encoded episodic memories.

scholarly journals Brain Long Noncoding RNAs: Multitask Regulators of Neuronal Differentiation and Function

Molecules ◽  
2021 ◽  
Vol 26 (13) ◽  
pp. 3951
Author(s):  
Sarva Keihani ◽  
Verena Kluever ◽  
Eugenio F. Fornasiero
Keyword(s):  
Neuronal Differentiation ◽  
Neuronal Excitability ◽  
Noncoding Rnas ◽  
Long Noncoding Rnas ◽  
Regulatory Mechanisms ◽  
Control Robustness ◽  
Living Organisms ◽  
And Function ◽  
Regulatory Functions ◽  
Neuronal Physiology

The extraordinary cellular diversity and the complex connections established within different cells types render the nervous system of vertebrates one of the most sophisticated tissues found in living organisms. Such complexity is ensured by numerous regulatory mechanisms that provide tight spatiotemporal control, robustness and reliability. While the unusual abundance of long noncoding RNAs (lncRNAs) in nervous tissues was traditionally puzzling, it is becoming clear that these molecules have genuine regulatory functions in the brain and they are essential for neuronal physiology. The canonical view of RNA as predominantly a ‘coding molecule’ has been largely surpassed, together with the conception that lncRNAs only represent ‘waste material’ produced by cells as a side effect of pervasive transcription. Here we review a growing body of evidence showing that lncRNAs play key roles in several regulatory mechanisms of neurons and other brain cells. In particular, neuronal lncRNAs are crucial for orchestrating neurogenesis, for tuning neuronal differentiation and for the exact calibration of neuronal excitability. Moreover, their diversity and the association to neurodegenerative diseases render them particularly interesting as putative biomarkers for brain disease. Overall, we foresee that in the future a more systematic scrutiny of lncRNA functions will be instrumental for an exhaustive understanding of neuronal pathophysiology.

scholarly journals Static and dynamic functional connectivity supports the configuration of brain networks associated with creative cognition

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Abhishek Uday Patil ◽  
Sejal Ghate ◽  
Deepa Madathil ◽  
Ovid J. L. Tzeng ◽  
Hsu-Wen Huang ◽  
...  
Keyword(s):  
Cognitive Processes ◽  
Large Scale ◽  
Brain Networks ◽  
Blood Oxygen Level Dependent ◽  
Detection Algorithm ◽  
Brain Regions ◽  
Creative Cognition ◽  
Network Flexibility ◽  
Community Detection Algorithm ◽  
Window Approach

AbstractCreative cognition is recognized to involve the integration of multiple spontaneous cognitive processes and is manifested as complex networks within and between the distributed brain regions. We propose that the processing of creative cognition involves the static and dynamic re-configuration of brain networks associated with complex cognitive processes. We applied the sliding-window approach followed by a community detection algorithm and novel measures of network flexibility on the blood-oxygen level dependent (BOLD) signal of 8 major functional brain networks to reveal static and dynamic alterations in the network reconfiguration during creative cognition using functional magnetic resonance imaging (fMRI). Our results demonstrate the temporal connectivity of the dynamic large-scale creative networks between default mode network (DMN), salience network, and cerebellar network during creative cognition, and advance our understanding of the network neuroscience of creative cognition.

scholarly journals Spine impairment in mice high-expressing neuregulin 1 due to LIMK1 activation

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Peng Chen ◽  
Hongyang Jing ◽  
Mingtao Xiong ◽  
Qian Zhang ◽  
Dong Lin ◽  
...  
Keyword(s):  
Neural Development ◽  
Protein Level ◽  
Brain Regions ◽  
Postmortem Brain ◽  
Pathophysiological Mechanism ◽  
Brain Disorders ◽  
Spine Density ◽  
Genes Encoding ◽  
High Level ◽  
And Function

AbstractThe genes encoding for neuregulin1 (NRG1), a growth factor, and its receptor ErbB4 are both risk factors of major depression disorder and schizophrenia (SZ). They have been implicated in neural development and synaptic plasticity. However, exactly how NRG1 variations lead to SZ remains unclear. Indeed, NRG1 levels are increased in postmortem brain tissues of patients with brain disorders. Here, we studied the effects of high-level NRG1 on dendritic spine development and function. We showed that spine density in the prefrontal cortex and hippocampus was reduced in mice (ctoNrg1) that overexpressed NRG1 in neurons. The frequency of miniature excitatory postsynaptic currents (mEPSCs) was reduced in both brain regions of ctoNrg1 mice. High expression of NRG1 activated LIMK1 and increased cofilin phosphorylation in postsynaptic densities. Spine reduction was attenuated by inhibiting LIMK1 or blocking the NRG1–LIMK1 interaction, or by restoring NRG1 protein level. These results indicate that a normal NRG1 protein level is necessary for spine homeostasis and suggest a pathophysiological mechanism of abnormal spines in relevant brain disorders.

scholarly journals HIV Infection Is Associated with Attenuated Frontostriatal Intrinsic Connectivity: A Preliminary Study

2015 ◽  
Vol 21 (3) ◽  
pp. 203-213 ◽  
Author(s):  
Jonathan C. Ipser ◽  
Gregory G. Brown ◽  
Amanda Bischoff-Grethe ◽  
Colm G. Connolly ◽  
Ronald J. Ellis ◽  
...  
Keyword(s):  
Hiv Infection ◽  
Brain Regions ◽  
Group Differences ◽  
Hiv Rna ◽  
Functional Connections ◽  
Intrinsic Connectivity ◽  
Dorsolateral Prefrontal ◽  
Independent Replication ◽  
Subcortical Regions ◽  
The Brain

AbstractHIV-associated cognitive impairments are prevalent, and are consistent with injury to both frontal cortical and subcortical regions of the brain. The current study aimed to assess the association of HIV infection with functional connections within the frontostriatal network, circuitry hypothesized to be highly vulnerable to HIV infection. Fifteen HIV-positive and 15 demographically matched control participants underwent 6 min of resting-state functional magnetic resonance imaging (RS-fMRI). Multivariate group comparisons of age-adjusted estimates of connectivity within the frontostriatal network were derived from BOLD data for dorsolateral prefrontal cortex (DLPFC), dorsal caudate and mediodorsal thalamic regions of interest. Whole-brain comparisons of group differences in frontostriatal connectivity were conducted, as were pairwise tests of connectivity associations with measures of global cognitive functioning and clinical and immunological characteristics (nadir and current CD4 count, duration of HIV infection, plasma HIV RNA). HIV – associated reductions in connectivity were observed between the DLPFC and the dorsal caudate, particularly in younger participants (<50 years, N=9). Seropositive participants also demonstrated reductions in dorsal caudate connectivity to frontal and parietal brain regions previously demonstrated to be functionally connected to the DLPFC. Cognitive impairment, but none of the assessed clinical/immunological variables, was also associated with reduced frontostriatal connectivity. In conclusion, our data indicate that HIV is associated with attenuated intrinsic frontostriatal connectivity. Intrinsic connectivity of this network may therefore serve as a marker of the deleterious effects of HIV infection on the brain, possibly via HIV-associated dopaminergic abnormalities. These findings warrant independent replication in larger studies. (JINS, 2015, 21, 1–11)

scholarly journals Differential Promotion of Glutamate Transporter Expression and Function by Glucocorticoids in Astrocytes from Various Brain Regions

2005 ◽  
Vol 280 (41) ◽  
pp. 34924-34932 ◽  
Author(s):  
Jürgen Zschocke ◽  
Nadhim Bayatti ◽  
Albrecht M. Clement ◽  
Heidrun Witan ◽  
Maciej Figiel ◽  
...  
Keyword(s):  
Glutamate Transporter ◽  
Brain Regions ◽  
And Function ◽  
Transporter Expression

Animal Models of Down Syndrome

2021 ◽  
Author(s):  
Anna J. Moyer ◽  
Roger H. Reeves
Keyword(s):  
Down Syndrome ◽  
Cognitive Impairment ◽  
Intellectual Disability ◽  
Animal Models ◽  
Brain Regions ◽  
Laboratory Mice ◽  
Tremendous Progress ◽  
New Treatments ◽  
And Function ◽  
Early Developmental

Is intellectual disability a treatable feature of persons with Down syndrome? Researchers have made tremendous progress in the last 30 years, from creating the first mouse model of Down syndrome to completing the first major clinical trial for cognitive impairment in people with Down syndrome. Until recently, normalizing brain development and function seemed too lofty a goal, and indeed, even proposing a candidate therapy requires answering a number of difficult questions. How does trisomy 21, a molecular diagnosis, cause the clinical phenotypes of Down syndrome? When, where, and how do trisomic genes act to disrupt normal development and which genes are involved with which outcomes? Which brain regions and behaviors are most impaired? Is there an early developmental window of time during which treatments are most effective? This article discusses how animal models such as laboratory mice can be used to understand intellectual disability and to develop new treatments for cognitive impairment.

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