Neuroanatomical Evidence for Distinct Cognitive and Affective Components of Self

2006 ◽  
Vol 18 (9) ◽  
pp. 1586-1594 ◽  
Author(s):  
J. M. Moran ◽  
C. N. Macrae ◽  
T. F. Heatherton ◽  
C. L. Wyland ◽  
W. M. Kelley

This study examines whether the cognitive and affective components of self-reflection can be dissociated using functional magnetic resonance imaging. Using a simple paradigm in which subjects judged the personal relevance of personality characteristics that were either favorable (e.g., “honest”) or unfavorable (e.g., “lazy”, we found that distinct neural circuits in adjacent regions of the prefrontal cortex subserve cognitive and emotional aspects of self-reflection. The medial prefrontal cortex responded only to material that was self-descriptive, and this did not differ as a function of the valence of the trait. When material was judged to be self-relevant, the valence of the material was resolved in an adjacent region of ventral anterior cingulate. The nature of self is one of the most enduring questions in science, and researchers are now beginning to be able to decompose the neural operations that give rise to a unitary sense of self.

2018 ◽  
Author(s):  
Keno Juechems ◽  
Jan Balaguer ◽  
Santiago Herce Castañón ◽  
María Ruz ◽  
Jill X. O’Reilly ◽  
...  

AbstractHumans and other animals make decisions in order to satisfy their goals. However, it remains unknown how neural circuits compute which of multiple possible goals should be pursued (e.g. when balancing hunger and thirst) and combine these signals with estimates of available reward alternatives. Here, humans undergoing functional magnetic resonance imaging (fMRI) accumulated two distinct assets over a sequence of trials. Financial outcomes depended on the minimum cumulate of either asset, creating a need to maintain “value homeostasis” by redressing any imbalance among the assets. BOLD signals in the dorsal anterior cingulate cortex (dACC) tracked the level of homeostatic imbalance among goals, whereas the ventromedial prefrontal cortex (vmPFC) signalled the level of homeostatic redress incurred by a choice, rather than the overall amount received. These results suggest that a network of medial frontal brain regions compute a value signal that maintains homeostatic balance among internal goals.


Author(s):  
Jiameng Xu

How do our brains process and attach positive and negative value to the objects around us, the sensations we feel, and the experiences that we have? One method of examining these questions is to detect, using functional magnetic resonance imaging (fMRI), which areas of the human brain are activated when subjects are exposed to rewarding and aversive stimuli. Although many fMRI studies have concentrated on identifying a network of areas that become active in processing either reward or aversion, there is evidence of significant overlap between the “reward” and “aversion” networks, suggesting that the brain might process rewarding and aversive stimuli in a similar manner regardless of valence. Thus, a meta-analysis of fMRI studies involving rewarding and aversive stimuli was undertaken to determine the areas of the brain that are commonly and differentially activated by reward and aversion. The preliminary results indicate that regions of the prefrontal cortex, anterior cingulate cortex, amygdala, nucleus accumbens, hippocampus, and basal ganglia were commonly activated by rewarding and aversive stimuli, while areas including the insula, midcingulate cortex, and parts of the hippocampus were differentially activated. Locating such commonalities and differences might help in our understanding of how the brain ascribes value to our environment.  


2020 ◽  
Author(s):  
Jayne Morriss ◽  
Tiffany Bell ◽  
Nicolò Biagi ◽  
Tom Johnstone ◽  
Carien M. van Reekum

AbstractHeightened responding to uncertain threat is associated with anxiety disorder pathology. Here, we sought to determine if individual differences in self-reported intolerance of uncertainty (IU) underlie differential recruitment of neural circuitry during instructed threat of shock (n = 42). During the task, cues signalled uncertain threat of shock (50%) or certain safety from shock. Ratings, skin conductance and functional magnetic resonance imaging was acquired. Overall, participants displayed greater amygdala activation to uncertain threat vs. safe cues, in the absence of an effect of IU. However, we found that high was associated with greater activity in the medial prefrontal cortex and dorsomedial rostral prefrontal cortex to uncertain threat vs safe cues. These findings suggest that, during instructed threat of shock, IU is specifically related, over trait anxiety, to activation in prefrontal cortical regions. Taken together, these findings highlight the potential of self-reported IU in identifying mechanisms that may be related to conscious threat appraisal and anxiety disorder pathology.


2016 ◽  
Vol 36 (12) ◽  
pp. 2177-2193 ◽  
Author(s):  
Cornelia Helbing ◽  
Marta Brocka ◽  
Thomas Scherf ◽  
Michael T Lippert ◽  
Frank Angenstein

Several human functional magnetic resonance imaging studies point to an activation of the mesolimbic dopamine system during reward, addiction and learning. We previously found activation of the mesolimbic system in response to continuous but not to discontinuous perforant pathway stimulation in an experimental model that we now used to investigate the role of dopamine release for the formation of functional magnetic resonance imaging responses. The two stimulation protocols elicited blood-oxygen-level dependent responses in the medial prefrontal/anterior cingulate cortex and nucleus accumbens. Inhibition of dopamine D1/5 receptors abolished the formation of functional magnetic resonance imaging responses in the medial prefrontal/anterior cingulate cortex during continuous but not during discontinuous pulse stimulations, i.e. only when the mesolimbic system was activated. Direct electrical or optogenetic stimulation of the ventral tegmental area caused strong dopamine release but only electrical stimulation triggered significant blood-oxygen level-dependent responses in the medial prefrontal/anterior cingulate cortex and nucleus accumbens. These functional magnetic resonance imaging responses were not affected by the D1/5 receptor antagonist SCH23390 but reduced by the N-methyl-D-aspartate receptor antagonist MK801. Therefore, glutamatergic ventral tegmental area neurons are already sufficient to trigger blood-oxygen-level dependent responses in the medial prefrontal/anterior cingulate cortex and nucleus accumbens. Although dopamine release alone does not affect blood-oxygen-level dependent responses it can act as a switch, permitting the formation of blood-oxygen-level dependent responses.


2009 ◽  
Vol 15 (3) ◽  
pp. 383-393 ◽  
Author(s):  
HELEN M. GENOVA ◽  
FRANK G. HILLARY ◽  
GLENN WYLIE ◽  
BART RYPMA ◽  
JOHN DELUCA

AbstractAlthough it is known that processing speed deficits are one of the primary cognitive impairments in multiple sclerosis (MS), the underlying neural mechanisms responsible for impaired processing speed remain undetermined. Using BOLD functional magnetic resonance imaging, the current study compared the brain activity of 16 individuals with MS to 17 healthy controls (HCs) during performance of a processing speed task, a modified version of the Symbol Digit Modalities Task. Although there were no differences in performance accuracy, the MS group was significantly slower than HCs. Although both groups showed similar activation involving the precentral gyrus and occipital cortex, the MS showed significantly less cerebral activity than HCs in bilateral frontal and parietal regions, similar to what has been reported in aging samples during speeded tasks. In the HC group, processing speed was mediated by frontal and parietal regions, as well as the cerebellum and thalamus. In the MS group, processing speed was mediated by insula, thalamus and anterior cingulate. It therefore appears that neural networks involved in processing speed differ between MS and HCs, and our findings are similar to what has been reported in aging, where damage to both white and gray matter is linked to processing speed impairments (JINS, 2009, 15, 383–393).


2012 ◽  
Vol 117 (4) ◽  
pp. 868-877 ◽  
Author(s):  
Marieke Niesters ◽  
Najmeh Khalili-Mahani ◽  
Christian Martini ◽  
Leon Aarts ◽  
Joop van Gerven ◽  
...  

Background The influence of psychoactive drugs on the central nervous system has been investigated with positron emission tomography and task-related functional magnetic resonance imaging. However, it is not known how these drugs affect the intrinsic large-scale interactions of the brain (resting-state functional magnetic resonance imaging connectivity). In this study, the effect of low-dose S(+)-ketamine on intrinsic brain connectivity was investigated. Methods Twelve healthy, male volunteers received a 2-h intravenous S(+)-ketamine infusion (first hour 20 mg/70 kg, second hour 40 mg/70 kg). Before, during, and after S(+)-ketamine administration, resting-state brain connectivity was measured. In addition, heat pain tests were performed between imaging sessions to determine ketamine-induced analgesia. A mixed-effects general linear model was used to determine drug and pain effects on resting-state brain connectivity. Results Ketamine increased the connectivity most importantly in the cerebellum and visual cortex in relation to the medial visual network. A decrease in connectivity was observed in the auditory and somatosensory network in relation to regions responsible for pain sensing and the affective processing of pain, which included the amygdala, insula, and anterior cingulate cortex. Connectivity variations related to fluctuations in pain scores were observed in the anterior cingulate cortex, insula, orbitofrontal cortex, and the brainstem, regions involved in descending inhibition of pain. Conclusions Changes in connectivity were observed in the areas that explain ketamine's pharmacodynamic profile with respect to analgesia and psychedelic and other side effects. In addition, pain and ketamine changed brain connectivity in areas involved in endogenous pain modulation.


Sign in / Sign up

Export Citation Format

Share Document