scholarly journals The Resting Brain Sets Support-Giving in Motion: Dorsomedial Prefrontal Cortex Activity During Momentary Rest Primes Supportive Responding

2020 ◽  
Vol 1 (1) ◽  
Author(s):  
Tristen K Inagaki ◽  
Sasha Brietzke ◽  
Meghan L Meyer

Abstract Humans give support, care, and assistance to others on a daily basis. However, the brain mechanisms that set such supportive behavior in motion are unknown. Based on previous findings demonstrating that activity in a portion of the brain’s default network—the dorsomedial prefrontal cortex (DMPFC)—during brief rest primes social thinking and behavior, momentary fluctuations in this brain region at rest may prime supportive responding. To test this hypothesis, 26 participants underwent functional magnetic resonance imaging (fMRI) while they alternated between deciding whether to give support to a close other in financial need, receive support for themselves, and make arbitrary decisions unrelated to support. Decisions were interleaved with brief periods of rest. Results showed that, within participants, spontaneous activity in the DMPFC during momentary periods of rest primed supportive-responding: greater activity in this region at the onset of a brief period of rest predicted, on a trial-by-trial basis, faster decisions to give support to the close other. Thus, activating the DMPFC as soon as our minds are free from external demands to attention may help individuals “default” to support-giving. Implications for understanding the prosocial functions of the resting brain are discussed.

2019 ◽  
Vol 15 (10) ◽  
pp. 1076-1085 ◽  
Author(s):  
Tristen K Inagaki ◽  
Meghan L Meyer

Abstract There is a growing appreciation for the health benefits of giving support, though variability in such behavior exists. Based on the possibility that the dorsomedial (DMPFC) default network subsystem is associated with social thinking and behavior, integrity of this subsystem may facilitate giving support to others. The current study tested associations between DMPFC subsystem connectivity at rest and tendencies related to giving support. During a functional magnetic resonance imaging session, 45 participants completed an emotional social cues task, a resting-state scan and self-report measures of social support. Supportive behavior during the month following the scan was also assessed. Greater DMPFC subsystem connectivity at rest was associated with greater support giving (though not receiving or perceiving support) at the time of the scan and one month later. Results held after adjusting for extraversion. In addition, greater resting-state DMPFC subsystem connectivity was associated with attenuated dorsal anterior cingulate cortex, anterior insula and amygdala activity to others’ negative emotional social cues, suggesting that DMPFC subsystem integrity at rest is also associated with the dampened withdrawal response proposed to facilitate care for others in need. Together, results begin to hint at an additional role for the ‘default’ social brain: giving support to others.


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.  


2018 ◽  
Vol 115 (42) ◽  
pp. 10630-10635 ◽  
Author(s):  
Lynda C. Lin ◽  
Yang Qu ◽  
Eva H. Telzer

Emotions usually occur in a social context; yet little is known about how similar and dissimilar others influence our emotions. In the current study, we examined whether ingroup and outgroup members have differential influence on emotion processing at the behavioral and neural levels. To this end, we recruited 45 participants to rate a series of images displaying people engaged in different emotional contexts. Participants then underwent an fMRI scan where they viewed the same images along with information on how ingroup and outgroup members rated them, and they were asked to rate the images again. We found that participants shifted their emotions to be more in alignment with the ingroup over the outgroup, and that neural regions implicated in positive valuation [ventral striatum (VS) and ventromedial prefrontal cortex (vmPFC)], mentalizing [dorsomedial prefrontal cortex (dmPFC), medial prefrontal cortex (mPFC), posterior superior temporal sulcus (pSTS), and temporal pole], as well as emotion processing and salience detection (amygdala and insula), linearly tracked this behavior such that the extent of neural activity in these regions paralleled changes in participants’ emotions. Results illustrate the powerful impact that ingroup members have on our emotions.


1990 ◽  
Vol 2 (4) ◽  
pp. 409-424 ◽  
Author(s):  
Nancy A. Breslin ◽  
Daniel R. Weinberger

AbstractSchizophrenia is being increasingly viewed as a neurodevelopmental disorder, that is, one in which early, fixed pathology becomes manifest clinically during the normal course of maturation of the brain. Evidence for this position comes first from neuroimaging research, such as (1) studies that demonstrate morphologic brain changes (such as ventriculomegaly on CT scans) even in first break patients; and (2) a lack of correlation between these morphologic changes and duration of illness. Another source of evidence is studies of normal brain development in rodents and primates, including research that shows (1) the prefrontal cortex is a late maturing part of the brain, and (2) lesions of the prefrontal cortex may be initially silent and show delayed onset of dysfunction as the brain matures. A neurodevelopmental approach to schizophrenia, in turn, has stimulated further work into the normal development of brain regions implicated in the illness, such as the frontal cortex. Thus, the fields of neuropsychiatry and neurodevelopment have been mutually stimulated during the course of this work. In addition, viewing schizophrenia in developmental terms may have implications for the understanding of changes in cognition and behavior during normal adolescence.


1985 ◽  
Vol 30 (12) ◽  
pp. 999-999
Author(s):  
Gerald S. Wasserman

Author(s):  
Burbaeva G.Sh. ◽  
Androsova L.V. ◽  
Vorobyeva E.A. ◽  
Savushkina O.K.

The aim of the study was to evaluate the rate of polymerization of tubulin into microtubules and determine the level of colchicine binding (colchicine-binding activity of tubulin) in the prefrontal cortex in schizophrenia, vascular dementia (VD) and control. Colchicine-binding activity of tubulin was determined by Sherlinе in tubulin-enriched extracts of proteins from the samples. Measurement of light scattering during the polymerization of the tubulin was carried out using the nephelometric method at a wavelength of 450-550 nm. There was a significant decrease in colchicine-binding activity and the rate of tubulin polymerization in the prefrontal cortex in both diseases, and in VD to a greater extent than in schizophrenia. The obtained results suggest that not only in Alzheimer's disease, but also in other mental diseases such as schizophrenia and VD, there is a decrease in the level of tubulin in the prefrontal cortex of the brain, although to a lesser extent than in Alzheimer's disease, and consequently the amount of microtubules.


2020 ◽  
Vol 25 (45) ◽  
pp. 4799-4805 ◽  
Author(s):  
Osvaldo Flores-Bastías ◽  
Gonzalo I. Gómez ◽  
Juan A. Orellana ◽  
Eduardo Karahanian

Background: High ethanol intake induces a neuroinflammatory response resulting in the subsequent maintenance of chronic alcohol consumption. The melanocortin system plays a pivotal role in the modulation of alcohol consumption. Interestingly, it has been shown that the activation of melanocortin-4 receptor (MC4R) in the brain decreases the neuroinflammatory response in models of brain damage other than alcohol consumption, such as LPS-induced neuroinflammation, cerebral ischemia, glutamate excitotoxicity, and spinal cord injury. Objectives: In this work, we aimed to study whether MC4R activation by a synthetic MC4R-agonist peptide prevents ethanol-induced neuroinflammation, and if alcohol consumption produces changes in MC4R expression in the hippocampus and hypothalamus. Methods: Ethanol-preferring Sprague Dawley rats were selected offering access to 20% ethanol on alternate days for 4 weeks (intermittent access protocol). After this time, animals were i.p. administered an MC4R agonist peptide in the last 2 days of the protocol. Then, the expression of the proinflammatory cytokines interleukin 6 (IL-6), interleukin 1-beta (IL-1β), and tumor necrosis factor-alpha (TNF-α) were measured in the hippocampus, hypothalamus and prefrontal cortex. It was also evaluated if ethanol intake produces alterations in the expression of MC4R in the hippocampus and the hypothalamus. Results: Alcohol consumption increased the expression of MC4R in the hippocampus and the hypothalamus. The administration of the MC4R agonist reduced IL-6, IL-1β and TNF-α levels in hippocampus, hypothalamus and prefrontal cortex, to those observed in control rats that did not drink alcohol. Conclusion: High ethanol consumption produces an increase in the expression of MC4R in the hippocampus and hypothalamus. The administration of a synthetic MC4R-agonist peptide prevents neuroinflammation induced by alcohol consumption in the hippocampus, hypothalamus, and prefrontal cortex. These results could explain the effect of α-MSH and other synthetic MC4R agonists in decreasing alcohol intake through the reduction of the ethanol-induced inflammatory response in the brain.


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