Emotion-specific clues to the neural substrate of empathy

2002 ◽  
Vol 25 (1) ◽  
pp. 22-23
Author(s):  
Anthony P. Atkinson

Research only alluded to by Preston & de Waal (P&deW) indicates the disproportionate involvement of some brain regions in the perception and experience of certain emotions. This suggests that the neural substrate of primitive emotional contagion has some emotion-specific aspects, even if cognitively sophisticated forms of empathy do not. Goals for future research include determining the ways in which empathy is emotion-specific and dependent on overt or covert perception.

2018 ◽  
Author(s):  
Jay Joseph Van Bavel

We review literature from several fields to describe common experimental tasks used to measure human cooperation as well as the theoretical models that have been used to characterize cooperative decision-making, as well as brain regions implicated in cooperation. Building on work in neuroeconomics, we suggest a value-based account may provide the most powerful understanding the psychology and neuroscience of group cooperation. We also review the role of individual differences and social context in shaping the mental processes that underlie cooperation and consider gaps in the literature and potential directions for future research on the social neuroscience of cooperation. We suggest that this multi-level approach provides a more comprehensive understanding of the mental and neural processes that underlie the decision to cooperate with others.


2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Damien S. Fleur ◽  
Bert Bredeweg ◽  
Wouter van den Bos

AbstractMetacognition comprises both the ability to be aware of one’s cognitive processes (metacognitive knowledge) and to regulate them (metacognitive control). Research in educational sciences has amassed a large body of evidence on the importance of metacognition in learning and academic achievement. More recently, metacognition has been studied from experimental and cognitive neuroscience perspectives. This research has started to identify brain regions that encode metacognitive processes. However, the educational and neuroscience disciplines have largely developed separately with little exchange and communication. In this article, we review the literature on metacognition in educational and cognitive neuroscience and identify entry points for synthesis. We argue that to improve our understanding of metacognition, future research needs to (i) investigate the degree to which different protocols relate to the similar or different metacognitive constructs and processes, (ii) implement experiments to identify neural substrates necessary for metacognition based on protocols used in educational sciences, (iii) study the effects of training metacognitive knowledge in the brain, and (iv) perform developmental research in the metacognitive brain and compare it with the existing developmental literature from educational sciences regarding the domain-generality of metacognition.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Huoyin Zhang ◽  
Shiyunmeng Zhang ◽  
Jiachen Lu ◽  
Yi Lei ◽  
Hong Li

AbstractPrevious studies in humans have shown that brain regions activating social exclusion overlap with those related to attention. However, in the context of social exclusion, how does behavioral monitoring affect individual behavior? In this study, we used the Cyberball game to induce the social exclusion effect in a group of participants. To explore the influence of social exclusion on the attention network, we administered the Attention Network Test (ANT) and compared results for the three subsystems of the attention network (orienting, alerting, and executive control) between exclusion (N = 60) and inclusion (N = 60) groups. Compared with the inclusion group, the exclusion group showed shorter overall response time and better executive control performance, but no significant differences in orienting or alerting. The excluded individuals showed a stronger ability to detect and control conflicts. It appears that social exclusion does not always exert a negative influence on individuals. In future research, attention to network can be used as indicators of social exclusion. This may further reveal how social exclusion affects individuals' psychosomatic mechanisms.


Author(s):  
Brandon Gunasekera ◽  
Kelly Diederen ◽  
Sagnik Bhattacharyya

Abstract Background Evidence suggests that an overlap exists between the neurobiology of psychotic disorders and the effects of cannabinoids on neurocognitive and neurochemical substrates involved in reward processing. Aims We investigate whether the psychotomimetic effects of delta-9-tetrahydrocannabinol (THC) and the antipsychotic potential of cannabidiol (CBD) are underpinned by their effects on the reward system and dopamine. Methods This narrative review focuses on the overlap between altered dopamine signalling and reward processing induced by cannabinoids, pre-clinically and in humans. A systematic search was conducted of acute cannabinoid drug-challenge studies using neuroimaging in healthy subjects and those with psychosis Results There is evidence of increased striatal presynaptic dopamine synthesis and release in psychosis, as well as abnormal engagement of the striatum during reward processing. Although, acute THC challenges have elicited a modest effect on striatal dopamine, cannabis users generally indicate impaired presynaptic dopaminergic function. Functional MRI studies have identified that a single dose of THC may modulate regions involved in reward and salience processing such as the striatum, midbrain, insular, and anterior cingulate, with some effects correlating with the severity of THC-induced psychotic symptoms. CBD may modulate brain regions involved in reward/salience processing in an opposite direction to that of THC. Conclusions There is evidence to suggest modulation of reward processing and its neural substrates by THC and CBD. Whether such effects underlie the psychotomimetic/antipsychotic effects of these cannabinoids remains unclear. Future research should address these unanswered questions to understand the relationship between endocannabinoid dysfunction, reward processing abnormalities, and psychosis.


2020 ◽  
Author(s):  
Christoph Fraenz ◽  
Dorothea Metzen ◽  
Christian J. Merz ◽  
Helene Selpien ◽  
Nikolai Axmacher ◽  
...  

AbstractResearch has shown that fear acquisition, in reaction to potentially harmful stimuli or situations, is characterized by pronounced interindividual differences. It is likely that such differences are evoked by variability in the macro- and microstructural properties of brain regions involved in the processing of threat or safety signals from the environment. Indeed, previous studies have shown that the strength of conditioned fear reactions is associated with the cortical thickness or volume of various brain regions. However, respective studies were exclusively targeted at single brain regions instead of whole brain networks. Here, we tested 60 young and healthy individuals in a differential fear conditioning paradigm while they underwent fMRI scanning. In addition, we acquired T1-weighted and multi-shell diffusion-weighted images prior to testing. We used task-based fMRI data to define global brain networks which exhibited increased BOLD responses towards CS+ or CS- presentations, respectively. From these networks, we obtained mean values of gray matter density, neurite density, and neurite orientation dispersion. We found that mean gray matter density averaged across the CS+ network was significantly correlated with the strength of conditioned fear reactions quantified via skin conductance response. Measures of neurite architecture were not associated with conditioned fear reaction in any of the two networks. Our results extend previous findings on the relationship between brain morphometry and fear learning. Most importantly, our study is the first to introduce neurite imaging to fear learning research and discusses how its implementation can be improved in future research.


2021 ◽  
Vol 15 ◽  
Author(s):  
Zhenyao Ye ◽  
Chen Mo ◽  
Song Liu ◽  
Kathryn S. Hatch ◽  
Si Gao ◽  
...  

Tobacco smoking is an addictive behavior that supports nicotine dependence and is an independent risk factor for cancer and other illnesses. Its neurogenetic mechanisms are not fully understood but may act through alterations in the cerebral white matter (WM). We hypothesized that the vertical pleiotropic pathways, where genetic variants influence a trait that in turn influences another trait, link genetic factors, integrity of cerebral WM, and nicotine addiction. We tested this hypothesis using individual genetic factors, WM integrity measured by fractional anisotropy (FA), and nicotine dependence-related smoking phenotypes, including smoking status (SS) and cigarettes per day (CPDs), in a large epidemiological sample collected by the UK Biobank. We performed a genome-wide association study (GWAS) to identify previously reported loci associated with smoking behavior. Smoking was found to be associated with reduced WM integrity in multiple brain regions. We then evaluated two competing vertical pathways: Genes → WM integrity → Smoking versus Genes → Smoking → WM integrity and a horizontal pleiotropy pathway where genetic factors independently affect both smoking and WM integrity. The causal pathway analysis identified 272 pleiotropic single-nucleotide polymorphisms (SNPs) whose effects on SS were mediated by FA, as well as 22 pleiotropic SNPs whose effects on FA were mediated by CPD. These SNPs were mainly located in important susceptibility genes for smoking-induced diseases NCAM1 and IREB2. Our findings revealed the role of cerebral WM in the maintenance of the complex addiction and provided potential genetic targets for future research in examining how changes in WM integrity contribute to the nicotine effects on the brain.


2021 ◽  
pp. 0271678X2110477
Author(s):  
Laura Michiels ◽  
Nathalie Mertens ◽  
Liselot Thijs ◽  
Ahmed Radwan ◽  
Stefan Sunaert ◽  
...  

Functional alterations after ischemic stroke have been described with Magnetic Resonance Imaging (MRI) and perfusion Positron Emission Tomography (PET), but no data on in vivo synaptic changes exist. Recently, imaging of synaptic density became available by targeting synaptic vesicle protein 2 A, a protein ubiquitously expressed in all presynaptic nerve terminals. We hypothesized that in subacute ischemic stroke loss of synaptic density can be evaluated with 11C-UCB-J PET in the ischemic tissue and that alterations in synaptic density can be present in brain regions beyond the ischemic core. We recruited ischemic stroke patients to undergo 11C-UCB-J PET/MR imaging 21 ± 8 days after stroke onset to investigate regional 11C-UCB-J SUVR (standardized uptake value ratio). There was a decrease (but residual signal) of 11C-UCB-J SUVR within the lesion of 16 stroke patients compared to 40 healthy controls (ratiolesion/controls = 0.67 ± 0.28, p = 0.00023). Moreover, 11C-UCB-J SUVR was lower in the non-lesioned tissue of the affected hemisphere compared to the unaffected hemisphere (ΔSUVR = −0.17, p = 0.0035). The contralesional cerebellar hemisphere showed a lower 11C-UCB-J SUVR compared to the ipsilesional cerebellar hemisphere (ΔSUVR = −0.14, p = 0.0048). In 8 out of 16 patients, the asymmetry index suggested crossed cerebellar diaschisis. Future research is required to longitudinally study these changes in synaptic density and their association with outcome.


Author(s):  
Zakia Z Haque ◽  
Ranshikha Samandra ◽  
Farshad Alizadeh Mansouri

The concept of working memory refers to a collection of cognitive abilities and processes involved in the short-term storage of task-relevant information to guide the ongoing and upcoming behaviour and therefore describes an important aspect of executive control of behaviour for achieving goals. Deficits in working memory and related cognitive abilities have been observed in patients with brain damage or neuropsychological disorders and therefore it is important to better understand neural substrate and underlying mechanisms of working memory. Working memory relies on neural mechanisms that enable encoding, maintenance and manipulation of stored information as well as integrating them with ongoing and future goals. Recently, a surge in brain stimulation studies have led to development of various non-invasive techniques for localized stimulation of prefrontal and other cortical regions in humans. These brain stimulation techniques can potentially be tailored to influence neural activities in particular brain regions and modulate cognitive functions and behaviour. Combined use of brain stimulation with neuroimaging and electrophysiological recording have provided a great opportunity to monitor neural activity in various brain regions and non-invasively intervene and modulate cognitive functions in cognitive tasks. These studies have shed more light on the neural substrate and underlying mechanisms of working memory in humans. Here, we review findings and insight from these brain stimulation studies about the contribution of brain regions, and particularly prefrontal cortex, to working memory.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A161-A161
Author(s):  
E Pardilla-Delgado ◽  
L Ramirez Gomez ◽  
A Y Baena ◽  
M I Montes ◽  
Y Bocanegra ◽  
...  

Abstract Introduction Alzheimer’s disease (AD) impacts brain regions that control circadian regulation systems such as wakefulness and daytime physical activity. Recent evidence shows that AD pathology is damaging for wake-promoting neurons. Whether early changes in wakefulness and daytime activity occur during asymptomatic stages of familial AD (fAD) remains unknown. In this study, we aimed to investigate whether daytime activity differs between cognitively-unimpaired carriers of early-onset fAD and age-matched non-carrier family members. Further, we examined the associations between daytime activity and memory performance. Methods A total of 25 members of the large Colombian kindred with the Presenilin1 (PSEN1) E280A mutation were included in the study (9 mutation carriers and 16 non-carriers, mean age=38.2). PSEN1 mutation carriers develop dementia before the age of 50. All subjects underwent wrist actigraphy for 7-14 days to measure daytime activity (average activity per minute and per epoch), and completed the CERAD Word List Learning and the Free and Cued Selective Reminding Test (FCSRT). Results Compared to non-carriers, mutation carriers had less average daytime activity (Mann-Whitney U Test p=.04). Higher average daytime activity was associated with better memory recall in both the CERAD word list delayed recall (r=.47, p=.05) and the FCRST delayed total recall (r=.53, p=.02). No associations with age were observed. Conclusion Our results suggest that cognitively-unimpaired mutation carriers have reduced daytime activity, years before the onset of dementia. Reduced daytime activity in carriers is also associated with lower memory performance. Our preliminary findings add to the growing evidence that circadian dysfunction is present in early AD, and may play an important role in subsequent memory impairment. Future research with large samples is needed to further examine sleep and circadian dysfunction in asymptomatic individuals at genetic risk for AD. Support NIA 5R01AG054671-03 to YTQ


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