Increased Activation of the Supragenual Anterior Cingulate Cortex during Visual Emotional Processing in Male Subjects with High Degrees of Alexithymia: An Event-Related fMRI Study

2010 ◽  
Vol 79 (6) ◽  
pp. 363-370 ◽  
Author(s):  
Alexander Heinzel ◽  
Ralf Schäfer ◽  
Hans-Wilhelm Müller ◽  
Andre Schieffer ◽  
Ariane Ingenhag ◽  
...  
2011 ◽  
Vol 26 (S2) ◽  
pp. 934-934
Author(s):  
C. Kraus ◽  
M. Savli ◽  
A. Hahn ◽  
P. Baldinger ◽  
A. Höflich ◽  
...  

IntroductionThe subgenual part of the anterior cingulate cortex (sgACC) has been frequently reported to be structurally and cytoarchitectually changed in major depressive disorder (MDD) and is also a promising target in deep brain stimulation in treatment-resistant MDD. Furthermore, substantial evidence demonstrates a high density of serotonin-1A (5-HT1A) receptors in the sgACC, a key area involved in emotional processing.ObjectivesHere, we investigated the relationship between the 5-HT1A receptor in the sgACC and changes in regional grey matter volume with voxel-based morphometry.MethodsPET ([carbonyl-11C]WAY-100635) was used to quantify 5-HT1A receptor binding (BPND) together with structural magnetic resonance images from 32 healthy subjects (mean 26.68 ± 5.1 years; 17 women). Regression analysis was performed in SPM8 (p < .001 uncorr.) using sgACC 5-HT1A BPND as regressor, controlling for sex, age and total grey matter volume (GMV).Results5-HT1A BPND in the sgACC was positively associated with regional GMV in the medial temporal gyri (T=4.37) and nucleus accumbens bilaterally (T = 4.19). Furthermore, sgACC 5-HT1A binding was negatively correlated with GMV within the inferior temporal gyri (T = 5.22) and putamen bilaterally (T = 5.12).ConclusionsOur findings demonstrate structural relationships between sgACC 5-HT1A receptor binding and grey matter volume in the ventral striatum as well as in temporal regions, which both exhibit close neuronal connections with the sgACC. Moreover, the GMV of the ventral striatum has been reported to be decreased in patients with MDD. Conclusively, our results underpin the role of serotonergic neuronal transmission in cytoarchitectural processes within regions involved in the modulation of mood.


NeuroImage ◽  
1998 ◽  
Vol 7 (4) ◽  
pp. S110 ◽  
Author(s):  
C.S. Carter ◽  
T. Braver ◽  
D.M. Barch ◽  
M. Botvinick ◽  
A. Sanders ◽  
...  

Author(s):  
Mikael A. Kowal ◽  
Arno Hazekamp ◽  
Lorenza S. Colzato ◽  
Henk van Steenbergen ◽  
Bernhard Hommel

2012 ◽  
Vol 18 (4) ◽  
pp. 739-748 ◽  
Author(s):  
Xingbao Li ◽  
Karen J. Hartwell ◽  
Jeffery Borckardt ◽  
James J. Prisciandaro ◽  
Michael E. Saladin ◽  
...  

2021 ◽  
Author(s):  
Anna M. Kazmierowska ◽  
Michal Szczepanik ◽  
Marek Wypych ◽  
Dawid Drozdziel ◽  
Artur Marchewka ◽  
...  

Humans often benefit from social cues when learning about the world. For instance, learning about threats from others can save the individual from dangerous first-hand experiences. Familiarity is believed to increase the effectiveness of social learning, but it is not clear whether it plays a role in learning about threats. Using functional magnetic resonance imaging, we undertook a naturalistic approach and investigated whether there was a difference between observational fear learning from friends and strangers. Participants (observers) witnessed either their friends or strangers (demonstrators) receiving aversive (shock) stimuli paired with colored squares (observational learning stage). Subsequently, participants watched the same squares, but without receiving any shocks (direct-expression stage). We observed a similar pattern of brain activity in both groups of observers. Regions related to threat responses (amygdala, anterior insula, anterior cingulate cortex) and social perception (fusiform gyrus, posterior superior temporal sulcus) were activated during the observational phase, reflecting the fear contagion process. The anterior insula and anterior cingulate cortex were also activated during the subsequent stage, indicating the expression of learned threat. Because there were no differences between participants observing friends and strangers, we argue that social threat learning is independent of the level of familiarity with the demonstrator.


Author(s):  
Ada Admin ◽  
Nicolas R. Bolo ◽  
Alan M. Jacobson ◽  
Gail Musen ◽  
Matcheri S. Keshavan ◽  
...  

The brain mechanisms underlying the association of hyperglycemia with depressive symptoms are unknown. We hypothesized that disrupted glutamate metabolism in pregenual anterior cingulate cortex (ACC) in type 1 diabetes (T1D) without depression affects emotional processing. Using proton magnetic resonance spectroscopy (MRS), we measured glutamate concentrations in ACC and occipital cortex (OCC) in 13 T1D without major depression (HbA1c=7.1±0.7% [54±7mmol/mol]) and 11 healthy non-diabetic controls (HbA1c=5.5±0.2% [37±3mmol/mol]) during fasting euglycemia (EU) followed by a 60-minute +5.5mmol/l hyperglycemic clamp (HG). Intrinsic neuronal activity was assessed using resting-state blood oxygen level dependent functional MRI to measure the fractional amplitude of low frequency fluctuations in slow-band 4 (fALFF4). Emotional processing and depressive symptoms were assessed using emotional tasks (Emotional-Stroop, Self-Referent-Encoding-Task SRET) and clinical ratings (HAM-D, SCL-90-R), respectively. During HG, ACC glutamate increased (1.2mmol/kg, +10%, p=0.014) while ACC fALFF4 was unchanged (-0.007, -2%, p=0.449) in T1D; in contrast, glutamate was unchanged (-0.2mmol/kg, -2%, p=0.578) while fALFF4 decreased (-0.05, -13%, p=0.002) in controls. OCC glutamate and fALFF4 were unchanged in both groups. T1D had longer SRET negative-word response-times (p=0.017) and higher depression-rating scores (HAM-D p=0.020; SCL-90-R-depression p=0.008). Higher glutamate change tended to associate with longer Emotional-Stroop response-times in T1D only. Brain glutamate must be tightly controlled during hyperglycemia due to the risk for neurotoxicity with excessive levels. Results suggest that ACC glutamate control mechanisms are disrupted in T1D, which affects glutamatergic neurotransmission related to emotional or cognitive processing. Increased prefrontal glutamate during acute hyperglycemic episodes could explain our previous findings of associations between chronic hyperglycemia, cortical thinning and depressive symptoms in T1D.


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