scholarly journals Acute Hyperglycemia Increases Brain Pregenual Anterior Cingulate Cortex Glutamate Concentrations in Type 1 Diabetes Mellitus

2020 ◽  
Author(s):  
Ada Admin ◽  
Nicolas R. Bolo ◽  
Alan M. Jacobson ◽  
Gail Musen ◽  
Matcheri S. Keshavan ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Depressive Symptoms ◽  
Anterior Cingulate Cortex ◽  
Emotional Processing ◽  
Response Times ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Emotional Stroop ◽  
Chronic Hyperglycemia

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.

scholarly journals Acute Hyperglycemia Increases Brain Pregenual Anterior Cingulate Cortex Glutamate Concentrations in Type 1 Diabetes Mellitus

2020 ◽  
Author(s):  
Ada Admin ◽  
Nicolas R. Bolo ◽  
Alan M. Jacobson ◽  
Gail Musen ◽  
Matcheri S. Keshavan ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Depressive Symptoms ◽  
Anterior Cingulate Cortex ◽  
Emotional Processing ◽  
Response Times ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Emotional Stroop ◽  
Chronic Hyperglycemia

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.

scholarly journals Hypoglycemic thalamic activation in type 1 diabetes is associated with preserved symptoms despite reduced epinephrine

2019 ◽  
Vol 40 (4) ◽  
pp. 787-798 ◽  
Author(s):  
Munachiso Nwokolo ◽  
Stephanie A Amiel ◽  
Owen O'Daly ◽  
Megan L Byrne ◽  
Bula M Wilson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Type 1 Diabetes ◽  
Cerebral Blood Flow ◽  
Anterior Cingulate Cortex ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Regional Cerebral Blood ◽  
Cerebral Blood Flow Change ◽  
Global Cerebral Blood Flow

Brain responses to low plasma glucose may be key to understanding the behaviors that prevent severe hypoglycemia in type 1 diabetes. This study investigated the impact of long duration, hypoglycemia aware type 1 diabetes on cerebral blood flow responses to hypoglycemia. Three-dimensional pseudo-continuous arterial spin labeling magnetic resonance imaging was performed in 15 individuals with type 1 diabetes and 15 non-diabetic controls during a two-step hyperinsulinemic glucose clamp. Symptom, hormone, global cerebral blood flow and regional cerebral blood flow responses to hypoglycemia were measured. Epinephrine release during hypoglycemia was attenuated in type 1 diabetes, but symptom score rose comparably in both groups. A rise in global cerebral blood flow did not differ between groups. Regional cerebral blood flow increased in the thalamus and fell in the hippocampus and temporal cortex in both groups. Type 1 diabetes demonstrated lesser anterior cingulate cortex activation; however, this difference did not survive correction for multiple comparisons. Thalamic cerebral blood flow change correlated with autonomic symptoms, and anterior cingulate cortex cerebral blood flow change correlated with epinephrine response across groups. The thalamus may thus be involved in symptom responses to hypoglycemia, independent of epinephrine action, while anterior cingulate cortex activation may be linked to counterregulation. Activation of these regions may have a role in hypoglycemia awareness and avoidance of problematic hypoglycemia.

scholarly journals Acute Hyperglycemia Increases Brain Pregenual Anterior Cingulate Cortex Glutamate Concentrations in Type 1 Diabetes

Diabetes ◽  
2020 ◽  
Vol 69 (7) ◽  
pp. 1528-1539
Author(s):  
Nicolas R. Bolo ◽  
Alan M. Jacobson ◽  
Gail Musen ◽  
Matcheri S. Keshavan ◽  
Donald C. Simonson
Keyword(s):  
Type 1 Diabetes ◽  
Anterior Cingulate Cortex ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Acute Hyperglycemia

370-P: Changes in Glutamate Dynamics in the Anterior Cingulate Cortex with Recurrent Hypoglycemia in Type 1 Diabetes

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 370-P
Author(s):  
YOUNG WOO PARK ◽  
DINESH DEELCHAND ◽  
ANJALI KUMAR ◽  
AMIR MOHEET ◽  
YUAN ZHANG ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Anterior Cingulate Cortex ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Recurrent Hypoglycemia

scholarly journals Modulation of anterior cingulate cortex reward and penalty signalling in medication-naive young-adult subjects with depressive symptoms following acute dose lurasidone

2019 ◽  
Vol 49 (08) ◽  
pp. 1365-1377 ◽  
Author(s):  
Selina A. Wolke ◽  
Mitul A. Mehta ◽  
Owen O'Daly ◽  
Fernando Zelaya ◽  
Nada Zahreddine ◽  
...  
Keyword(s):  
Depressive Symptoms ◽  
Anterior Cingulate Cortex ◽  
Cingulate Cortex ◽  
Reward Processing ◽  
Anterior Cingulate ◽  
Depression Severity ◽  
Placebo Condition ◽  
Double Blind ◽  
Monetary Incentive Delay ◽  
Reward Functions

AbstractBackgroundAberrations in reward and penalty processing are implicated in depression and putatively reflect altered dopamine signalling. This study exploits the advantages of a placebo-controlled design to examine how a novel D2antagonist with adjunctive antidepressant properties modifies activity in the brain's reward network in depression.MethodsWe recruited 43 medication-naïve subjects across the range of depression severity (Beck's Depression Inventory-II score range: 0–43), including healthy volunteers, as well as people meeting full-criteria for major depressive disorder. In a double-blind placebo-controlled cross-over design, all subjects received either placebo or lurasidone (20 mg) across two visits separated by 1 week. Functional magnetic resonance imaging with the Monetary Incentive Delay (MID) task assessed reward functions via neural responses during anticipation and receipt of gains and losses. Arterial spin labelling measured cerebral blood flow (CBF) at rest.ResultsLurasidone altered fronto-striatal activity during anticipation and outcome phases of the MID task. A significant three-way Medication-by-Depression severity-by-Outcome interaction emerged in the anterior cingulate cortex (ACC) after correction for multiple comparisons. Follow-up analyses revealed significantly higher ACC activation to losses in high-v.low depression participants in the placebo condition, with a normalisation by lurasidone. This effect could not be accounted for by shifts in resting CBF.ConclusionsLurasidone acutely normalises reward processing signals in individuals with depressive symptoms. Lurasidone's antidepressant effects may arise from reducing responses to penalty outcomes in individuals with depressive symptoms.

T136. Anterior Cingulate Cortex and Depressive Symptoms: A Structural MRI Study

2018 ◽  
Vol 83 (9) ◽  
pp. S181
Author(s):  
Hisham Ibrahim ◽  
Kulikova Alexandra ◽  
A. John Rush ◽  
E. Sherwood Brown
Keyword(s):  
Depressive Symptoms ◽  
Anterior Cingulate Cortex ◽  
Cingulate Cortex ◽  
Structural Mri ◽  
Anterior Cingulate ◽  
Mri Study

scholarly journals Testing a Developmental Model of Parental Warmth, Amygdala–Subgenual Anterior Cingulate Cortex Connectivity, and Depressive Symptoms in Adolescents During the COVID-19 Pandemic

2021 ◽  
Author(s):  
Jonas G. Miller ◽  
Tiffany C. Ho ◽  
Jaclyn Schwartz Kirshenbaum ◽  
Rajpreet Chahal ◽  
Anthony Gifuni ◽  
...  
Keyword(s):  
Depressive Symptoms ◽  
Anterior Cingulate Cortex ◽  
Family Environment ◽  
Mental Health Problems ◽  
Predictive Marker ◽  
Cingulate Cortex ◽  
Developmental Model ◽  
Anterior Cingulate ◽  
Parental Warmth ◽  
Subgenual Anterior Cingulate Cortex

Background: Neurobiological measures may serve as predictive markers of risk for and resilience to depressive symptoms during the COVID-19 pandemic. We tested a developmental model linking variation in amygdala–subgenual anterior cingulate cortex (sgACC) resting-state connectivity both to earlier experiences in the family environment and to subsequent vulnerability to depressive symptoms during the pandemic.Methods: We used data from a longitudinal study that included three waves (N=214 adolescents; ages 9-15 years at Time 1 (T1), 11-17 years at Time 2 (T2), and 12-19 years during the pandemic at Time 3 [T3]). We assessed parental warmth (T1), depressive symptoms (T1 to T3), and functional connectivity between the sgACC and basolateral (BLA) and centromedial amygdala (CMA) (T1 and T2). We modeled associations among early parental warmth, amygdala–sgACC connectivity, and depressive symptoms before and during the pandemic.Results: Less parental warmth was associated prospectively with stronger BLA–sgACC connectivity approximately two years later (=-.23, p=.021) over and above the effect of BLA–sgACC connectivity at T1. Stronger BLA–sgACC connectivity, in turn, was associated with heightened depressive symptoms, both before (r=.21, p=.031) and during the pandemic (=.22, p=.031; independent of the effect of pre-pandemic symptoms). Conclusion: Adolescents who experience less parental warmth may develop a pattern of BLA–sgACC connectivity that increases their risk for mental health problems during the pandemic. BLA–sgACC connectivity in early to middle adolescence may be a predictive marker of risk for depressive symptoms in general and specifically during periods of heightened stress.

Serotonin - 1A binding in the subgenual anterior cingulate cortex is associated with regional grey matter volume in striatum and temporal areas

2011 ◽  
Vol 26 (S2) ◽  
pp. 934-934
Author(s):  
C. Kraus ◽  
M. Savli ◽  
A. Hahn ◽  
P. Baldinger ◽  
A. Höflich ◽  
...  
Keyword(s):  
Anterior Cingulate Cortex ◽  
Receptor Binding ◽  
Emotional Processing ◽  
Grey Matter ◽  
Ventral Striatum ◽  
Cingulate Cortex ◽  
Magnetic Resonance Images ◽  
Anterior Cingulate ◽  
Grey Matter Volume ◽  
Matter Volume

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.

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