Metabolic rate in the right amygdala predicts negative affect in depressed patients

Abstract

The role of the amygdala in major depression was investigated. Resting regional cerebral metabolic rate (rCMRglu) was measured with [18F]fluorodeoxyglucose positron emission tomography (PET) in two samples of subjects using two different PET cameras. The samples consisted of 10 and 17 medication-free depressives and 11 and 13 controls, respectively. Using coregistration of PET and magnetic resonance images, regions were individually delineated for the amygdala and thalamus, the latter of which was used as a control region. Within the depressed groups, right amygdalar rCMRglu was positively correlated with negative affect. Thalamic rCMRglu was not related to negative affect, and amygdalar rCMRglu accounted for a significant portion of variance in depressives' negative affect scores over and above the contribution of thalamic rCMRglu.

Decreased prefrontal, anterior cingulate, insula, and ventral striatal metabolism in medication-free depressed outpatients with bipolar disorder

“…Of note however, Tutus et al (1998) employed a different radiotracer ( 99m Tc-HMPAO) than used in all the remaining studies (FDG), which may have contributed to their failure to detect prefrontal hypometabolism. We did not find evidence of relative hypermetabolism in the left amygdala as reported in some (Drevets, 1999;Drevets et al, 2002Drevets et al, ,1992 but not all (Abercrombie et al, 1998) prior studies of unipolar major depressive disorder. Ketter et al found relative but not absolute increases in amygdala metabolism in treatment-resistant primarily rapid-cycling bipolar inpatients.…”

A pilot study of amygdala volumes in pediatric generalized anxiety disorder

“…Our results are also interesting in light of a recent PET study (Abercrombie et al 1998), showing that right amygdalar metabolic rates positively correlated with negative affect in depressed patients. Because behaviorally inhibited children were shown to be predisposed to depression, but not anxiety disorders, during young adulthood (Caspi et al 1996), prospective studies of right amygdalar function in pediatric GAD patients may foster a better understanding of the pathophysiology of adult onset depressive disorders.…”

Blockade of the GLT-1 Transporter in the Central Nucleus of the Amygdala Induces both Anxiety and Depressive-Like Symptoms

“…Deep brain stimulation data in patients with treatment-resistant depression suggest that there is a baseline increase in activation of area Cg25 that is normalized by deep brain stimulation treatment (Mayberg et al, 2005). And, some data suggest that there is an increase in activity of the amygdala that is positively correlated with MDD symptom severity (Abercrombie et al, 1998). These two sets of findings are likely related because the amygdala has dense connections and close proximity to area Cg25 (Ongur and Price, 2000).…”

“…These changes have been attributed to a decrease in glial cells, with both astrocytes and oligodendrocytes being reduced in number without a concomitant loss of neurons (Bowley et al, 2002;Gosselin et al, 2009;Altshuler et al, 2010). Treatment-resistant depression is also associated with increased metabolic activity in the amygdala (Ketter et al, 2001) which is positively correlated with negative affect (Abercrombie et al, 1998), suggesting that abnormally high amygdala activity may contribute to symptom severity. Increased glutamate levels in both the amygdala and prefrontal cortex have also been associated with MDD (Sanacora et al, 2004;Hashimoto et al, 2007), suggesting that increases in amygdala activity could be due to higher glutamate levels.…”