The effect of antidepressant drugs on regional cerebral glucose utilization in the rat

Gerber, J; Choki, Jun-ichiro; Brunswick, David J.; Reivich, Martin; Frazer, Alan

doi:10.1016/0006-8993(83)90142-7

Cited by 38 publications

(14 citation statements)

References 18 publications

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“…These data are compatible with preclinical evidence that chronic antidepressant drug treatments suppress amygdala function 33–36. Horovitz35 observed that direct injection of antidepressant drugs (ADs) into and specific lesions of the centromedial amygdaloid nucleus produced identical effects in animal models used to predict AD efficacy.…”

Section: Neuroimaging Abnormalities In the Amygdala In Mood Disorderssupporting

confidence: 52%

Neuroimaging Abnormalities in the Amygdala in Mood Disorders

Drevets¹

2003

Annals of the New York Academy of Sciences

471

254

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Neuroimaging technology has been applied to investigate the pathophysiology of mood disorders in studies aimed at characterizing the anatomical correlates of depressive symptoms, the neurophysiological effects of antidepressant treatments, and the trait‐like abnormalities that persist despite symptom remission. These studies have identified cerebral blood flow and metabolic differences between depressives and controls in the amygdala and anatomically related areas of the prefrontal cortex, striatum, and thalamus. Taken together with converging evidence from neuroendocrine, lesion analysis, and postmortem studies of clinically depressed subjects, these data suggest that emotional/stress‐response systems that include the amygdala are pathologically activated in major depression and that this activity is associated with dysfunction of the prefrontal cortex and monoamine neurotransmitter systems that normally modulate such responses.

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Section: Neuroimaging Abnormalities In the Amygdala In Mood Disorderssupporting

confidence: 52%

Neuroimaging Abnormalities in the Amygdala in Mood Disorders

Drevets¹

2003

Annals of the New York Academy of Sciences

471

254

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“…48 Initial observations supported that treatment with desmethylimipramine for 7 days resulted in increase in glucose utilization in several brain areas, but that treatment for 28 days was inhibitory. 49 Data on oxidative energy metabolism suggest that IMI had a maximum stimulation of respiration in the brain mitochondria that was sustained after 1-and 2-week treatment. 50 It should however be noted that IMI at high concentrations can inhibit ATPase activity; 51 moreover, uncoupling effects on oxidative phosphorylation in rat liver mitochondria have been described with melipramine.…”

Section: Discussionmentioning

confidence: 99%

St John's wort and imipramine-induced gene expression profiles identify cellular functions relevant to antidepressant action and novel pharmacogenetic candidates for the phenotype of antidepressant treatment response

Wong¹,

O'Kirwan²,

Hannestad³

et al. 2004

Mol Psychiatry

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Both the prototypic tricyclic antidepressant imipramine (IMI) and the herbal product St John's wort (SJW) can be effective in the treatment of major depressive disorder. We studied hypothalamic gene expression in rats treated with SJW or IMI to test the hypothesis that chronic antidepressant treatment by various classes of drugs results in shared patterns of gene expression that may underlie their therapeutic effects. Individual hypothalami were hybridized to individual Affymetrix chips; we studied three arrays per group treatment. We constructed 95% confidence intervals for expression fold change for genes present in at least one treatment condition and we considered genes to be differentially expressed if they had a confidence interval excluding 1 (or À1) and had absolute difference in expression value of 10 or greater. SJW treatment differentially regulated 66 genes and expression sequence tags (ESTs) and IMI treatment differentially regulated 74 genes and ESTs. We found six common transcripts in response to both treatments. The likelihood of this occurring by chance is 1.14 Â 10 À23 . These transcripts are relevant to two molecular machines, namely the ribosomes and microtubules, and one cellular organelle, the mitochondria. Both treatments also affected different genes that are part of the same cell function processes, such as glycolytic pathways and synaptic function. We identified single-nucleotide polymorphisms in the human orthologs of genes regulated both treatments, as those genes may be novel candidates for pharmacogenetic studies. Our data support the hypothesis that chronic antidepressant treatment by drugs of various classes may result in a common, final pathway of changes in gene expression in a discrete brain region.

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“…For example, neurophysiological activity in the amygdala decreases in rats, monkeys, and/or humans during several antidepressant treatments, including drugs, vagal nerve stimulation, or deep brain stimulation of the anterior capsule, potentially reducing efferent transmission via the ACe (Drevets et al, 2002a;Sheline et al, 2001;Fu et al, 2004;Van Laere et al, 2006;Gerber et al, 1983;Henry et al, 1998). Notably, in rats Horovitz (1966) observed that injection of antidepressant drugs into the amygdala produced identical effects as lesions of the ACe in animal models used to predict antidepressant drug efficacy.…”

Section: Antidepressant Treatment Effectsmentioning

confidence: 99%

Neurocircuitry of Mood Disorders

Price

Drevets

2009

Neuropsychopharmacol

1,401

1,101

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This review begins with a brief historical overview of attempts in the first half of the 20th century to discern brain systems that underlie emotion and emotional behavior. These early studies identified the amygdala, hippocampus, and other parts of what was termed the 'limbic' system as central parts of the emotional brain. Detailed connectional data on this system began to be obtained in the 1970s and 1980s, as more effective neuroanatomical techniques based on axonal transport became available. In the last 15 years these methods have been applied extensively to the limbic system and prefrontal cortex of monkeys, and much more specific circuits have been defined. In particular, a system has been described that links the medial prefrontal cortex and a few related cortical areas to the amygdala, the ventral striatum and pallidum, the medial thalamus, the hypothalamus, and the periaqueductal gray and other parts of the brainstem. A large body of human data from functional and structural imaging, as well as analysis of lesions and histological material indicates that this system is centrally involved in mood disorders.

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The effect of antidepressant drugs on regional cerebral glucose utilization in the rat

Cited by 38 publications

References 18 publications

Neuroimaging Abnormalities in the Amygdala in Mood Disorders

Neuroimaging Abnormalities in the Amygdala in Mood Disorders

St John's wort and imipramine-induced gene expression profiles identify cellular functions relevant to antidepressant action and novel pharmacogenetic candidates for the phenotype of antidepressant treatment response

Neurocircuitry of Mood Disorders

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