Reduced Volume of Limbic System–Affiliated Basal Ganglia in Mood Disorders:

Baumann, B.; Dános, P.; Krell, Dieter; Diekmann, Susanne; Leschinger, A.; Stauch, Renate; Wurthmann, C.; Bernstein, Hans‐Gert; Bogerts, Bernhard

doi:10.1176/jnp.11.1.71

Cited by 185 publications

(105 citation statements)

References 58 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…VS defining lines are displayed on an MRI coronal image, namely a bisector of the internal capsule (IC bisector) and VS separator, which is perpendicular to the IC bisector and passes through the dorsal corner of the lateral ventricles (Baumann et al, 1999). Table 3 displays the correlation coefficients for the baseline and poststress TSST cortisol levels (AUC) and subjective responses (AUC) to AMPH adjusted for age, gender, and saline-induced subjective response (AUC).…”

Section: Tsst Plasma Cortisol Levels and Subjective Drug Responsesmentioning

confidence: 99%

Association of Amphetamine-Induced Striatal Dopamine Release and Cortisol Responses to Psychological Stress

Wand

Oswald

McCaul

et al. 2007

Neuropsychopharmacol

148

View full text Add to dashboard Cite

Preclinical studies have shown that stress and glucocorticoids increase mesolimbic dopamine (DA) and thereby facilitate psychostimulant self-administration. The relationship between stress-induced cortisol and mesolimbic DA responses to psychostimulants has not been studied in humans. To test the hypotheses that glucocorticoid responses to psychological stress are correlated with DA and subjective responses to psychostimulants in humans, 25 healthy adults (18-29 years) completed the Trier Social Stress Test (TSST) and two positron emission tomography (PET) scans with high-specific [ 11 C]raclopride. The first scan was preceded by intravenous saline and the second by amphetamine (AMPH). Findings showed that stress-induced cortisol levels were positively associated with AMPH-induced DA release in the ventral striatum and other striatal regions. Subjects with higher cortisol responses to stress also reported more positive subjective drug effects with AMPH than subjects with lower responses. The results are consistent with preclinical findings showing an interrelationship between glucocorticoids and mesolimbic DA dynamics, which may influence psychostimulant self-administration in humans.

show abstract

Section: Tsst Plasma Cortisol Levels and Subjective Drug Responsesmentioning

confidence: 99%

Association of Amphetamine-Induced Striatal Dopamine Release and Cortisol Responses to Psychological Stress

Wand

Oswald

McCaul

et al. 2007

Neuropsychopharmacol

148

View full text Add to dashboard Cite

show abstract

“…Most studies of atrophy and survival of neurons in response to stress, as well as hormones of the hypothalamic-pituitary-adrenal (HPA) axis, have focused on the hippocampus. This is owing, in part, to the well-defined and easily studied neuronal populations of this limbic brain region, including the (Rajkowska et al 1999) • Laminar cortical thickness in layers III, V, and VI in subgenual anterior cingulate cortex (area 24) in BPD (Bouras et al 2001) • Volume of subgenual prefrontal cortex in familial MDD and BPD (Ongur et al 1998) • Volumes of nucleus accumbens (left), basal ganglia (bilateral) in MDD and BPD (Baumann et al 1999) • Para hippocampal cortex size (right) in suicide (Altshuler et al 1990) Reduced Neuronal Size and/or Density…”

Section: Stress and Glucocorticoids Modulate Neural Plasticity: Implimentioning

confidence: 99%

Enhancing neuronal plasticity and cellular resilience to develop novel, improved therapeutics for Difficult-to-Treat depression

Manji

Quiróz

Sporn

et al. 2003

Biological Psychiatry

445

259

View full text Add to dashboard Cite

“…Baumann and associates 43,44 reported reduced volumes of the left nucleus accumbens, the right putamen and bilateral pallidum externum in postmortem brain samples obtained from patients with unipolar MDD or BPD.…”

Section: Postmortem Morphometric Findingsmentioning

confidence: 99%

Neuroplasticity and cellular resilience in mood disorders

et al. 2000

View full text Add to dashboard Cite

Although mood disorders have traditionally been regarded as good prognosis diseases, a growing body of data suggests that the long-term outcome for many patients is often much less favorable than previously thought. Recent morphometric studies have been investigating potential structural brain changes in mood disorders, and there is now evidence from a variety of sources demonstrating significant reductions in regional CNS volume, as well as regional reductions in the numbers and/or sizes of glia and neurons. Furthermore, results from recent clinical and preclinical studies investigating the molecular and cellular targets of mood stabilizers and antidepressants suggest that a reconceptualization about the pathophysiology and optimal long-term treatment of recurrent mood disorders may be warranted. It is proposed that impairments of neuroplasticity and cellular resilience may underlie the pathophysiology of mood disorders, and further that optimal long-term treatment for these severe illnesses may only be achieved by the early and aggressive use of agents with neurotrophic/ neuroprotective effects. It is noteworthy that lithium, valproate and antidepressants indirectly regulate a number of factors involved in cell survival pathways including CREB, BDNF, bcl-2 and MAP kinases, and may thus bring about some of their delayed long-term beneficial effects via underappreciated neurotrophic effects. The development of novel treatments which more directly target molecules involved in critical CNS cell survival and cell death pathways have the potential to enhance neuroplasticity and cellular resilience, and thereby modulate the long-term course and trajectory of these devastating illnesses. Molecular Psychiatry (2000) 5, 578-593.Keywords: atrophy; cell death; neuroprotection; lithium; bcl-2; MAP kinase; neurite; neurotrophic; neurogenesis; N-acetylaspartate; gray matter There is mounting evidence that recurrent mood disorders-once considered 'good prognosis diseases'-are, in fact, often very severe and life-threatening illnesses. Recurrent mood disorders can have devastating long-term effects, and the cost of these illnesses in terms of human suffering, productivity and health care is enormous. Suicide is the cause of death in 10-20% of individuals, and in addition to suicide, mood disorders are associated with many other deleterious health-related effects. 1-5 Indeed, a recent study which controlled for physical illness, smoking and alcohol consumption found that the magnitude of the increased mortality risk conferred by the presence of high depressive symptoms was similar to that of stroke and congestive heart failure. 5 Not surprisingly, the costs associated with disability and premature death represent an economic burden of tens of billions of dollars annually in the United States alone. 1,6,7 It is now recognized that, for many patients, the long-term outCorrespondence: HK Manji, MD,

show abstract

Reduced Volume of Limbic System–Affiliated Basal Ganglia in Mood Disorders:

Cited by 185 publications

References 58 publications

Association of Amphetamine-Induced Striatal Dopamine Release and Cortisol Responses to Psychological Stress

Association of Amphetamine-Induced Striatal Dopamine Release and Cortisol Responses to Psychological Stress

Enhancing neuronal plasticity and cellular resilience to develop novel, improved therapeutics for Difficult-to-Treat depression

Neuroplasticity and cellular resilience in mood disorders

Contact Info

Product

Resources

About