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1.
Psychol Med ; 42(5): 989-1001, 2012 May.
Article in English | MEDLINE | ID: mdl-22017808

ABSTRACT

BACKGROUND: The aim of this study is to examine the efficacy of mindfulness-based cognitive therapy (MBCT) in addition to treatment as usual (TAU) for recurrent depressive patients with and without a current depressive episode. METHOD: A randomized, controlled trial comparing MBCT+TAU (n=102) with TAU alone (n=103). The study population consisted of patients with three or more previous depressive episodes. Primary outcome measure was post-treatment depressive symptoms according to the Hamilton Rating Scale for Depression. Secondary outcome measures included the Beck Depression Inventory, rumination, worry and mindfulness skills. Group comparisons were carried out with linear mixed modelling, controlling for intra-group correlations. Additional mediation analyses were performed. Comparisons were made between patients with and without a current depressive episode. RESULTS: Patients in the MBCT+TAU group reported less depressive symptoms, worry and rumination and increased levels of mindfulness skills compared with patients receiving TAU alone. MBCT resulted in a comparable reduction of depressive symptoms for patients with and without a current depressive episode. Additional analyses suggest that the reduction of depressive symptoms was mediated by decreased levels of rumination and worry. CONCLUSIONS: The study findings suggest that MBCT is as effective for patients with recurrent depression who are currently depressed as for patients who are in remission. Directions towards a better understanding of the mechanisms of action of MBCT are given, although future research is needed to support these hypotheses.


Subject(s)
Cognitive Behavioral Therapy/methods , Depressive Disorder/therapy , Meditation/methods , Meditation/psychology , Psychotherapy, Group/methods , Awareness , Depressive Disorder/psychology , Female , Humans , Male , Middle Aged , Psychiatric Status Rating Scales/statistics & numerical data , Recurrence , Treatment Outcome
2.
J Neuroendocrinol ; 18(10): 797-805, 2006 Oct.
Article in English | MEDLINE | ID: mdl-16965298

ABSTRACT

In Xenopus laevis, corticotrophin-releasing factor (CRF) and urocortin 1 are present in the brain and they both are potent stimulators of alpha-melanophore stimulating hormone (MSH) secretion by melanotroph cells in the pituitary gland. Because both CRF and urocortin 1 bind with high affinity to CRF receptor type 1 (CRF1) in mammals and Xenopus laevis, one of the purposes of the present study was to identify the sites of action of CRF and urocortin 1 in the Xenopus brain and pituitary gland. Moreover, we raised the hypothesis that the external light intensity is a physiological condition controlling CRF1 expression in the pituitary melanotroph cells. By in situ hybridisation, the presence of CRF1 mRNA is demonstrated in the olfactory bulb, amygdala, nucleus accumbens, preoptic area, ventral habenular nuclei, ventromedial thalamic area, suprachiasmatic nucleus, ventral hypothalamic area, posterior tuberculum, tectum mesencephali and cerebellum. In the pituitary gland, CRF1 mRNA occurs in the intermediate and distal lobe. The optical density of the CRF1 mRNA hybridisation signal in the intermediate lobe of the pituitary gland is 59.4% stronger in white-adapted animals than in black-adapted ones, supporting the hypothesis that the environmental light condition controls CRF1 mRNA expression in melanotroph cells of X. laevis, a mechanism likely to be responsible for CRF- and/or urocortin 1-stimulated secretion of alpha-MSH.


Subject(s)
Brain Chemistry/genetics , Pituitary Gland/physiology , Receptors, Corticotropin-Releasing Hormone/physiology , Adaptation, Physiological , Animals , Brain Chemistry/drug effects , Corticotropin-Releasing Hormone/pharmacology , In Situ Hybridization , Lighting , Melanins/metabolism , Melanins/physiology , Pituitary Gland/drug effects , RNA, Messenger/biosynthesis , RNA, Messenger/genetics , Receptors, Corticotropin-Releasing Hormone/biosynthesis , Receptors, Corticotropin-Releasing Hormone/genetics , Urocortins , Xenopus laevis
3.
Gen Comp Endocrinol ; 147(3): 237-46, 2006 Jul.
Article in English | MEDLINE | ID: mdl-16483575

ABSTRACT

In mammals complex interactions between various brain structures and neuropeptides such as corticotropin-releasing factor (CRF) and urocortin 1 (Ucn1) underlay the control of feeding by the brain. Recently, in the amphibian Xenopus laevis, CRF- and Ucn1-immunoreactivities were shown in the hypothalamic magnocellular nucleus (Mg) and evidence was obtained for their involvement in food intake. To gain a better understanding of the brain structures controlling feeding in X. laevis, the effects of 16 weeks starvation on neurones immunoreactive (ir) to Fos and neuropeptides in various brain structures were quantified. In the Mg, compared to controls, starved animals showed fewer neurones immunopositive for Fos (-55.9%), Ucn1 (-44.0%), cocaine and amphetamine-regulated transcript (CART) (-94.3%) and metenkephalin (ENK) (-65.0%), whereas CRF-ir neurones were 2.1 times more numerous. These differences were mainly apparent in the ventral part of the Mg, followed by the medial and dorsal part of the nucleus. In the neural lobe of the pituitary gland a 22.5% lower optical density of CART-ir was observed. In the four other brain structures investigated, starvation had different effects. The dorsomedial part of the suprachiasmatic nucleus showed 5.9 times more NPY-ir cells and in the ventromedial thalamic area a lower number of NPY-ir cells (-33.6%) was found, whereas the Edinger-Westphal nucleus contained fewer CART-ir cells (-42.2%); no effect of starvation was seen in the ventral hypothalamic nucleus. Our results support the hypothesis that in X. laevis, the Mg plays a pivotal role in feeding-related processes and, moreover, that starvation also has neuropeptide- and brain structure-specific effects in other parts of the brain and in the pituitary gland, suggesting particular roles of these structures and their neuropeptides in physiological adaptation to starvation.


Subject(s)
Brain/metabolism , Neuropeptides/metabolism , Pituitary Gland/metabolism , Proto-Oncogene Proteins c-fos/metabolism , Starvation/metabolism , Xenopus/physiology , Animals , Appetite Regulation , Cell Size , Corticotropin-Releasing Hormone/metabolism , Enkephalin, Methionine/analogs & derivatives , Enkephalin, Methionine/metabolism , Immunohistochemistry , Nerve Tissue Proteins/metabolism , Neuropeptide Y/metabolism , Urocortins , Ventral Thalamic Nuclei/cytology , Ventral Thalamic Nuclei/physiology
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