Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have created transgenic mouse lines with impaired glucocorticoid receptor function by expression of a type II glucocorticoid receptor antisense RNA in brain tissues. These animals have endocrinological characteristics similar to those seen in depression, including a hyperactive hypothalamic-pituitary-adrenal axis as indicated by elevated plasma corticosterone and adrenocorticotropin hormone levels. Treatment of transgenic animals with the tricyclic antidepressant desipramine increased hypothalamic glucocorticoid receptor mRNA concentration and dexamethasone-binding activity while decreasing plasma adrenocorticotropin hormone concentration and corticosterone levels. These results support the hypothesis that antidepressants exert action on the hypothalamic-pituitary-adrenal axis through modulation of glucocorticoid receptor gene expression.
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PMID:Antidepressant drug action in a transgenic mouse model of the endocrine changes seen in depression. 148 Jan 37

Cerebrospinal fluid concentrations of corticotropin-releasing hormone (CRH), thyrotropin-releasing hormone (TRH) and somatostatin (SRIF) were measured in 77 female inpatients with moderate to extreme dementia and in 17 elderly female controls. Both multi-infarct (MID) and Alzheimer-type (SDAT) demented patients had equally elevated CSF CRH and TRH but not SRIF levels as compared with the controls. This elevation was, however, not seen in patients with simple dementia while it was most prominent in those exhibiting marked depressive symptoms. It is concluded that depression rather than dementia itself may be associated with CSF CRH and TRH elevation in elderly patients with cognitive impairment.
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PMID:Cerebrospinal fluid neuropeptides in dementia. 148 50

Controversy continues over the characteristics of beta-endorphin secretion in depression. Beta-endorphin plasma levels were measured in 30 drug-free male patients with a DSM-III-R major depressive disorder and 21 healthy controls. Depressed patients displayed significantly lower beta-endorphin plasma levels in baseline conditions, after the single dose metyrapone test, and after the dexamethasone suppression test. The activation of hypothalamic-pituitary-adrenal (HPA) axis in depression might be due, at least in part, to low levels of beta-endorphin. These results suggest that HPA axis dysregulation in depression may involve peptides other than ACTH.
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PMID:Beta-endorphin responses to metyrapone and dexamethasone in depressed patients. 149 94

1. There are major changes in progesterone, oestrogen, cortisol and beta-endorphin level associated with parturition, and as all these can be psychoactive it is likely that they contribute to the mood changes that can occur at this time. However evidence for their involvement is, at present, indirect. 2. Postnatal depression itself appears to be a heterogeneous condition with different times of onset, and it is probable that various biological and social factors play a role to a differing degree in different individuals. 3. About half of postnatal depression appears to arise in the first two weeks after childbirth. Some cases follow a period of early euphoria. 4. A different subgroup is associated with thyroid dysfunction, which peaks two to five months postpartum. 5. The tyramine test does not predict vulnerability to postnatal depression. 6. It is suggested that in future research the time course of onset of the depression, and the nature of the mood changes that occur in the first postpartum week, are investigated as possibly relevant variables.
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PMID:Do biochemical factors play a part in postnatal depression? 149 22

To determine whether the well-documented hyperactivity of the hypothalamic-pituitary-adrenal axis in depressed patients includes adrenal gland hypertrophy, adrenal gland size was evaluated by computed tomography. Assessments consisted of (1) global ratings by two radiologists ignorant of the diagnostic identity of the subjects and (2) calculation of adrenal volume. Of the 38 patients with major depression, 12 were rated as exhibiting adrenal hypertrophy. Adrenal volumes in the depressed patients were significantly increased when compared with those of normal controls. Adrenal gland size was not correlated with dexamethasone suppression test results, patient age, duration of the depressive episode, or depression severity. These results are concordant with the hypothesis that chronic corticotropin hypersecretion in depression results in adrenocortical hypertrophy. Adrenal gland enlargement may be a measure of cumulative lifetime depression.
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PMID:Adrenal gland enlargement in major depression. A computed tomographic study. 821 8

Mood states of cancer patients were assessed pre- and post-41.8 degrees C whole-body hyperthermia using the Profile of Mood States questionnaire. Results demonstrated a statistically significant increase in fatigue associated with decreased vigour which returned to baseline values by 72 h. In contrast, a significant improvement in depression was evident through 72 h following treatment. The relationship of this result to earlier studies of WBH-induced beta-endorphin is discussed.
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PMID:Changes in mood state following whole-body hyperthermia. 160 35

Advances in neuropeptide neurobiology in the last decade are illustrated by studies of corticotropin-releasing factor (CRF), the 41 amino acid-containing peptide that controls the anterior pituitary secretion of adrenocorticotropin and other pro-opiomelanocortin products. Corticotropin-releasing factor is synthesized in both hypothalamic and extrahypothalamic perikarya in a large prohormone form, (186 amino acids), then it is processed and transported to nerve terminals where it is released in its active form by a calcium-dependent mechanism. Corticotropin-releasing factor biosynthesis can now be measured by in situ hybridization because of the elucidation of the CRF gene sequence. Once released, CRF acts on high-affinity CRF receptors, and signal transduction is mediated by activation of adenylate cyclase in certain brain areas, and perhaps by phosphoinositide hydrolysis. In other brain areas CRF is inactivated by peptidases that degrade the hormone, though these are not well characterized. A CRF binding protein has been identified in plasma, and perhaps in brain. Considerable evidence exists from cerebrospinal fluid studies, postmortem tissue receptor measurements, and CRF stimulation test studies to support the hypothesis that CRF is hypersecreted in depression, resulting in both pituitary-adrenal axis hyperactivity and certain signs and symptoms of depression, e.g., decreased libido, insomnia, and decreased appetite. There is also evidence for an involvement of CRF in the pathophysiology of anxiety disorders and in the mechanism of action of benzodiazepines. The development of selective CRF-receptor antagonists will permit direct testing of the hypothesis that CRF hypersecretion is responsible for certain of the cardinal features of affective and anxiety disorders.
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PMID:New vistas in neuropeptide research in neuropsychiatry: focus on corticotropin-releasing factor. 161 Apr 87

This study examined the effects of a computerized functional electrical stimulation exercise program on plasma beta-endorphin-like immunoreactivity (BEP-ir), cortisol levels and depression parameters in spinal cord-injured individuals. Nine subjects from 1.2 to 33.5 yr postinjury with both motor and sensory complete lesions between C5 and T12 participated. It was determined that patients who sustained spinal cord-injuries less than 5 yr before this study had lower than normal baseline levels of BEP-ir and flattened circadian rhythms. Patients who sustained their injury greater than 5 yr before this study had higher baseline levels of BEP-ir with some return to normal circadian rhythmicity. Baseline cortisol levels, regardless of time since injury, appeared to be dysregulated. Regular exercise with computerized functional electrical stimulation caused significantly (P less than 0.05) sustained increases in BEP-ir in all patients and improved the regulation of cortisol. Furthermore, the more strenuous the exercise training, greater increases in BEP-ir levels were seen. Last, depression scores improved, which suggests a possible association between subjective mood and BEP-ir levels.
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PMID:Neuroendocrine changes during functional electrical stimulation. 162 80

The aim of this study was to determine the significance of the "coronary factor" in patients with essential hypertension (EH). Electrocardiogram Holter monitoring was performed in 61 patients with EH stage II (according to the World Health Organization criteria). Silent, ie, painless ST-segment depression, was found in 34 patients on whom echocardiography, a treadmill test, and transesophageal pacing were performed. In 21 patients with EH and silent ischemia, the examination included 201Tl stress scintigraphy, coronary angiography, and a platelet aggregation test. In 15 patients, catecholamines and beta-endorphins were obtained in blood samples during silent ischemia. 201Tl scintigraphy showed transient defects of perfusion without clearance abnormalities (group I) and with clearance abnormalities (group II). The patients in group I had more severe left ventricular hypertrophy (LVH) and a significantly higher platelet aggregation response to 0.5 mumol/L adenosine diphosphate; one patient in this group had coronary atherosclerosis. LVH and the platelet aggregation response was less pronounced in the patients in group II, but atherosclerotic lesions of a coronary artery were observed in four patients. In both groups, norepinephrine and beta-endorphin levels were increased during silent episodes of ischemia. The results suggest that there are different pathogenetic mechanisms of coronary insufficiency in patients with EH, a hypertensive heart, and silent ischemia.
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PMID:Silent myocardial ischemia in patients with essential hypertension. 163 37

Plasma beta-endorphin-like immunoreactivity (BEP-ir) and cortisol levels were measured by radioimmunoassay (RIA) in nine patients who were at least 12 months status post spinal cord injury (SCI). Plasma levels were obtained at 8:00 am and 4:00 pm to determine circadian rhythm, and on the day following administration of 1 mg dexamethasone, levels were again obtained at 8:00 am and 4:00 pm. The mean morning levels of plasma BEP-ir were significantly lower than control values for this laboratory (6.2 +/- 1.2 v 12.0 +/- 2.3 pg/mL). The morning BEP-ir values were lowest in patients who were closer to the time of injury (described by a second-order polynomial regression, R = .89; P less than .01). Mean morning cortisol levels were not significantly different from controls, but showed greater variability (mean, 15.1; range, 0.7 to 22.7 micrograms/dL v control, 15.5; range, 7 to 35). Dexamethasone suppressed cortisol secretion in all patients and BEP-ir levels in six of nine patients. Failure to detect BEP-ir suppression occurred in patients whose BEP-ir levels were less than 4.5 pg/mL and close to the minimum detection limit of the assay. Depression was present in five of nine patients as measured by the Beck Depression Inventory (BDI) and in three of nine patients as measured by the Hamilton Depression Scale (HSRD). However, the depression indices did not correlate with the neuroendocrine measures.
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PMID:beta-Endorphin and cortisol abnormalities in spinal cord-injured individuals. 164 Aug 43


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