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

When retinas from dark-adapted C57BL/6 mice were incubated in the dark for 5 min at 37 degrees C in Earle's medium, they contained 80-120 pmol/mg protein of cGMP and about 13 pmol/mg protein of cAMP. When the incubation in darkness was in calcium-deficient Earle's medium with 3 mM EGTA, a 10-20 fold increase occurred in the cGMP level, peaking at 2-3 min, but no change occurred in cAMP. This elevated level fell in 3 min to normal dark levels on return to normal Earle's medium, but was still about three times that of control levels after 15 min in EGTA-containing solution. Bright light after 2 min of dark incubation of dark-adapted retinas resulted in a 40-50% fall in cGMP, and bright light sharply reduced the elevated dark cGMP level of retinas in calcium-deficient media with 3 mM EDTA. However, no depression of normal dark levels of cGMP has thus far been obtained by increasing external calcium levels, even in the presence of the ionophore A23187. All the above phenomena involving dark cGMP levels and calcium are similar in Earle's medium with 100 mM of K+ substituted for Na+. Congenic rodless (rd/rd) mouse retinas have less than 5% of control cGMP and show only traces of calcium sensitivity. Thus, the above phenomena in controls are likely to be largely occurring in rods. The data suggest a dependency of the dark cGMP level on the calcium level, but that the light-induced fall in cGMP may largely be calcium insensitive.
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PMID:Calcium and cyclic nucleotide regulation in incubated mouse retinas. 20 16

Six patients with bipolar II seasonal affective disorder (SAD) and seven normal control subjects rated their moods in winter at six fixed times each week-day during 1 week of dim and 2 weeks of bright light. The scales rated represent the mood dimension specifically associated with depression, a dimension here called behavioral engagement (BE). Compared with controls, depressed SAD subjects (1) showed lower BE levels across all rating times of the day, (2) were more likely to show diurnal variation in BE, (3) displayed more between-day instability in BE diurnal rhythm, and (4) exhibited greater short-term lability (change within 3 hours) in BE. Bright light reduced or eliminated all group differences in BE level and variability.
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PMID:Behavioral engagement level, variability, and diurnal rhythm as a function of bright light in bipolar II seasonal affective disorder: an exploratory study. 141 70

The 24-h rhythms of blood serotonin and serum melatonin were determined in 39 unmediated inpatients with nonseasonal affective disorder and in 14 healthy men and women after 7 days of morning bright-light (2500 lx) or dim-light (50 lx) treatment. Bright-light treatment led to a more than 50% decrease in the Hamilton Rating Scale for Depression (HRSD) score in 4/19 patients and dim light in 1/17 patients. After light treatment the mesor (the daily mean estimated by cosinor analysis) of patients' and subjects' melatonin levels did not change significantly, nor was there a correlation between phase change and decrease in HRSD score. We observed after bright- and dim-light treatment a consistent increase in blood serotonin in patients and healthy subjects, which differed significantly between healthy subjects and patients. These findings suggest the involvement of serotonergic mechanisms following light therapy.
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PMID:Blood serotonin, serum melatonin and light therapy in healthy subjects and in patients with nonseasonal depression. 152 35

Psychotropic drug-free hospitalized veterans with nonseasonal major depressive disorders or depressed forms of bipolar disorder were treated with light for 1 week. Twenty-five patients were randomly assigned to bright white light treatment (2000-3000 lux), and 26 patients were randomized to dim red light placebo control treatment. Unlike those treated with dim red light, those treated with bright white light showed declines in three measures of depression during treatment. Partial relapse appeared within 2 days. A global depression score showed a statistically significant (p = 0.02) difference favoring bright white light treatment. Two bright-light-treated patients became mildly hypomanic, but side effects were mild. Improvement was not correlated with patient expectations; indeed, patients expected somewhat greater benefit from the placebo. Patients treated in summer responded as well as those treated in winter. Baseline electroencephalogram (EEG) sleep stage data (e.g., rapid eye movement; REM latency) did not predict treatment responses. These 1-week treatment results suggest that bright light might produce benefits for patients with nonseasonal depression. Bright light should not be recommended for routine clinical application before additional assessments with longer treatment durations are done.
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PMID:Controlled trial of bright light for nonseasonal major depressive disorders. 173 74

In a randomized crossover design 19 patients with winter depression were treated with 7 days of bright morning light (6:00 to 8:00 AM) and 7 days of evening light (7:00 to 9:00 PM). Bright light in the morning reduced the Hamilton Depression Rating Scale score from 22.3 to 5.5; bright light in the evening decreased the Hamilton score from 21.0 to 12.2. Improvement in the depression as measured by the Hamilton Depression Rating scores was greater with morning light compared with evening lights. Hypersomnia was associated (p less than 0.05) with a superior response to morning light.
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PMID:Morning or evening bright light treatment of winter depression? The significance of hypersomnia. 199 83

Bright artificial light is used to treat patients with major depression with a seasonal component ("Winter Depression"). Hyperactivity of muscarinic cholinergic systems is implicated in the pathophysiology of depression. Continual exposure to bright light for 7 days or during discrete portions of the photoperiod blunts the thermic response to a muscarinic agonist (oxotremorine) in the rat. Exposure to either 24 hours per day of bright light (in contrast to periods of circumscribed exposure) or darkness would tend to produce free-running. Observers have suggested that the reduced responsiveness to oxotremorine may result from the induction of free-running (the "free-running hypothesis"). The "free-running hypothesis" leads to the prediction that rats exposed to constant darkness will exhibit a reduction in thermic responsiveness to oxotremorine. The authors hypothesized that constant exposure to darkness would, contrary to the "free-running hypothesis," enhance the thermic response to oxotremorine. Rats (n = 12) exposed to constant darkness for 7 days exhibited super-sensitivity to oxotremorine 5 days after return to standard light/dark cycle in the vivarium. This argues against the hypothesis that the induction of free-running enhances sensitivity to the thermic effects of oxotremorine.
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PMID:Exposure to constant darkness enhances the thermic response of the rat to a muscarinic agonist. 201 50

Similar symptomatology has been described for both seasonal affective disorder (SAD) and atypical depression. For example, hyperphagia, hypersomnia, and intense lethargy are common to both, suggesting that they might be subtypes of the same disorder. If SAD and atypical depression are different manifestations of the same underlying pathophysiology, treatment effective for one might also benefit the other. Bright artificial lights (2500 lux, 6-8 a.m. and p.m.) were significantly less effective in treating eight patients diagnosed as having atypical depression without a seasonal pattern than 25 SAD patients. Differential treatment outcome suggests that SAD and atypical depression are separate disorders.
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PMID:Is seasonal affective disorder a variant of atypical depression? Differential response to light therapy. 224 88

In a randomized crossover design, 7 patients with winter depression were treated with 7 d of bright morning light (0600 to 0800) and 7 d of evening light (2000 to 2200). Bright lights in the morning significantly reduced the Hamilton Rating Scale for Depression (HRSD) score (18.4 to 5.0); the bright light in the evening moderately decreased the HRSD score (19.4 to 15.1). The improvement in the HRSD score was significantly greater with morning light than with evening light.
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PMID:Bright light treatment of winter depression: morning versus evening light. 228 2

Bright light exposure has been found to alleviate the symptoms of recurrent winter depression in many patients. The mechanism of light therapy may involve shifts in the timing (phase) of circadian rhythms. In this study, morning light exposure (which shifts rhythms earlier) was compared with evening light exposure (which shifts rhythms later) in a double-blind, crossover design. The onset of melatonin secretion in the evening was measured under dim light conditions as a marker for circadian timing (phase) before and after each treatment. Eight patients with winter depression and five control subjects were studied. Morning light was found to be significantly better than evening light in reducing depressive symptoms. At baseline, there was a trend for the onset of melatonin production to be later in the patients than in the controls. Morning light shifted the melatonin onset significantly earlier in the patients but not the controls. Our findings suggest that patients with winter depression have circadian rhythms that are abnormally delayed and that bright light therapy benefits winter depression by providing a corrective advance.
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PMID:Morning vs evening light treatment for winter depression. Evidence that the therapeutic effects of light are mediated by circadian phase shifts. 232 85

Bright light is an effective treatment of winter depression. Study of the effects of this treatment on mechanisms thought to be involved in the pathophysiology of depressive disorders is reviewed. Measurement of a physiological parameter, namely the change in core temperature using an intraperitoneally implanted radio transmitter sensitive to temperature in freely moving rats, indicates that treatment with bright light under various experimental conditions tends to powerfully subsensitize muscarinic and nicotinic mechanisms. Pulses of bright light during the phase delay portions of the PRC blunt sensitivity to clonidine. Our studies with bright light are consistent with those indicating that heterocyclic antidepressants and a monoamine oxidase inhibitor produce subsensitivity to the thermic effects of nicotine. Reports of the influences of full-spectrum bright light and its impact on targeted neurotransmitter mechanisms call attention to the anatomical substratum mediating its effects. Possible receptor changes are measurable using receptor binding techniques and quantitative autoradiography. The physiological effects of this interesting treatment raises questions of its impact on coupling mechanisms and second messengers.
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PMID:Neurobiologic effects of bright artificial light. 262 98


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