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)

Previous investigations have indicated that one of the most consistent EEG sleep findings in depressive patients has been a shortened REM latency. On the basis of these studies, we have concluded that with the exception of drug withdrawal states (such as CNS depressant or amphetamine withdrawal and narcolepsy) shortened REM latency points to a strong affective component in the patient's illness. Short REM latency has also been observed in patients suffering from schizo-affective illness as well as in certain schizophrenic patients who require tricyclic antidepressants in their management. Furthermore, this psychobiologic marker is a persistent, rather than a transient phenomenon, and can be observed over a period of several weeks unless a patient's condition becomes more favorable through clinical intervention. This present report indicates that short REM latency is found in virtually all primary depressive illness and is absent in secondary depression. Thus, REM latency appears to be a dependable, measurable marker for diagnosing primary depression, and we argue that the phenomenon is independent of age, drug effect and changes in other sleep parameters. It is expected that EEG sleep and motor measurements can yield further significant data and improve differential diagnosis in psychiatry, in much the same way that laboratory data support other medical specialities.
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PMID:REM latency: a psychobiologic marker for primary depressive disease. 18 39

Chronic administration of amphetamine to cats (twice daily, in doses increasing from 5 to 15 mg/kg over a 10-day period) elicited a number of behaviors, e.g., limb flick and abortive groom, characteristic of the action of hallucinogenic drugs and dependent on a depression of central serotonergic neurotransmission. This drug treatment produced large decreases (-40 to -60%) in central nervous system serotonin (5-HT) and its major metabolite, 5-hydroxyindoleacetic acid (5-HIAA), when measured either 6 or 24 hr after the last amphetamine injection. The rate of limb flicking returned to a predrug level approximately 5 days after drug withdrawal, at which time 5-HT and 5-HIAA levels had returned to within 30 to 40% of base line. Both 5-HT and 5-HIAA returned to base-line levels within 14 days after drug withdrawal. Norepinephrine (NE), dopamine (DA) and DA metabolites were decreased 60 to 95% by chronic amphetamine treatment and showed little recovery within the 14 days after drug withdrawal. A second experiment examined the latency to onset of the behavioral and neurochemical changes with a constant dose of amphetamine (7.5 mg/kg, twice daily). Limb flicking was significantly increased above base-line levels following 3 days of amphetamine administration, at which time 5-HT and 5-HIAA levels were decreased 30 to 40%. NE, DA and DA metabolites were decreased approximately 50 to 90% by this treatment regimen. A third experiment examined the effects of a low dose of amphetamine (3.75 mg/kg), injected more frequently (every 6 hr for 6 days), to approximate the administration pattern in human amphetamine abuse. This treatment produced significant increases in limb flicking and abortive grooming on days 5 and 6 and resulted in 30 to 40% depletions of 5-HT and 5-HIAA. NE, DA and DA metabolites were decreased by approximately 50 to 90%. These data are discussed in relation to a role for serotonin in amphetamine psychosis and schizophrenia.
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PMID:Chronic amphetamine administration to cats: behavioral and neurochemical evidence for decreased central serotonergic function. 50 68

Patients with stable coronary artery disease commonly have transient myocardial ischemia with or without experiencing angina, but the prognostic implications of this "total ischemic burden" is still a matter of debate. We studied 112 consecutive patients with coronary artery disease, normal left ventricular function at rest and exercise-induced myocardial ischemia, a 24-hour ambulatory EKG was performed after drug withdrawal. The mean exercise duration was 572 +/- 192 seconds, with an ischemic threshold (ST depression = 1 mm) of 390 +/- 190 seconds). By Holter monitoring 30 patients had no ischemia and 82 (73%) had a total of 332 episodes of ST segment changes, the majority of which were asymptomatic (242/332, 73%). Among 82 patients with transient myocardial ischemia, 44 (54%) had only asymptomatic episodes. Nine patients (11%) complained of angina coincident to ST changes. Twenty-nine patients (35%) had both painful and painless ST segment alterations. All patients were prospectively followed-up while on conventional medical therapy. During a mean follow up of 25 +/- 10 months cardiac events occurred in 31 patients; there were 5 cardiac deaths, 3 non-fatal myocardial infarctions, 2 hospitalization for unstable angina and 21 revascularization procedures (PTCA or CABG). By multivariate analysis the number of stenotic vessels on coronary angiography was predictive of the events during the follow-up (p = 0.03), while other demographic, clinical, ergometric and angiographic variables were not influential. Event-free survival was similar for all subsets of transient myocardial ischemia (silent, symptomatic, or none).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prognostic value of total ischemic burden in patients with stable ischemic heart disease. 176 34

The authors sought a demonstration of the validity of brain stimulation reward (BSR) models of depression. It was predicted that chronic, but not acute antidepressant treatment would enhance BSR responding. Rats with medial forebrain bundle electrodes were separated into 4 groups that received either saline or desmethylimipramine at 5, 10, or 20 mg/kg daily. A rate-free, threshold measure that has not previously been employed in studies of BSR and antidepressants was used. BSR thresholds were monitored every 3rd day over a 9-day baseline period and an 18-day drug treatment period, and after 12 days of drug withdrawal. Groups did not differ from one another till the 15th and 18th day of drug treatment. The greatest effects were seen in the 10 and 20 mg groups. The 20 mg group returned to baseline after drug withdrawal, but the 10 mg group did not. The absolute size of the effect was considered to be small, leading the authors to speculate that antidepressants act on homeostatic mechanisms that stabilize BSR substrates, only indirectly enhancing transmission of the reward signal.
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PMID:Chronic DMI reduces thresholds for brain stimulation reward in the rat. 192 90

The main adverse reaction to the immunosuppressive drug cyclosporine is dose-dependent renal dysfunction. Although renal vasoconstriction without major tubular dysfunction is usually noted, recent studies have demonstrated an inhibition of renal cortical microsomal protein synthesis. Sprague-Dawley rats and appropriate pair-fed controls were given cyclosporine orally in doses of 5, 10, 25, and 50 mg/kg/day for periods up to 10 days. A dose-dependent decline in glomerular filtration rate and effective renal plasma flow was maximal by day 3 and did not worsen despite continued dosing. Microsomal protein synthesis as measured by [3H]leucine incorporation was also depressed in a dose-dependent fashion; however, inhibition did not reach the nadir until day 4, 1 day after renal dysfunction was established. When cyclosporine was discontinued, microsomal protein synthesis was normalized by 4 days after drug withdrawal; in contrast, the return of glomerular filtration rate and effective renal plasma flow to normal required 8 days after drug discontinuation. Tubular function as measured by fractional excretion of lithium, enzymuria, and urinary osmolality was well maintained despite the depression of renal hemodynamics. There was no evidence of tubular necrosis by light or electron microscopy. Although cyclosporine produces reductions in renal microsomal protein synthesis, measured by "run-off" translation assays, these effects appear unlikely to be the direct cause of acute renal dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cyclosporine-induced renal dysfunction: correlations between cellular events and whole kidney function. 193 33

We report the cases of three elderly patients presenting with insidious mental impairment whilst receiving both lipophilic and hydrophilic beta-adrenoceptor blocking agents (propranolol and atenolol respectively). In each case marked improvement occurred on drug withdrawal. Two of our cases probably had early senile dementia of the Alzheimer's type and continued to exhibit signs of mild mental impairment, but the third was restored to normal functioning. We found no evidence of impaired perfusion to suggest a vascular basis for the effect or of depression. We believe that beta-blockade may cause or exacerbate mental impairment in the elderly.
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PMID:Cognitive impairment associated with beta-blockade in the elderly. 208 52

This study suggests that depressive symptoms are less common in severe, chronic, schizophrenic inpatients than would be predicted if these symptoms were manifestations of negative symptoms or drug-induced parkinsonism. The findings further suggest that depressive symptoms in such patients are independent phenomena which conform to a depressive syndrome. This depression does not represent a misidentification of the negative symptoms affective flattening and alogia, as measured by the SANS, or parkinsonism or akathisia. The study findings fail to support the view that long-term depot antipsychotic medication plays an important role in the genesis of depression and dysphoria in chronic schizophrenic patients. Depressive symptoms were found to occur as frequently, and dysphoria more frequently, in schizophrenic patients in the year after drug withdrawal compared with patients continuing on maintenance drug treatment for the same period.
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PMID:Dysphoric and depressive symptoms in chronic schizophrenia. 257 73

A 28-day oral dosage test of miporamicin (MPM), a new macrolide antibiotic, was performed to assess its toxicologic potential in groups of male and female rats receiving the compound in feed. Five graded dosage levels of 0, 3,200, 8,000, 20,000, and 50,000 ppm were employed for treatment with MPM in feed and the treatment period was followed by a 28-day recovery phase observation period. 1. No deaths occurred throughout the course of the experiment. Animals receiving 50,000 ppm developed signs: ruffled hair coat and emaciation, which disappeared following withdrawal of the drug. 2. The MPM-50,000 group displayed depression of weight gain and decrease of feed and water intake during the treatment period. During the posttreatment recovery phase observation period the animals showed recovery in weight gain rate as well as in feed and water intake. 3. The achieved compound dosage was 273 mg/kg/day in males and 288 mg/kg/day in females in the MPM-3,200 group, 721 and 773 mg/kg/day respectively in the MPM-8,000 group, 1,738 and 1,856 mg/kg/day in the MPM-20,000 group, and 3,405 and 3,611 mg/kg/day in the MPM-50,000 group. 4. Hematological examinations revealed low values for RBC, WBC, hematocrit and hemoglobin concentration and decreased platelet counts in the MPM-50,000 group, which were considered to be due to the decreased feed intake. These changes disappeared or abated following withdrawal. 5. Of various serum biochemical parameters assessed, total protein, albumin, glucose and triglycerides showed lowered values in the MPM-50,000 group. All these changes were considered to be attributable to the decreased feed intake. During the ensuing recovery phase observation period, all these parameters showed restoration or abatement in parallel with the recovery in feed intake. 6. Urine analysis disclosed decrease of urine volume, lowered electrolyte concentration and elevation of urine osmolarity in the MPM-20,000 and the MPM-50,000 groups. These changes were considered to be secondary to cecal enlargement which is commonly seen with antibiotic medication, or to the decreased feed and water intake. Following drug withdrawal, all these changes disappeared with the recovery in feed and water intake and abatement of cecal hyperplasia. 7. At terminal necropsy, diminution of body fat and atrophy of the spleen and thymus that correlated with emaciation were noted in the MPM-50,000 group. Dose-related enlargement of the caecum was also noted in the treated groups. All these changes disappeared or abated following withdrawal.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Subacute toxicity study of miporamicin in rats by twenty-eight-day administration in feed]. 262 84

The effect of three dosage schedules on the expression of a withdrawal syndrome indicative of physical dependence on pentobarbital was determined in male Sprague-Dawley rats. Rats were prepared with an intraperitoneal cannula and were continuously infused with either saline (control) or pentobarbital sodium, using an escalating drug dosage schedule, for either 5 (PB-5), 13 (PB-13) or 20 (PB-20) days. Final doses reached were 500 mg/kg/day (PB-5) and 1000 mg/kg/day (PB-13). PB-20 rats reached 1000 mg/kg/day on day 13 and were maintained at this dose for an additional 7 days. Body weight, water consumption and assessment of CNS depression were obtained daily. Following the last day of pentobarbital infusion all rats were infused with saline for a 72-hour drug-free period. Water consumption, body weight and assessment of overt behavioral signs indicative of a drug withdrawal syndrome were obtained at specific times during the drug-free period. PB-5 rats showed little evidence of withdrawal while PB-20 rats demonstrated the greatest degree of withdrawal. Peak withdrawal scores were observed to be 1, 3.8 and 5 for PB-5, PB-13, and PB-20, respectively. Withdrawal scores for group PB-13 and PB-20 were found to be significantly greater than either control or PB-5 but were not significantly different from each other. Body weight for PB-13 and PB-20 mice declined slightly (nonsignificant) during the drug-free period while a significant decrease (40% decline) in water consumption was demonstrated by 24 hours of this period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intensity of the withdrawal syndrome varies with duration of pentobarbital administration. 262 53

Neuroendocrine abnormalities in depression have been regarded, by many authors, as relatively specific markers of nosological subtypes of the disorder, e.g. primary vs. secondary, endogenous vs. non-endogenous or unipolar vs. bipolar depression. They should reflect the same changes in central neurotransmitters (e.g. noradrenergic insufficiency and/or cholinergic hyperactivity) that were hypothesized as the cause of clinical symptoms. This view is challenged on the basis of our own neuroendocrine investigations in 317 psychiatric patients and 103 normal controls. According to these studies the abnormalities are nosologically rather unspecific. They are induced by a large variety of factors, e.g. emotional stress associated with the clinical symptomatology, weight loss due to malnutrition as a consequence of reduced appetite, medication and drug withdrawal. Stress-induced hypercortisolism appears to be the most common abnormality that may trigger other neuroendocrine dysfunctions, such as a blunted TSH response to TRH. Differences in neuroendocrine abnormalities of depressives are probably due to variations in the manifold factors influencing the hormonal axes involved, to temporal changes in hormonal patterns (e.g. one abnormality triggering another) and to individual differences in the basic activity and the responsiveness of the various axes.
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PMID:The nature of neuroendocrine abnormalities in depression: a controversial issue in contemporary psychiatry. 288 Mar 46


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