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)

The s.c. administration of 20 mg/kg of morphine-HCl produced a decrease in the spontaneous locomotor activity (SLMA) of rats. The decrease in SLMA was significantly antagonized by p-chlorophenylalanine (p-CPA). When rats pretreated with p-CPA were given 5-hydroxytryptophan before morphine injection, the marked sedative response to morphine was restored, suggesting that the morphine-induced decrease in SLMA of rats may depend on the release of 5-hydroxytryptamine by morphine. By contrast, the s.c. administration of 5 mg/kg of morphine-HCl produced a significant increase in SLMA of rats. The magnitude of the increase was reduced by atropine, scopolamine or alpha-methyl-p-tyrosine. It appears that both adrenergic and cholinergic mechanisms participate in the increase in SLMA of rats induced by morphine. Both the increase in SLMA produced by 5 mg/kg of morphine and the decrease in SLMA induced by 20 mg/kg of morphine were completely antagonized by the s.c. administration of naloxone-HCl, 0.0625 and 0.25 mg/kg, respectively. Thus, it appears that the receptor with which morphine interacts to produce stimulation is chemically identical with or very similar to the receptor with which morphine combines to induce depression. The former receptors, however, are likely to be located on different neurons from the latter.
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PMID:Effects of humoral modulators and naloxone on morphine-induced changes in the spontaneous locomotor activity of the rat. 0 52

The effect of the factor that inhibits the release of melanocyte stimulating hormone (MSH), i.e., L-prolyl-L-leucyl-glycinamide (MIF), and L-prolyl-N-methyl-D-leucyl-glycinamide, an analog, on brain norepinephrine (NE), dopamine (DA) and serotonin (5-HT) turnover was examined in rats. The analog (40 mg/kg i.p.), in a fashion similar to MIF (40 and 5 mg/kg i.p.), increased brain DA turnover; only MIF (40 mg/kg i.p.) increased endogenous DA levels. The analog (40 and 5 mg/kg i.p.) decreased brain NE turnover; MIF at the same doses was ineffective. Neither MIF nor the analog affected rat brain 5-HT turnover or the 5-HTP-induced behavioural syndrome in the mouse. These results indicate that the analog, like MIF, exerts effects on central catecholamine turnover. The different biochemical profile of the analog compared to MIF may be importance with regard to potential clinical use in the treatment of Parkinson's disease and depression.
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PMID:Synthetic melanocyte stimulating hormone release-inhibiting factor (MIF). Part III: effect of L-prolyl-N-methyl-D-leucyl-glycinamide and MIF on biogenic amine turnover. 2 96

Biological functions are regulated by feedback mechanisms. In old age disorders occur in this regulation by insufficiency of biochemical transmitters. The synthesizing enzymes of Tyrosine Hydroxylase, Tryptophan Hydroxylase, Dopa Decarboxylase and 5-Hydroxytryptophan Decarboxylase are diminished in old age. Minus symptoms as depression, or exhaustion and disorders of circulation occur. A substitution by biogenic transmitters is not possible, because these don't pass the blood-brain-barriere. Therefore a medication of psychopharmacological drugs is necessary. For instance Anxiety--tranquilizer, exhaustion--anti depressive drugs.
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PMID:[Psychological problems of incurable patients in old age (author's transl)]. 4 75

The influence of serotonergic system on the changes in locomotor activity of mice and rats brought about by morphine, fentanyl, codeine and pentazocine and on morphine induced catalepsy in rats was studied. p-Chlorophenylalanine (pCPA) did not affect the behavioral changes produced in mice by morphine, fentanyl, codeine and pentazocine but reduced the behavioral depression produced by these drugs in rats. 5-Hydroxytryptophan (5-HTP) but not tryptophan (TP) reversed the action of pCPA on the effect of morphine and fentanyl. After reserpine the depression produced in rats by morphine and fentanyl was more pronounced. TP did not change the depression produced by combination of reserpine and morphine but counteracted the depression observed after combination of reserpine and fentanyl. In mice reserpine protected against hypermotility produced by morphine or fentanyl and TP potentiated the depression produced by the combination of reserpine and morphine or reserpine and fentanyl. Serotonin precursors, 5-HTP and TP evidently potentiated the morphine induced catalepsy. pCPA counteracted only the enhancement of the catalepsy observed after TP administration. Naloxone abolished the catalepsy after combined treatment with morphine and TP. Similarly but weaker acted cyproheptadine. The results suggest that the serotonin system plays a role in the effects of morphine and fentanyl on rat locomotor activity. An increase in the cerebral serotonin level increases the morphine catalepsy in rats.
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PMID:Central action of narcotic analgesics. V. Participation of serotonin in the mechanism of action of narcotic analgesics. 4 45

Tryptophan and 5-hydroxytryptophan have now been extensively investigated in affective disorders. There is now very good evidence that tryptophan increases the antidepressant activity of monoamine oxidase inhibitors. The antidepressant activity of tryptophan and 5-hydroxytryptophan has also been the subject of numerous investigations. There is evidence that patients with decreased cerebrospinal fluid concentration of 5-hydroxyindoleacetic acid respond particularly favourably to this treatment. The therapeutic activity of tryptophan has led to the investigation of the plasma concentration of tryptophan. Free plasma tryptophan, that is tryptophan unbound to plasma protein, appears decreased. There is also evidence that tryptophan and 5-HT transported are abnormal in depression.
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PMID:[Indoleamine precursors in depression (author's transl)]. 9 9

Central serotonin (5-hydroxytryptamine; 5-HT) metabolism can be disturbed in a subgroup of patients with vital (endogenous, primary) depression. Presumably these disturbances do not result from the depression and have a predisposing rather than a causative relationship to it. This latter statement is based on two observations. First, in a majority of patients, the 5-HT disturbances persist after depression has abated. Secondly, 5-hydroxytryptophan seems to have prophylactic value, in particular in patients with persistent abnormalities in central 5-HT metabolism. In this study we approached the hypothesis that 5-HT disturbances are a predisposing factor to the occurrence of depression from still another perspective. If this hypothesis is correct, then depressive patients with persistent 5-HT disturbances should have higher frequencies of depression than depressive patients without demonstrable 5-HT disturbances. This was indeed demonstrated. The same was true for family members of probands with low levels of 5-hydroxyindoleacetic acid. No cerebrospinal fluid data are available for family members. The reported findings strongly support the predisposition hypothesis.
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PMID:Central serotonin metabolism and frequency of depression. 9 33

The effect of L-5-hydroxytryptophan (L-5-HTP) against the depression of tumor-resisting power in host animal, which is induced by a whole body x-irradiation of 500 R, was studied. Host animal and tumor cell used were LAF, hybrid mouse and mastocytoma cell, respectively. The i.p. injected dose of L-5-HTP was 6.25 mg per mouse, which is most effective for protecting mice from radiation-induced hematopoietic death. In the experimental conditions, the agent was not effective to prevent the radiation-induced depression of tumor-resisting power of the animal.
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PMID:[Incapacity of 5-hydroxytryptophan to act against the depression of tumor-resisting power of host animal which is induced by whole body x-irradiation]. 12 90

C-fiber reflex were recorded from an ipsilateral S1 ventral root in the acute decerebrate spinal (T10) cat after stimulation of the superficial peroneal nerve. L-Tryptophan, infused in a dose of 150 mg/kg, increased the C-fiber reflex to 210% (S.E.M. +/- 30.1%) of control. This effect was antagonized by cyproheptadine, 0.5 mg/kg. L-Tryptophan increased the C-fiber reflex to 176% (S.E.M. +/- 13.0%) of control after p-chlorophenylalanine pretreatment. Pretreatment of the cats with the decarboxylase inhibitor alpha-methyldopa, 100 mg/kg, 30 minutes before infusion, antagonized the facilitatory effects of L-Tryptophan. L-Tryptophan, 150 mg/kg, had no effect on the monosynaptic or short latency polysynaptic reflexes. 5-Hydroxytryptophan, 20 mg/kg, had erratic effects on the C-fiber reflex producing both facilitation and depression which were not statistically significant. The recovery of tryptamine from brain perfusates, after perfusion of the anterior cerebellum and pons, with a modified Gaddum push-pull cannula, decreased across time. L-Tryptophan caused a slight increase in tryptamine release which was not statistically significant, whereas in cats pretreated with p-chlorophenyl alanine, a significant increase in tryptamine release was seen.
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PMID:The effect of L-tryptophan on spinal cord C-fiber reflexes. 13 Apr 82

The relative abilities of 1--3 mg/kg of desipramine (DES), imipramine (IMIP), amitriptyline (AMI), and chlorimipramine (CI-IMIP) to enhance synaptic transmission mediated by either NE or 5-HT were determined by testing their effects directly on NE or 5-HT transmission to sympathetic preganglionic neurons in unanesthetized, spinal cats. Effects on NE transmission were assessed on intraspinal excitatory pathways which utilize NE as a transmitter. Effects on 5-HT transmission were assessed on 5-HT-mediated depression of spinal sympathetic reflexes produced by 30 mg/kg of 5-HTP. Both DES and IMIP markedly enhanced transmission through the intraspinal excitatory NE pathways whereas AMI and CI-IMIP depressed transmission. However, both AMI and CI-IMIP modestly enhanced transmission in cats depleted of central 5-HT by pretreatment with parachlorophenylalanine. The relative potencies of the four drugs on excitatory NE transmission were DES greater than IMIP greater than AMI greater than CI-IMIP. Each of the four drugs also enhanced the 5-HTP-induced depression of spinal sympathetic reflexes, but their relative potencies on 5-HT transmission were just the opposite to those found on NE transmission. Therefore, all four drugs enhanced transmission by both NE and 5-HT, but their relative selectivities for the two transmitters differed markedly and were complementary. In general, the results support those of previous studies based on less direct methods for assessing inhibition of amine reuptake by tricyclic antidepressants.
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PMID:Enhancement of central norepinephrine and 5-hydroxytryptamine transmission by tricyclic antidepressants. A comparison. 22 Jun 58

There is a suggestive evidence for a relationship between central 5-HT and the occurrence of certain types of depressions. This evidence is derived from three sources: postmortem studies; measurement of CSF 5-HIAA; accumulation of CSF 5-HIAA after transport blockade by probenecid. Disturbances of central 5-HT metabolism are not typical for any depression but for certain types of vital (endogenous) depression. This implies that the group of vital depression, though tending towards homogeneity in terms of symptomatology, is heterogenous in biochemical terms and comprises patients with and without disorders in central 5-HT metabolism. It is plausible that disorders of the 5-HT metabolism play a role in the pathogenesis of depression, instead of resulting from them. This statement is based on the following findings: (i) 5-HTP can abolish or alleviate the depressive syndrome or some of its elements. (ii) This 5-HTP effect can be potentiated by clomipramine (Anafranil), a relative selective inhibitor of 5-HT reuptake. (iii) There exists a negative correlation between 5-HT turnover in the CNS and the therapeutic effect of clomipramine. The alleged distrurbances in central 5-HT are more likely to be predisposing than of direct causative significance. This assumption is based on two observations: (i) In more that 50% of cases, the 5-HT turnover remains low after clinical recovery, the patient being drug-free. (ii) There is suggestive evidence that abolition of the 5-HT deficit (by means of 5-HTP) exerts a prophylactic effect in uni-and bipolar depression.
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PMID:The Harold E. Himwich Memorial Lecture. Significance of biochemical parameters in the diagnosis, treatment, and prevention of depressive disorders. 30 32


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