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)

1. The antidepressant trazodone and its main metabolite m-chlorophenylpiperazine (mCPP) were investigated for their analgesic properties and their sensitivity to a threshold dose of morphine in acetic acid abdominal constriction and hot plate tests. 2. The drugs elicited hypoalgesic effects at about the same doses in the two analgesic assays. 3. Naloxone (2 mg/kg i.p.) prevented the hypoalgesia of trazodone but not of mCPP in the hot plate test. The opiate antagonist did not affect the responses of both drugs to the writhing test. 4. Subanalgesic doses of the two drugs increased the sensitivity to morphine in both assays. The results further support the suggested role played by opioid and 5-HT systems on depression.
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PMID:Antinociceptive effects of trazodone and m-chlorophenylpiperazine (mCPP) in mice: interaction with morphine. 205 Feb 81

In a passive avoidance test, intracerebroventricular administration (post-trial treatment) of the somatostatin-depleting compound cysteamine decreased the avoidance latency of the rats in a dose-related manner, while the effect of pantethine (which is metabolized to cysteamine) was less pronounced. In open-field studies, both compounds decreased the motor activity (ambulation, rearing) of the animals 15 min after the injection followed by a subsequent recuperation of the locomotor depression. Following pantethine, the ambulation increased during the later tests (60 min, 240 min, 24 hr). Cysteamine decreased the noradrenaline and increased the dopamine and dihydroxyphenyl acetic acid content in the hypothalamus, whereas the effects of pantethine were less expressed. Both compounds slightly decreased the striatal noradrenaline and increased the dihydroxyphenyl acetic acid levels at 15 and 60 min after administration. However, contrary to pantethine, 4 hr after treatment with cysteamine, there was a decrease in dihydroxyphenyl acetic acid concentration in this brain region. These findings suggest that both pantethine and cysteamine attenuate passive avoidance latency after intracerebroventricular treatment. The different efficiency of pantethine and its metabolite cysteamine might be connected to the low pantetheinase activity of the brain tissue; however, some direct effects of pantethine cannot be excluded. The different effects of the two compounds on the open-field activity are possibly associated with the diverse effects of the compounds on the striatal dopaminergic neurotransmission.
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PMID:Comparative studies of intracerebroventricularly administered cysteamine and pantethine in different behavioral tests and on brain catecholamines in rats. 224 25

23Na nuclear magnetic resonance (NMR) spectroscopy was utilized to measure intracellular Na+ in perfused ferret hearts exposed to the shift reagent dysprosium triethylenetramine-hexa-acetic acid [Dy(TTHA)3-]. The intracellular Na+ signal was small under normal perfusion conditions; resolution was enhanced by using a Jump-Return NMR pulse protocol. During 20 min of total global ischemia at 30 degrees C, intracellular Na+ concentration ([Na+]i) increased steadily to a peak value fivefold greater than control. [Na+]i declined monotonically back to control levels within 9 min of reperfusion. In contrast, the mean contractile pressure only recovered to 54% of control levels. Thus major alterations in Na+ homeostasis occur during severe ischemia. [Na+] recovers rapidly during reperfusion and is therefore dissociated from the lingering postischemic depression of contractile function known as "stunning."
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PMID:23Na-NMR measurements of intracellular sodium in intact perfused ferret hearts during ischemia and reperfusion. 226 Jul 1

The present investigation sought to examine the importance of substance P in the altered respiratory activity after neonatal capsaicin administration. Halothane-anesthetized adult rats given capsaicin neonatally exhibit a decreased basal minute ventilation with PaCO2 equal to and PaO2 greater than vehicle injected controls. In addition, the minute ventilation-PaCO2 curve was displaced to the right. Acute bilateral cervical vagotomy severely blunted the minute ventilation response to PaCO2 and abolished the differences in ventilation between capsaicin treated and control rats. Neonatal capsaicin significantly reduced pons-medulla substance P content but not TRH, serotonin or 5-hydroxyindole acetic acid. Immunohistochemical studies revealed that substance P fibers of the trigeminal spinal nucleus were the most severely affected in the brain stem and that substance P fibers in the lung were totally absent. The intracerebroventricular administration of substance P increased minute ventilation similarly in both control and capsaicin treated rats, largely as a result of increases in tidal volume. The minute ventilation-PaCO2 curve was similar in both groups after substance P administration. Simultaneous administration of the peptidase inhibitor captopril with substance P increased the respiratory response to substance P in normal rats. Administration of captopril to capsaicin treated rats restored the ventilation-PaCO2 curve to the position observed in normal rats. The hypotensive response to intracerebroventricular captopril alone in control rats was less profound in rats given neonatal capsaicin. These results are consistent with the thesis that respiratory depression after capsaicin treatment is at least in part due to the loss of substance P primary afferent nerve terminals in the brain stem, suggesting that substance P fibers in the brain stem may participate in the normal modulation of respiratory activity.
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PMID:Altered respiratory response to substance P in capsaicin-treated rats. 241 26

Male rats (100 g) previously adapted to a 20% casein diet were fed diets containing from 0 to 55% of casein and were killed after 20, 60, 150, 240, or 330 min. Food intake of rats fed a protein-free diet or a diet containing greater than 35% of casein was depressed within 20 min and remained depressed for up to 5.5 h. Depressed food intake of rats fed protein-free diets was accompanied by a rapid reduction in plasma and brain total concentrations of free indispensable amino acids (IAA). Food intake depression among groups fed diets containing in excess of 35% casein was associated with elevated plasma and brain total IAA concentrations, compared with those of animals fed diets containing 15-20% of casein. No consistent relationships were observed between food or protein intakes and whole-brain concentrations of 5-hydroxytryptamine, 5-hydroxyindole-3-acetic acid, or their sum. Our results suggest that in animals fed a single diet, food intake is depressed if the total concentration of free IAA in brain either falls below a certain critical minimum or exceeds some maximum tolerable level.
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PMID:Acute effects of dietary protein on food intake, tissue amino acids, and brain serotonin. 243 9

The role of serotonin in the anorexic response of rats to an amino acid-imbalanced diet was investigated. After chronic depletion of serotonin with parachlorophenylalanine (PCPA, 300 mg/kg) or 5,7-dihydroxytryptamine (DHT, 200 micrograms/rat, intracisternally), initial intake of a mild isoleucine-imbalanced diet was reduced by 60% vs. a 17% reduction after saline injection. After acute treatment with the agonist, quipazine (quip, 5 mg/kg ip) or the precursor, tryptophan (TRP, 1% added to the diet), imbalanced diet intake was also exacerbated. PCPA and DHT may have caused receptor supersensitivity, such that the food intake depression after serotonin depletion was similar to that seen with the quip and TRP treatments. Injection of the autoreceptor agonist, 8-hydroxy-2(di-n-propylamino)tetralin (8-OH-DPAT, 500 micrograms/kg sc), to reduce transmission in the serotonergic systems resulted in an attenuation of the usual food intake depression of the amino acid-imbalanced diet (only a 7%, nonsignificant reduction). Also measurements made in the absence of pharmacological treatment showed that the ratio 5-hydroxyindole acetic acid-to-serotonin, a putative index of serotonin turnover, was increased 155% in the raphe nuclei and 140% in the hippocampus 3.5 h after ingestion of the mild isoleucine-imbalanced diet. Therefore increased serotonergic activity in some brain areas may be associated with the initial depression of food intake in rats fed an imbalanced amino acid diet.
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PMID:Serotonin and feeding responses of rats to amino acid imbalance: initial phase. 244 14

The ototoxicity of an otic drop preparation containing 2% acetic acid and 3% propylene glycol (VoSol, Denver Chemical Co., Humacao, PR) was investigated according to measurements of endocochlear potential (EP) and inner ear fluid pH. The application of this preparation to the round window membrane for 30 minutes caused a depression in EP from 80.5 +/- 2.5 mV (mean +/- SD; n = 6) to 11.7 +/- 7.7 mV, and lowered inner ear fluid pH from 7.55 +/- 0.09 to 5.06 +/- 0.19 (n = 6) in perilymph and from 7.52 +/- 0.07 to 5.88 +/- 0.63 (n = 6) in endolymph. Two percent acetic acid produced similar changes after 30 minutes: EP was reduced from 83.0 +/- 2.2 mV to 34.0 +/- 2.9 mV and endolymphatic pH from 7.49 +/- 0.04 to 6.83 +/- 0.21 (n = 4). However, the application of artificial perilymph of pH 4 titrated with HCl induced no significant changes in either EP or endolymphatic pH. We suggest that the mechanisms of ototoxicity in the otic drop preparation are Na+ and K+-ATPase inhibition, and that such inhibition is due to the intracellular acidification of strial cells resulting from the penetration of acetic acid across the cell membrane, and to the direct and synergistic actions of propylene glycol.
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PMID:The preparation of acetic acid for use in otic drops and its effect on endocochlear potential and pH in inner ear fluid. 259 25

The study of morphines influence on vocalization and movement, nociceptive reactivity in rats in free behavior, during trauma of an extremity, intraperitoneal acetic acid administration and two-hour restraint allow us to reveal specific analgesic actions of this substance in doses comparable to that used for pain relief in man. This action consisted in the almost disappearance of trauma-induced hyperalgesia or a significant reduction of visceral stimulation-induced hypalgesia without any significant changes in movement reactivity depression typical to these states. Moreover, analysis or morphines influence on movement reactivity depression in free behaving rats of different groups or parts of one group previously housed in different aversive conditions allow to understand the reasons of variability in the action of opiates and the significance of previous living conditions in determination of their effects. Furthermore, the enhancement of morphines action on movement reactivity 3-4 hours after a single naloxone administration was observed, which indicates the possibility of artificial regulation of opiate effects by direct action on opiate receptors by naloxone. Subchronic naloxone administration (0.5 mg/kg, 3 times per day for 3 days) led to substantial and longterm enhancement of morphines depressive effect on movement reactivity (20 and 105 hours after the last naloxone use) and to decrease in movement reactivity depression typical to restraint stress.
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PMID:Morphine: some puzzles of well-known substance. 274 64

Comparing the pattern of serotonin, 5-hydroxyindole acetic acid, 3,4-dihydroxyphenyl acetic acid and homovanillic acid in five brain areas of one dysphoric patient to those of 3 depressed patients it seems that dysphoria biochemically is a state between depression and mania. Dynamically, dysphoria may possibly be seen as a behavioral correlate of a switch process between high and low turnover of neurotransmitters (rather high frequency in comparison to bipolar disorder with very low frequency). However, the biochemical data are obviously in agreement with psychiatric findings, i.e. that dysphoria in any case is an extremely labile state.
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PMID:Biochemical aspects of dysphoria: case study for hypothesis generation. 289 24

Relatively high concentrations of verapamil or EGTA [ethylene glycol-bis (beta-aminoethyl ether) N, N, N',N'-tetra acetic acid] inhibit contraction (P) of the rat phrenic nerve-hemidiaphragm preparation elicited by direct or indirect stimulation. The inhibitory effect of verapamil is greater (P less than 0.002) with direct (I50 = 26.3 +/- 1.7 microM) than indirect = I50 = 37.6 +/- 1.9 microM) stimulation. For EGTA the reverse is true: I50 is 1320 +/- 80 microM with direct and 1100 +/- 60 microM with indirect stimulation. The greater than 90% verapamil-induced depression of P can only be partially reversed by washout. Increasing the [Ca2+] or the addition of 4-aminopyridine (4AP) has insignificant antagonist effect. Except for the antagonism by 4AP during direct stimulation, the EGTA-induced depression of P is better antagonized by washout, increase of the [Ca2+], or the addition of 4AP than that caused by verapamil. Neostigmine did not antagonize the depression of P caused by either verapamil or EGTA. The findings presented indicate that the primary site of action of verapamil is postjunctional and that of EGTA is prejunctional.
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PMID:The effect of verapamil and EGTA on the rat phrenic nerve-hemidiaphragm preparation. 298 88


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