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)

Feedforward and feedback inhibition are two fundamental modes of operation widespread in the nervous system. We have functionally identified synaptic connections between rat CA1 hippocampal interneurons of the stratum oriens (SO) and interneurons of the stratum lacunosum moleculare (SLM), which can act as feedback and feedforward interneurons, respectively. The unitary inhibitory postsynaptic currents (uIPSCs) detected with K-gluconate-based patch solution at -50 mV had an amplitude of 20.0 +/- 2.0 pA, rise time 2.2 +/- 0.2 ms, decay time 25 +/- 2.2 ms, jitter 1.4 +/- 0.2 ms (average +/- SEM, n = 39), and were abolished by the gamma-aminobutyric acid (GABA)(A) receptor antagonist 2-(3-carboxypropyl)-3-amino-6-methoxyphenyl-pyridazinium bromide (SR 95531). Post hoc anatomical characterization revealed that all but one of the identified presynaptic neurons were oriens-lacunosum moleculare (O-LM) cells, whereas the postsynaptic neurons were highly heterogeneous, including neurogliaform (n = 4), basket (n = 4), Schaffer collateral-associated (n = 10) and perforant path-associated (n = 9) cells. We investigated the short-term plasticity expressed at these synapses, and found that stimulation at 10-40 Hz resulted in short-term depression of uIPSCs. This short-term plasticity was determined by presynaptic factors and was not target-cell specific. We found that the feedforward inhibition elicited by the direct cortical input including the perforant path onto CA1 pyramidal cells was modulated through the inhibitory synapses we have characterized. Our data show that the inhibitory synapses between interneurons of the SO and SLM shift the balance between feedback and feedforward inhibition onto CA1 pyramidal neurons.
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PMID:Specific inhibitory synapses shift the balance from feedforward to feedback inhibition of hippocampal CA1 pyramidal cells. 1818 15

Antidepressant drug imipramine hydrochloride (IMP) is amphiphilic which shows surfactant-like behavior in aqueous solutions. We have studied the effect of adding electrolytes and non-electrolytes on the micellar behavior of IMP by making cloud point (CP) and dye solubilization measurements. The CP of a 100mM IMP solution (prepared in 10mM sodium phosphate (SP) buffer) was found to decrease with increasing pH, both in the absence as well as presence of added salts. Increase in pH increased the visible absorbance of Sudan III dye solubilized in the drug micelles, implying micellar growth. Addition of increasing amounts of salts to 100mM IMP solutions (at pH 6.7) caused continuous increase in CP due to micellar growth. On the basis of these studies, the binding-effect orders of counter- and co-ions have been deduced, respectively, as: Br(-)>Cl(-)>F(-) and Li(+)<Na(+)<K(+)<NH(4)(+). The trend of increasing CP with addition of increasing amounts of quaternary salts (tetramethylammonium bromide, TMeAB; tetraethylammonium bromide, TEtAB; tetra-n-propylammonium bromide, TPrAB; tetra-n-butylammonium bromide, TBuAB; tetra-n-pentylammonium bromide, TPeAB) to 100mM IMP solutions (at pH 6.7) was found to be dependent upon the alkyl chain length of the particular salt. Ureas caused CP depression, which was found to be dependent upon the number of methyl groups present in the molecule. Contrary to this, thioureas increased the CP slightly, but the presence of methyl group(s) had effect similar to that of alkylureas. The visible absorbance due to solubilized dye increased/decreased with addition of electrolytes/ureas. The overall behavior has been discussed in terms of electrostatic interactions, micellar growth, and mixed micelle formation.
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PMID:Investigation of the role of electrolytes and non-electrolytes on the cloud point and dye solubilization in antidepressant drug imipramine hydrochloride solutions. 1842 90

A 66-year-old man received medical treatment of depression for several years. He had a suspected malignant syndrome and in addition the symptom had deteriorated, and the electroconvulsive therapy (ECT) was administered. Though suxamethonium chloride is usually used as a muscular relaxant in the electroconvulsive therapy, we used vecuronium bromide (VCB) considering malignant syndrome. Maintenance of anesthesia was necessary because of the long effect of VCB. Anesthesia was induced and maintained by target controlled infusion (TCI) of propofol. Because propofol suppresses the convulsion, it is necessary to adjust the depth of anesthesia by propofol, and we used TCI of propofol. When the predicted blood propofol concentrations were 1.5 microg x ml(-1) and 2.0 microg x ml(-1), electric stimulation was given to the patient and enough seizure duration was obtained. TCI of propofol is useful for ECT to patients for whom suxamethonium chloride can not be used.
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PMID:[Anesthetic management for electroconvulsive therapy using target-controlled infusion of propofol]. 1864 46

The limits of detection, precision and matrix effects in the inductively coupled plasma spectrometry of platinum group metals (PGMs) and gold were measured and evaluated for four ICP-AES and one ICP-MS instrument. The sample matrix was a cationic surfactant used for the PGMs and gold preconcentration on a modified silica gel (C18). A sorption of ion associates of PGMs and gold chlorocomplexes with the cation of onium salt N(1-carbaethoxypentadecyl)-trimethyl ammonium bromide was considered. The calibration curves, limits of detection and matrix effects were evaluated in the presence of 0.003 mol dm(-3) of onium salt (1.3 mg cm(-3)) and 0.1 mol dm(-3) HCl. The values of limits of detection (3 sigma(bl)) of PGMs for all axial ICP instruments were mostly below 10 ng cm(-3). Lateral observation on dual view ICP instrument yielded only 3 times higher detection limits in comparison to the axial mode of the same spectrometer and the detection limits for ICP-MS instrument were on the levels of units or tens of pg cm(-3). These limits of detection did not significantly differ from values obtained with pure solutions. Matrix effects in the presence of onium salt did not exceed 12% depression in the analytical signals. Besides the coefficients of correlation, the uncertainties on centroids of concentrations were calculated for calibration graphs obtained by linear regression.
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PMID:Comparison of some analytical performance characteristics in inductively coupled plasma spectrometry of platinum group metals and gold. 1896 28

The modern antiepileptic drug (AED) era--spanning a period of more than 150 years from the first use of bromide in 1857 to 2008--has seen the introduction into clinical practice of a diverse group of effective and safe drugs. These AEDs have provided considerable benefits for those afflicted with epilepsy of all kinds. In as many as 60-70% of newly treated patients, current AEDs lead to satisfactory control of seizures and a favorable risk-benefit balance for the great majority of patients, albeit with considerable differences in response depending on the type of seizure and epilepsy syndrome and rare serious adverse events. Unfortunately, in 20-30% of patients, epilepsy cannot be controlled. Patients with drug-resistant epilepsy often have serious comorbidity, including injury, depression, anxiety, and increased mortality. The aim of antiepileptic treatment should be to control seizures as quickly as possible with no or minimal side effects and with no negative impact on the quality of life. Improved seizure control is likely to reduce the morbidity and increased mortality associated with uncontrolled epilepsy. In this short overview, the options and the limitations of treating patients with epilepsy are briefly summarized.
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PMID:Drug treatment of epilepsy: options and limitations. 1923 51

We report three patients with a history of neuroleptic malignant syndrome for whom modified electroconvulsive therapy (m-ECT) was scheduled. Two patients suffered from schizophrenia, and one suffered from depression. Their symptoms, such as hyperthermia, consciousness disturbance, myotonus, tremor, sweating, and tachycardia, improved gradually with administration of dantrolene and fluid infusion. However, their psychotic state was exacerbated. Therefore, m-ECT was scheduled. When patients were restless at the hospital ward, they were sedated with propofol and transferred to the operating room. General anesthesia was induced with thiopental 2.5-5 mg x kg(-1). After loss of consciousness, vecuronium bromide 0.01 mg x kg(-1) followed by a dose of 0.1 mg x kg(-1) was administered and ventilation was assisted using a face mask and 100% oxygen. After the ECT stimulus, the patients were sedated with propofol until full recovery from muscle relaxation. Although anesthesia time (mean 38 min) was slightly longer (19 min) than in those anesthetized with thiopental and suxamethonium chloride, m-ECT was performed safely and effectively.
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PMID:[Anesthetic management for electroconvulsive therapy in the patients with a history of neuroleptic malignant syndrome]. 1946 6

Previous reports have shown that antidepressants increase neuronal cell proliferation and enhance neuroplasticity both in vivo and in vitro. This study investigated the direct effects of one such antidepressant, fluoxetine , on cell proliferation and on the production of neurotrophic factors in neuronal precursors derived from human embryonic stem cells (hESCs; H9). Fluoxetine induced the differentiation of neuronal precursors, strongly enhancing neuronal characteristics. The rate of proliferation was higher in fluoxetine -treated cells than in control cells, as determined by MTT [3(4,5-dimethylthiazol-2-yl) 2,5-diphenyltetrazolium bromide] assay. The CPDL (cumulative population doubling level) of the fluoxetine-treated cells was significantly increased in comparison to that of control cells (p<.001). Bromodeoxyuridine incorporation and staurosporine-induced apoptosis assays were elevated in fluoxetine-treated cells. Quantitative RT-PCR analysis revealed no significant differences in the expression of neurotrophic factors, brain-derived neurotrophic factor (BDNF);glial-derived neurotrophic factor (GDNF) and cAMP-responsive element-binding protein (CREB) between cells treated with fluoxetine for two weeks and their untreated counterparts. These results may help elucidate the mechanism of action of fluoxetine as a therapeutic drug for the treatment of depression. Data presented herein provide more evidence that, in addition to having a direct chemical effect on serotonin levels, fluoxetine can influence hESC-derived neuronal cells by increasing cell proliferation, while allowing them to maintain their neuronal characteristics.
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PMID:Increased cellular turnover in response to fluoxetine in neuronal precursors derived from human embryonic stem cells. 1959 7

Human ovarian granulosa cells obtained from women undergoing in vitro fertilization were exposed to 15.6, 31.25, 62.5, 125, 250, 500, 1000 muM Ni(2+) for 48 h. To determine the site of action of Ni(2+), the granulosa cells were stimulated to produce progesterone (P) by using maximally stimulating amounts of human chorionic gonadotropin (0.1 IU/ml hCG) or dibutyryl cyclic adenosine monophosphate (1 mM db-cAMP). The luteinizing hormone (LH) analog hCG was chosen because resultant P production requires an intact membrane receptor and db-cAMP was used to test for post LH receptor defects caused by Ni(2+). Progesterone content of the culture medium was determined by radioimmunoassay (RIA), and viability of the cells was measured by MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) reduction test. Concentration-dependent depression in both hGC and db-cAMP stimulated P production was seen at 15.625 muM or higher concentration of Ni(2+), which is not cytotoxic on human ovarian granulosa cells. The viability of cells was unaffected up to 31.25 muM and decreased significantly at 62.5 muM. Our results show a dose-related depression in stimulated P production of granulosa cells at a dose that does not induce significant cytotoxic action. These data indicate that the effect of Ni(2+) on P production is not due to cytotoxicity, and the cellular site(s) of inhibitory action appears to be subsequent to the membrane receptor and production of cAMP.
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PMID:Effect of nickel (ni(2+)) on primary human ovarian granulosa cells in vitro. 2002 Nov 8

The release of [(3)H]noradrenaline from rat hippocampal synaptosomes by 25 mM K(+) and 5 ?M veratridine, but not by the Ca(2+) ionophore A23187 was depressed by baclofen. This depression was reversed by 8-Bromo-cAMP. This action of baclofen was stereospecific and mimicked both that of GABA in the presence of bicuculline and that of clonidine. The ?(2)-adrenoceptor antagonists yohimbine and Wy25309 antagonised the action of clonidine and baclofen but not that of GABA. Specific binding of [(3)H]clonidine was displaced by Wy25309 and baclofen, but not by GABA. Specific binding of [(3)H]GABA in the presence of Ca(2+) was displaced by baclofen but not by Wy25309. It is concluded that baclofen is not a specific agonist at GABA(B) receptors in the brain.
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PMID:Effect of baclofen on in vitro noradrenaline release from rat hippocampus and cerebellum: an action at an ?(2)-adrenoceptor. 2049 11

Bovine viral diarrhea virus (BVDV) infections cause respiratory, reproductive, and enteric disease in cattle. Vaccination raises herd resistance and limits the spread of BVDV among cattle. Both killed and modified live vaccines against BVDV are available. While modified live vaccines elicit an immune response with a broader range and a longer duration of immunity, killed vaccines are considered to be safer. One way to improve the performance of killed vaccines is to develop new adjuvants. The goal of this research was evaluate new adjuvants, consisting of combinations of Quil A cholesterol and dimethyldioctadecylammonium (DDA) bromide, for use in killed vaccines. Responses to three novel killed vaccines, using combinations of Quil A and DDA as adjuvants, were compared to responses to a commercial modified live and a commercial killed vaccine. Vaccination response was monitored by measuring viral neutralizing antibodies (VN) levels and by response to challenge. All three novel vaccines were efficacious based on reduction in virus isolation, pyrexia, and depression. Compared to a commercial killed vaccine, the three novel vaccines elicited higher VN levels and reduced injection site inflammation.
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PMID:Evaluation of three experimental bovine viral diarrhea virus killed vaccines adjuvanted with combinations of Quil A cholesterol and dimethyldioctadecylammonium (DDA) bromide. 2087 89


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