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)

The physical origins of neuromagnetic signals are described from which it is concluded that magnetoencephalography is potentially much more applicable than electroencephalography for localizing the sources of a variety of neural activities in the brain. The magnitudes of typical neuromagnetic signals are discussed. Selected examples of MEG studies are given. Recent experiments which appear to indicate directly the association of spreading cortical depression with migraine headache are briefly described.
 ...
PMID:Neuromagnetism: a new approach for localizing brain function. 269 10

Many studies have been performed on the effects of various features of head geometry on electroencephalograms (EEG's) and magnetoencephalograms (MEG's) and on the accuracy with which electrical sources in the brain can be localized using these measurements. However, to date no studies have been performed of the effects of local variations in skull and scalp thickness. This paper presents a computer modeling study of the effects of such local variations. The results obtained in this study indicate that local variations in skull and scalp thickness have effects on EEG's and MEG's which range from a simple intuitive effect to complex effects which depend on such factors as source depth and orientation, the geometry of the variation in skull and scalp thickness, etc. These results also indicate that local variations in skull and scalp thickness cause EEG localization errors which are generally much less than 1 cm and MEG localization errors which are even smaller. These results also indicate that multichannel and single-channel MEG measurements will produce localization errors of approximately the same amplitude when there is a bump on the external surface of the head but that multichannel measurements will produce significantly smaller localization errors than single-channel measurements when a depression is present in that surface.
 ...
PMID:Effects of local variations in skull and scalp thickness on EEG's and MEG's. 846 75

The mechanisms involved in myocardial dysfunction during septic shock are not well understood. We have investigated the effects of endotoxin and the role of nitric oxide (NO) in the beta-adrenoceptor responsiveness of rat isolated, ejecting hearts perfused at 60 mmHg of head pressure. In vivo pretreatment with endotoxin (4 mg/kg, i.p., 3 h before heart isolation) significantly attenuated the inotropic response (increase in left ventricular developed pressure, LVP) to isoprenaline (0.15 microgram) after 30 min equilibration and after a further 90 min of perfusion. The peak rate of LVP development (dP/dtmax) in response to isoprenaline was reduced by endotoxin pretreatment, as was the increase of coronary flow. The depression of ventricular contraction was prevented by pretreatment with dexamethasone (1 mg/kg, i.p., 30 min before endotoxin), and was also restored by perfusion with NG-nitro-L-arginine (L-NA, 10 microM) for 60 min, but not by NG-nitro-D-arginine (D-NA, 10 microM). Mercaptoethylguanidine (MEG, 30 microM), a selective inhibitor of the inducible NO synthase (isoform 2), also reversed the depression of the isoprenaline response caused by endotoxin pretreatment. However, treatment with endotoxin, dexamethasone, L-NA, D-NA or MEG had minimal effects on the baseline parameters of LVP, dP/dtmax and coronary flow, which all tended to decline over the 2 h perfusion period. Western blot analysis using an antibody to NO synthase (isoform 2, but not to isoform 3) revealed the induction of a protein corresponding to NO synthase 2 in the endotoxin-treated hearts but not in control hearts or those treated with dexamethasone or MEG. In summary, these results indicate the endotoxin depresses myocardial contractile function and reduces inotropic responsiveness to beta-adrenoceptor activation. The effect of endotoxin on the inotropic response is mediated, at least in part, by products of an endogenous NO synthase that is suppressed by dexamethasone and a specific inhibitor of NO synthase (isoform 2).
 ...
PMID:Depression of the inotropic action of isoprenaline by nitric oxide synthase induction in rat isolated hearts. 904 99

Endogenous nitric oxide (NO) signalling pathways within the myocardium depress myocardial contractile function in septic shock and some cardiomyopathies. We have explored the role of NO synthases (NOSs) in mediating the cardiodepressant actions of interferon-gamma (IFN-gamma) and lipopolysaccaride (LPS) in rat papillary muscle. Muscles from the right ventricle were electrically stimulated (0.2 Hz) at 30 degrees C and isometric contraction monitored. Exposure to IFN-gamma and LPS for 15 h in vitro significantly decreased the peak tension (PT for IFN-gamma + LPS, from 0.13 +/- 0.03 to 0.07 +/- 0.02 g) and rate of tension development (dT/dt for IFN-gamma + LPS, from 1.78 +/- 0.36 to 1.17 +/- 0.28 g/s) compared to untreated controls, and this was prevented by dexamethasone (1 microM) and partly reversed by a non-specific NOS inhibitor, NG-nitro-L-arginine (NOLA, 30 microM). Likewise, the maximum inotropic response of the papillary muscles to isoprenaline (0.001-10 microM) decreased significantly after 15 h treatment with IFN-gamma and LPS (PT from 83 +/- 18 to 28 +/- 6%; +dT/dt from 83 +/- 12 to 31 +/- 7%; -dT/dt from 83 +/- 12 to 38 +/- 6%). Again, the depressant effects of IFN-gamma and LPS on inotropic responsiveness to isoprenaline were completely prevented by pretreatment with dexamethasone (1 microM), by a specific inhibitor of NOS2, mercaptoethylguanidine (MEG, 30 microM) and by NOLA. Whereas dexamethasone and NOLA protected against the attenuation of baseline contractions induced by LPS and IFN-gamma, MEG did not. Western blot analysis of cardiac myocytes showed that there was no constitutive expression of NOS2, but IFN-gamma and LPS induced expression of NOS2, and this was prevented by dexamethasone. Thus IFN-gamma, in the presence of LPS, reduced papillary muscle contraction and decreased responsiveness to beta-adrenoceptor stimulation through induction of NOS2 in the muscle. Increased NO production may contribute to the cardiac depression during septic shock and anti-cancer therapy with cytokines, and perhaps in heart failure.
 ...
PMID:Cardiodepressant effects of interferon-gamma and endotoxin reversed by inhibition of NO synthase 2 in rat myocardium. 961 39

The I1-imidazoline receptor is a novel brainstem modulator of sympathetic outflow that is elevated on platelets and in brains of depressed patients. A positive correlation has been reported (accompanying manuscript) between plasma norepinephrine (NE) concentrations and the densities (Bmax) of platelet I1 binding sites (I1 sites). I1-candidate proteins of 33 kDa and 85 kDa are now identified on Western blots probed with anti-imidazoline receptor antiserum (IRBP antiserum), that correlate with Bmax values for I1 sites. Furthermore, a human megakaryoblastoma cell line (MEG-01) has been used to study the regulation of these proteins on megakaryocytic cells, while bovine adrenal chromaffin cells provide a standard I1 cell type for comparison. Both the 33 kDa and 85 kDa IRBP-immunoreactive bands were enriched in plasma membrane fractions. IRBP antiserum did not cross-react with I2 imidazoline binding sites located on platelet mitochondrial membranes. The 85 kDa band was enhanced under conditions lacking fetal bovine serum (FBS) from the culture medium 6 h prior to harvesting. Conversely, 33 kDa protein was enhanced on MEG-01 cells grown in the presence of 10% FBS; suggesting that a precursor (85 kDa) and product (33 kDa) relationship might be induced by serum. The 85 kDa band was robustly up-regulated in response to imidazoline receptor-sensitive ligands; moxonidine, idazoxan and agmatine (10 microM each for 6 h). NE also up-regulated the 85 kDa IRBP-immunoreactive protein on MEG-01 membranes, but to a lesser extent. Idazoxan, an imidazoline alpha 2-antagonist, off-set its induction of 85 kDa protein by reducing the 33 kDa band. Yohimbine, a non-imidazoline alpha 2-antagonist, was ineffective alone, or in combination with moxonidine (up to 40 microM), but yohimbine blocked NE's induction of the 85 kDa band. Therefore, a rise in either plasma NE and/or endogenous I-site ligands (i.e. agmatine) could explain an elevation of imidazoline receptors observed in depression.
 ...
PMID:Imidazoline receptor proteins are regulated in platelet-precursor MEG-01 cells by agonists and antagonists. 969 2

We apply a recently developed multivariate statistical data analysis technique--so called blind source separation (BSS) by independent component analysis--to process magnetoencephalogram recordings of near-dc fields. The extraction of near-dc fields from MEG recordings has great relevance for medical applications since slowly varying dc-phenomena have been found, e.g., in cerebral anoxia and spreading depression in animals. Comparing several BSS approaches, it turns out that an algorithm based on temporal decorrelation successfully extracted a dc-component which was induced in the auditory cortex by presentation of music. The task is challenging because of the limited amount of available data and the corruption by outliers, which makes it an interesting real-world testbed for studying the robustness of ICA methods.
 ...
PMID:Independent component analysis of noninvasively recorded cortical magnetic DC-fields in humans. 1085 3

The presence of depression is common among the elderly and it often complicates the early diagnosis of Alzheimer's disease (AD). In this study, we searched for brain activity measures that characterise AD. We compared brain magnetic activity profiles during a memory task, obtained from patients with AD, elderly patients with late onset depression, and age matched volunteers without history of neurological or psychiatric disease. AD patients showed significantly reduced activity in left temporal lobe regions during late portions of the event related magnetic response (400 ms or later after stimulus onset), compared with both groups of patients who did not present with serious cognitive decline. This finding highlights the potential usefulness of MEG protocols supporting the differential diagnosis of AD and major depression related cognitive decline in the elderly.
 ...
PMID:Profiles of brain magnetic activity during a memory task in patients with Alzheimer's disease and in non-demented elderly subjects, with or without depression. 1525 20

DC-magnetoencephalography (DC-MEG)waveforms arising during migraine aura were used to determine the effectiveness of prophylactic medication therapy on neuronal hyperexcitability. Nine patients were prescribed valproate (Depakote) for migraine prophylaxis. MEG scans were recorded during visual stimulation before commencing medication and again after 30 days of daily use of valproate. Cortical brain activity was recorded during stimulation with a black-and-white circular checkerboard pattern alternating at 8 Hz and were analyzed with MR-FOCUSS. Large-amplitude DC-MEG signals, imaged to extended areas of occipital cortex, were seen before therapy. After 30 days of prophylactic treatment, reduced DC-MEG shifts in the occipital cortex and reduced incidence of migraine attacks were observed. Using visual stimulation, the authors demonstrated the hyperexcitability of widespread regions throughout occipital cortex in migraine patients, explaining the susceptibility for triggering spreading cortical depression and migraine aura. This study confirms that MEG can noninvasively determine the status of neuronal excitability before and after therapy. This finding may be helpful in determining which prophylactic medications will be most effective in reducing hyperexcitability in particular patients.
 ...
PMID:Cortical hyperexcitability in migraine patients before and after sodium valproate treatment. 1568 15

The non-invasive electrical recording of Direct Current (DC) phenomena in the frequency range below 0.1 Hz, e.g., occurring in metabolic injuries to brain cells in stroke or migraine (anoxic depolarization, peri-infarct depolarization, spreading depression), is technically restricted due to large drift artifacts caused by electrochemical instabilities at the electrode-skin interface. This limitation could be overcome by invasive approaches only. However, as early as 1969 first magnetic fields in this frequency range have been recorded over the human torso by oscillating the subject vertically in front of a magnetic field detector using a see-saw. By this technique the DC field is conversed to a higher frequency, where the external noise level is less. In the last decade, the modulation based DC-magnetoencephalography (DC-MEG) has been methodically refined, which allowed monitoring low-amplitude magnetic fields in this frequency domain arising not only from injured tissue, but also generated by functional cortical activation. Furthermore, the combination of DC-MEG and NearInfraRed Spectroscopy (NIRS) opens up a new avenue to study cortical neurovascular coupling, as vascular and neuronal activations could be analyzed simultaneously even without averaging in a single-trial mode. Recordings inside the novel magnetically shielded room (BMSR-2 of the Physikalisch-Technische Bundesanstalt, Berlin) exhibiting an extremely low background noise level in the DC frequency range, and alleviating the need of sensor-to-source modulation, allow to resolve additionally the short-term (subsecond) dynamics of neuronal DC-processes.
 ...
PMID:The discovery of slowness--recent progress in DC-MEG research. 1601 3

Long-term depression (LTD) of parallel fibre (PF)-Purkinje cell synapses in the cerebellum is recognized as a cellular substrate of motor learning. Although the delta2 glutamate receptor (GluRdelta2) has been shown to be crucial for LTD, the mechanisms by which GluRdelta2 functions remain elusive. In this study, we developed a virus vector-based gene transfer approach to rescue impaired LTD in GluRdelta2-null Purkinje cells in cerebellar slice preparations. We demonstrated that LTD was restored in GluRdelta2-null Purkinje cells transduced with wild-type but not with mutant GluRdelta2, which lacked the PDZ-ligand domain in the C-terminus. Immunohistochemical analysis revealed no difference in expression levels or spine localization patterns between virally introduced wild-type and mutant GluRdelta2 proteins. Similarly, LTD was abrogated in Purkinje cells that had been acutely perfused with peptides, hampering the interaction of GluRdelta2 with PDZ proteins such as PSD-93, PTPMEG and S-SCAM but not with delphilin. Together, these results indicate that PDZ proteins that bind to the C-terminus of GluRdelta2 are not essential for localizing GluRdelta2 at synapses but are crucial for conveying signals necessary for the induction of LTD.
 ...
PMID:The extreme C-terminus of GluRdelta2 is essential for induction of long-term depression in cerebellar slices. 1742 62


1 2 3 Next >>