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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with obstructive sleep apnea show a fall in arterial oxygen saturation during apneas. Whether this is causing myocardial ischemia and consecutively ST segment depressions in the electrocardiogram is not known. Therefore 15 consecutive patients (53 +/- 8 years, apnea index 45 +/- 28, minimal oxygen saturation 71 +/- 14%) with OSA were studied by Holter electrocardiogram and polysomnography. History and exercise testing gave no evidence of coronary heart disease. Three patients had ventricular arrhythmias Lown IVA and 10 had Lown I or III. Three patients showed unspecific negative T waves or ST segment elevations. In no patient significant ST segment depression was found. It is concluded that OSA does not lead to ischemic ST segment depression in the absence of coronary heart disease. The cause of ventricular arrhythmias in OSA seems not be related to myocardial ischemia.
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PMID:[ST segmental changes and arrhythmias in obstructive sleep apnea]. 194 65

To examine whether or not the location of local abnormalities on body surface isochrone maps reflects the site of myocardial ischemia, 48 coronary artery disease patients without myocardial infarction were studied. Eighty-seven unipolar electrocardiograms distributed over the anterior chest and the back were recorded simultaneously before and after the submaximal treadmill exercise. For each lead, the duration from the QRS onset to the time of the most rapid decrease in QRS voltage was measured (index of ventricular activation [IVA]). Based o the data provided by these 87 leads, IVA isochrone maps (IVA map) in preexercise and in postexercise, as well as IVA maps showing the difference between preexercise and postexercise, were constructed. The IVA was defined as abnormal when it exceeded (mean + 2 SD) the normal range. We called the area with the abnormal IVA, the "+2SD area." In patients having a stenosis in the left anterior descending artery, the +2SD area in each map was located mainly on the left anterior chest, whereas in patients having a stenosis in the right coronary artery, the +2SD area in each map was located mainly on the right lower thoracic surface. Moreover, the +2SD area of patients with both left anterior descending and right coronary artery disease appeared on both the left anterior chest and the right lower thoracic surface. In patients with left circumflex artery disease, however, the location of the +2SD area did not suggest a stenotic site because of its small population. On the other hand, it was difficult to determine the ischemic site from the body surface distribution of ST segment depression.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relation between localization of coronary artery disease and local abnormalities in ventricular activation during exercise tests. 229 56

Anatomical studies have confirmed that isolated right ventricular and anterior biventricular infarcts are rare. However, RV extension is found in 36 to 50 per cent of cases of postero-inferior infarcts, which confirms the findings of invasive and non-invasive investigations which detect acute RV dysfunction with the same frequency after this type of infarct. It is difficult to create right ventricular infarction experimentally because of the relative protection against ischaemia of the RV. In man, this condition almost always implies an associated thrombosis of the proximal right coronary artery and significant stenosis of the IVA, which justifies the broad indications for coronary angiography. The two major haemodynamic consequences of right ventricular infarction are due to original pathophysiological mechanisms: the adiastole seems to be due to a limitation of RV dilatation by the pericardium, the reduced output is due to faulty LV filling as a result of RV systolic dysfunction and associated factors such as the absence of efficient and synchronous atrial systole secondary to AVB (60%) or to acute right atrial paralysis. The choice of treatment is based on these pathophysiological data. The diagnosis of infarction of the RV is straightforward, often suggested on clinical examination (RVI syndrome: reduced output in 45% of cases) and the surface E.C.G. (ST-T depression 1 mm in V3R-V4R-V5R). The diagnosis is confirmed by more sophisticated investigations which can evaluate the degree of systolic dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Infarction of the right ventricle]. 669 84

1. We investigated the effect of nimodipine on the calcium current in dissociated cerebellar granule cells from 8-day-old rats. We measured the whole cell current and the depolarization-induced internal calcium elevation in Fura2-loaded cells exposed to high-potassium solutions. 2. Nimodipine maximally depressed the peak calcium current from holding potential (Vh) = -80 mV by 25% and the inactivation resistant residual current from Vh = -50 mV by 44%. The nimodipine-sensitive current had the same amplitude under both conditions and the half-maximal inhibition concentration (IC50) was close to 50 nM. 3. In contrast to other components of the calcium current, the nimodipine-sensitive current did not inactivate significantly during 1-s depolarization and it was weakly sensitive to the holding potential and to depolarizing conditioning prepulses. The effect of nimodipine was higher on the current elicited by small depolarizations and the current at -30 mV was depressed by < or = 70%. Depolarizing prepulses enhanced the effect of 1 nM (but not that of 1 microM) nimodipine. 4. In Fura2-loaded cells, nimodipine strongly antagonized the internal calcium rise due to superfusion with 15-75 mM potassium. The effect was significantly more potent on the internal calcium rise determined by lower depolarizations, with 80% inhibition of the peak response to 25 mM KCl. The dose dependence of this depression was best approximated by a two-site curve with IC50(1) = 0.27 nM and IC50(2) = 65 nM. The time course of recovery was dependent on the duration of treatment, suggesting a close interaction between nimodipine and the lipid membrane. 5. The effect of 1 microM nimodipine was not influenced by predepolarizations determined by treatments with calcium-free elevated potassium solutions, but when doses as low as 1 nM were applied the fast decay of the calcium level suggested a voltage dependence of the effect. Nimodipine also depressed < or = 90% of the plateau phase of the depolarization-induced internal calcium rise at different depolarizations. 6. Incubation in omega-conotoxin, fraction GVIA (5 microM) did not cause any significant decrease in the calcium response, whereas omega-agatoxin, fraction IVA (0.5 microM) depressed the calcium peak by 40-60% and its effect was additive with that of nimodipine. 7. We conclude that the nimodipine-sensitive current is a persistent, inactivation-resistant current that activates at a membrane potential lower than the other components and is likely to be responsible for the elevation of calcium determined by nonovershooting, prolonged depolarizations in these cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Functional characterization of the effect of nimodipine on the calcium current in rat cerebellar granule cells. 760 63

Calcium channels participate in the events linking axon terminal depolarization to neurotransmitter secretion. We wished to evaluate the role of N-type and non-N-type calcium channels in glutamatergic transmission at corticostriatal synapses, since this is a well defined excitatory synapse. In addition, these synapses are subject to a variety of forms of presynaptic modulation, some of which may involve alterations in calcium channel function. Application of the selective N-type channel blocker omega-conotoxin GVIA produced an irreversible depression of excitatory synaptic transmission in rat neostriatal slices shown by a decrease of approximately 50% in the amplitude of the synaptically driven population spike during field potential recording and a similar decrease in the amplitude of excitatory postsynaptic potentials during whole-cell recording. The component of transmission which was resistant to omega-conotoxin GVIA was blocked by omega-conotoxin MVIIC. omega-Agatoxin IVA had little effect on transmission. Activation of a presynaptic metabotropic glutamate receptor depressed transmission to a similar extent before and after omega-conotoxin GVIA treatment. Likewise, protein kinase C-activating phorbol esters potentiated transmission to the same extent before and after omega-conotoxin GVIA treatment. N-type calcium channels appear to be crucial for a component of excitation-secretion coupling at corticostriatal synapses. A component of transmission involves non-N-, non-L-type high-voltage-activated calcium channels. The effects of presynaptic metabotropic receptors and protein kinase C activation cannot be accounted for solely by alterations in the N-type channel function.
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PMID:Involvement of N- and non-N-type calcium channels in synaptic transmission at corticostriatal synapses. 781 9

1. This study examined the regulation of calcium currents in differentiated NG108-15 cells that had been stably transfected with cDNA encoding the short isoform of the human D2 dopamine receptor. Whole cell calcium currents were recorded by nystatin-perforated patch clamp recording. 2. Transient low-threshold calcium currents elicited by depolarizations from -100 mV to -20 mV were reversibly depressed by NiCl2 (84 +/- 8% at 30 microM; n = 3) and by omega-agatoxin IVA (15 +/- 5%; 100 nM, n = 7). These currents were unaffected by hD2 receptor activation. 3. High-threshold calcium currents elicited by depolarizations from -80 mV to 0 mV were partly blocked by omega-conotoxin GVIA (67 +/- 6% at 100 nM, n = 4) and by the subsequent addition of the dihydropyridine, nisoldipine (94 +/- 3% at 1 microM). Consistent with the presence of at least two distinct types of high-threshold calcium channels, nisoldipine alone (38 +/- 15% at 1 microM, n = 6) did not preclude the inhibition caused by omega-conotoxin GVIA (69 +/- 13% at 100 nM, n = 4). The residual current was completely blocked by 100 microM CdCl2 (98.8 +/- 0.4%, n = 7). 4. In hD2-transfected cells, but not untransfected cells, high-threshold currents were depressed by quinpirole (30 +/- 4% at 100 nM; n = 15) with a pEC50 of 8.61 +/- 0.22 (n = 5), as well as by (-)-noradrenaline (28 +/- 5% at 1 microM, n = 9). Responses to both agonists were selectively antagonized by S-(-)sulpiride (100 nM) but not by the alpha-adrenoceptor antagonist, phentolamine (1O microM). The depression caused by (-)-noradrenaline was positively correlated with that of quinpirole for each cell(r2 = 0.91, slope = 0.99).5. hD2-receptor-mediated inhibition of high-threshold calcium currents was abolished by pretreatment of cells with omega-conotoxin GVIA (100 nM; n = 4). However, a component of the high-threshold current was reversibly depressed by omega-conotoxin GVIA (67% to 45% depression after 10 min wash). This current was also depressed by hD2 receptor activation (59 +/- 9% depression in 100 nM quinpirole, n = 3),and was completely blocked by nisoldipine (95 +/- 2% at 1 MicroM).6. These data demonstrate that activation of hD2(short) dopamine receptors can regulate both wconotoxinGVIA, and dihydropyridine-sensitive high-threshold calcium currents in neuroblastoma cells.Morever, the ability of human D2 dopamine receptors to regulate more than one type of calcium current supports the notion that these receptors have a diverse functional role in the central nervous system.
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PMID:Depression of high-threshold calcium currents by activation of human D2 (short) dopamine receptors expressed in differentiated NG108-15 cells. 803 91

1. Whole-cell calcium currents were recorded from visually identified inhibitory interneurones located in stratum radiatum (near the border with stratum lacunosum-moleculare) of area. CA1 in rat hippocampal slices. Current-voltage (I-V) relationships in relatively well-clamped neurones showed that inward current activated between -50 and -40 mV (holding potential, -80 mV) and was maximal near -10 mV. Currents showed little inactivation over the course of 85 ms steps, and were completely blocked by removal of Ca2+ or addition of Cd2+. Prominent low-threshold currents were not observed under these conditions. 2. The calcium channels contributing to whole-cell currents in interneurones were examined using selective channel antagonists. The selective N-type calcium channel blocker omega-conotoxin GVIA (omega-CgTX-GVIA; 10 microM) irreversibly blocked 23.2 +/- 2.8% of whole-cell currents. The P/Q-type antagonist omega-agatoxin IVA (omega-Aga-IVA; 1-5 microM) blocked 10.4 +/- 3.3% of whole-cell currents. Block by omega-Aga-IVA was highly variable, ranging from 0 to 30%. The less selective conotoxin, omega-conotoxin MVIIC (omega-CTX-MVIIC; 5 microM) blocked 31.0 +/- 2.7% of whole-cell currents. The selective L-type channel antagonist nifedipine (20 microM) blocked 27.5 +/- 3.5% of whole-cell currents. 3. Whole-cell calcium currents were reversibly inhibited by the selective GABA(B) receptor agonists (+/-)-baclofen or CGP 27492 (1-3 microM; 18.9 +/- 1.4%). This inhibition was reversed or prevented by the selective GABAB receptor antagonist CGP 55845A (1 microM). Inhibition of inward current activated by voltage ramps was voltage dependent, being greatest near -10 mV, and less pronounced at more positive or negative potentials. Inhibition of calcium currents by GABAB receptor agonists was accompanied by an apparent change in the kinetics of whole-cell currents consistent with a slowing of the rate of activation. CGP 27492 depressed calcium currents by 16.1 +/- 1.9% before application of omega-CgTX-GVIA, and by 3.9 +/- 2.0% after application of omega-CgTX-GVIA in the same cells (P < 0.005), consistent with preferential block of N-type calcium channels. 4. Neither adenosine (200 microM) nor the selective mu-opioid receptor agonist Tyr-D-Ala-Gly-MePhe-Gly-ol (DAMGO; 2 microM) inhibited calcium currents. Similarly, CGP 27492, but not adenosine or DAMGO, induced an outward current (at - 70 mV) consistent with activation of inwardly rectifying potassium channels. 5. These results indicate that hippocampal inhibitory neurones located in stratum radiatum possess multiple calcium channel subtypes, including N-type, L-type, and at least two other types of high-threshold channels. Activation of GABAB receptors (but not adenosine or mu-opioid receptors) preferentially inhibits N-type channels in these neurones. Similar inhibition occurring in the terminals of interneurones could contribute to depression of inhibitory synaptic transmission by activation of GABAB autoreceptors.
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PMID:High-threshold Ca2+ currents in rat hippocampal interneurones and their selective inhibition by activation of GABA(B) receptors. 873 May 88

1. A gradual and prolonged decrease of the response, termed here "depression," evoked by repeated activation with transmembrane current stimuli was analyzed in rat CA1 hippocampal pyramidal cells under single-electrode current clamp by the use of the in vitro slice technique. 2. Depression was induced by 2-s duration 0.3- to 0.7-nA current pulses presented as a sequence of 12 stimuli at 3- to 60-s intervals. Sinusoidal currents (0.5-1.0 nA) at 5-Hz or 200-ms pulses repeated at 0.3-0.5/s, which may be more natural stimulations, also induced depression. 3. Depression outlasted stimulation up to 170 s in all cells tested. The initial high rate spike burst changed little (< 20%), whereas the lower rate adapted response decreased markedly (> 40%). Thus neurons increased their rate of adaptation. The afterhyperpolarizations following pulse-evoked responses increased in duration and amplitude with depression. There were input resistance (Rin) reductions at depolarized membrane potentials and during pulses. However, Rin reductions were considerably smaller or altogether absent late during interpulse intervals. Sub-threshold current stimuli were ineffective, indicating that spike activity was necessary to elicit depression. 4. Depression was 1) insensitive to the toxin omega-Agatoxin-IVA (omega-Aga-IVA; 0.5 microM), which blocked synaptic transmission, revealing a key involvement of intrinsic properties and little if any synaptic participation; 2) insensitive to 4-aminopyrydine (2.00-4.00 mM), which greatly enhanced excitatory and inhibitory synaptic efficacy, again suggesting little synaptic involvement and a principal postsynaptic participation, and no participation of the K(+)-mediated currents IA and ID; 3) abolished by carbamalcholine (5.0-20.0 microM)- an effect blocked by atropine (1.0-10.0 microM)- and reduced by Ca(2+)-free solutions, and by intracellular injection of the Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), suggesting that Ca(2+)-dependent K(+)-mediated currents are key factors, with a less important participation of the K(+)-mediated IM current. 5. We conclude that depression was due to activity-dependent modifications in intrinsic properties, with little if any synaptic participation. Depression may be functionally significant because it was induced by potentially natural stimulations. A model is proposed that accounts for the main traits of depression. In the model, depression was induced by a gradual decline of the speed at which Ca2+ was buffered intracellularly; an increase in the IK(Ca)S activation rate constant also simulated depression.
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PMID:Activity-dependent response depression in rat hippocampal CA1 pyramidal neurons in vitro. 898 7

Previous studies have demonstrated that the voltage-dependent Ca2+ current recorded from the cell body of the crayfish abdominal motoneuron, F3, undergoes a long-term reduction as a result of increased impulse activity. The properties of the Ca2+ channels undergoing this long-term change were examined with the use of two-electrode voltage-clamp techniques. The Ca2+ current was activated at -50 to -40 mV and its amplitude was maximal at 0 mV (-135.0 +/- 25.8 nA, mean +/- SE, n = 14). The current-voltage relationship and the greater sensitivity of the Ca2+ channel to Cd2+ than Ni2+ indicated that Ca2+ influx occurs through high-voltage-activated (HVA) Ca2+ channels. Loose-patch recordings demonstrated that the Ca2+ current was generated by the membrane of the cell body. When Ba2+ was substituted for extracellular Ca2+, there was a 40% increase in the amplitude of the inward current and a negative shift of approximately 10 mV in the I-V relationship. Application of the P-type Ca2+ channel antagonist omega-agatoxin IVA (omega-AgTX IVA) produced a significant 33% (n = 6) reduction in the peak amplitude of the Ba2+ current, whereas neither the L-type Ca2+ channel antagonist nifedipine nor the N-type channel antagonist omega-conotoxin GVIA produced a reduction in the Ba2+ current. The voltage-dependent activation of this P-type (omega-AgTX-IVA-sensitive) Ca2+ channel was similar to previously identified P-type channels, but different from that of the non-P-type (omega-AgTX-IVA-resistant) Ca2+ channels. When Ca2+ currents were measured 6-7 h after an increase in impulse activity (5-Hz stimulation for 45-60 min), there was a 43% reduction in the amplitude of the P-type current, but no significant changes in the non-P-type current amplitude. These results demonstrate that at least two subtypes of HVA Ca2+ channels contribute to the macroscopic Ca2+ current observed in the cell body of this crayfish phasic motoneuron: one belongs to the previously described P-type Ca2+ channel and the other(s) does not belong to the N-, L-, or P-type Ca2+ channel. The long-term, Ca(2+)-dependent reduction in Ca2+ current previously demonstrated in motoneuron F3 is produced by the selective reduction of this P-type Ca2+ current. This activity-dependent reduction in the P-type Ca2+ current is likely involved in the long-term depression of transmitter release observed at the neuromuscular synapses of this motoneuron.
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PMID:Characterization of a P-type calcium current in a crayfish motoneuron and its selective modulation by impulse activity. 912 May 98

The effects of glutamate metabotropic receptors (mGluRs) on excitatory transmission in the nucleus accumbens were investigated using electrophysiological techniques in rat nucleus accumbens slices. The broad-spectrum mGluR agonist (1S,3R)-1-aminocyclopentyl-1,3-dicarboxylate, the mGluR group 2 selective agonists (S)-4-carboxy-3-hydroxyphenylglycine, (1S,3S)-ACPD) and (2S,1'S,2'S)-2-(2'-carboxycyclopropyl)glycine (L-CCG1), and the mGluR group 3 specific agonist L-2-amino-4-phosphonobutyrate (L-AP4) all reversibly inhibited evoked excitatory synaptic responses. The specific group 1 mGluR agonist (R,S)-3,5-dihydroxyphenylglycine [(R,S)-DHPG] did not depress transmission. Dose-response curves showed that the rank order of agonist potencies was: L-CCG1 > L-AP4 > (1S,3S)-ACPD. Group 2 and 3 mGluRs inhibited transmission via a presynaptic mechanism, as they increased paired-pulse facilitation, decreased the frequency of miniature excitatory postsynaptic currents and had no effect on their amplitude. The mGluRs did not inhibit transmitter release by reducing voltage-dependent Ca2+ currents through N- or P-type Ca2+ channels, as inhibition persisted in the presence of omega-conotoxin-GVIA or omega-Aga-IVA. The depression induced by mGluRs was not affected by specific antagonists of dopamine D1, GABA-B or adenosine A1 receptors, indicating direct effects. Finally, (R,S)-DHPG specifically blocked the postsynaptic afterhyperpolarization current (I(AHP)). Our results represent the first direct demonstration of functional mGluRs in the nucleus accumbens of the rat.
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PMID:Metabotropic glutamate receptors in the rat nucleus accumbens. 924 Apr 9


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