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)

Isoproterenol induced long-lasting potentiation (LLP) of the medial perforant path-evoked excitatory post-synaptic potential (EPSP) and long-lasting depression (LLD) of the lateral perforant path-evoked EPSP in the absence of perforant path activation. The NMDA receptor antagonist D-(-)-2-amino-5-phosphonovaleric acid [D(-)APV] blocked the induction of LLP and LLD. After wash, a subsequent exposure to isoproterenol induced only LLP of medial perforant path EPSPs; LLD of lateral perforant path-evoked EPSPs did not occur. Our results are consistent with the hypothesis that beta-adrenergic agonist-induced synaptic modifications in the dentate gyrus arise from pre- and postsynaptic events.
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PMID:Beta-adrenergic agonist-induced long-lasting synaptic modifications in hippocampal dentate gyrus require activation of NMDA receptors, but not electrical activation of afferents. 197 21

A 21-year-old young man with Down's syndrome presented with depressive symptoms and intermittent features of a Parkinsonian like syndrome. After treatment with amitriptyline for 18 months he slowly improved and almost regained his former personality. Neither imaging procedures nor clinical features were able to establish a definitive cause of this patient's depression. There was no evidence of either neurodegenerative or premature aging processes. Discussion focused on increasing clinicians' awareness of frequently undiagnosed but treatable depressive disorders within the Down's syndrome population.
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PMID:Differential diagnosis and treatment of depressive features in Down's syndrome: a case illustration. 214 93

When perfused with high K+ (8.1 to 14.9 mM)-Tyrode's solution, the upstroke of action potentials in the isolated guinea-pig ventricular muscle is composed of two components and there are two separable peaks in the first derivative, i.e., Vmax, fast and Vmax, slow. The Vmax, fast was a measure of activation of the residual fast channel, while the Vmax, slow was that of the slow channel. Isoproterenol depressed Vmax, fast with increase in Vmax, slow, in a concentration-dependent manner (10(-8) to 10(-6) M). This depression of Vmax, fast was greater at more depolarized levels of membrane potential. Therefore, the isoproterenol-induced depression of Vmax, fast may be due to a negative shift of the curve relating Vmax, fast to the take-off potential (Em) (Vmax--Em relationship), along the voltage axis. The negative shift of Vmax--Em relationship by isoproterenol was also recognized in small preparations the size of which is well within the space constant. The negative shift was inhibited in the presence of beta-blockers (pindolol 1 microgram/ml or atenolol 10 micrograms/ml) but not by a calcium antagonist, 1-verapamil (1 microgram/ml). These results suggest that isoproterenol blocks sodium channels in the depolarized ventricular muscle via stimulation of the beta-adrenoceptors and that the depression of Vmax, fast is not mediated by the well-known effects of isoproterenol on Vmax, slow, i.e., increased influx of Ca2+ ions.
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PMID:Isoproterenol inhibits residual fast channel via stimulation of beta-adrenoceptors in guinea-pig ventricular muscle. 241 Jun 22

The excitatory responses of neurones in the anterior cingulate cortex of the rat to iontophoretically applied substance P (SP) are reduced by noradrenaline (NA) applied iontophoretically or released from noradrenergic pathways. In order to determine the receptor involved in this inhibitory effect we have studied the effects of a number of receptor-specific adrenergic agonists and antagonists on responses of cingulate neurones to SP in rats anaesthetized with chloral hydrate. Low iontophoretic currents (0-15 nA) of NA, adrenaline and the beta-agonist, clenbuterol, all strongly reduced responses to SP. Isoprenaline was also effective but less consistently so, although problems were experienced with its iontophoretic release from micropipettes. The alpha 1-agonists, phenylephrine and methoxamine were also able to reduce responses to SP. However, this reduction required higher iontophoretic currents (15-60 nA) and was associated with depressant effects on baseline firing rate. The alpha 2-agonist clonidine was only weakly active at high currents and this too was associated with depression of baseline firing. Similar weak effects were noted with dopamine. The inhibitory effects of NA on SP responses were convincingly blocked or reversed by the beta-antagonist, practolol, but not by the alpha 1-antagonist, prazosin. The reduction of SP responses by phenylephrine was also blocked by practolol but unaffected by prazosin. Finally, reduction of SP excitations by activation of the coeruleocortical pathway was also blocked by practolol applied iontophoretically to the cortical cells. These results are consistent with the hypothesis that the effect of NA on SP responsiveness in the cingulate cortex is mediated by beta-adrenoreceptors.
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PMID:Pharmacological characterization of the receptor mediating the adrenergic inhibition of responses to substance P in the cingulate cortex. 242 29

1. The longitudinal muscle isolated from the uterus of oestrogen-treated rats was not spontaneously active in Locke solution, and electrical stimulation evoked phasic contraction. Isoprenaline (3 x 10(-11) - 10(-8) M) and dibutyryl cyclic AMP (db cyclic AMP, 0.1-0.8 mM) depressed the phasic contraction; the depression was enhanced in the presence of 0.6 mM Mg. 2. The contracture generated by 40 mM K was partially relaxed by isoprenaline (10(-11) - 10(-8) M) and db cyclic AMP (0.1-0.8 mM). Mg (0.6 mM) enhanced the isoprenaline-induced relaxation, but not that induced by db cyclic AMP. 3. The membrane potential of the muscle was -61 mV, and electrical stimulation induced an action potential which consisted of spike and plateau components. Application of isoprenaline and db cyclic AMP mainly reduced the duration of the plateau potential. The effect was potentiated by 0.6 mM Mg. 4. The membrane was hyperpolarized, accompanied by a decrease in membrane resistance, when 10(-8) M isoprenaline or 0.8 mM db cyclic AMP was applied. The effects of isoprenaline were prominently augmented in the presence of 1.2 mM Mg, while those of db cyclic AMP were slightly potentiated. 5. Forskolin (0.1 microM) or papaverine (10 microM) inhibited the phasic contraction and the K-contracture. The effect on the phasic contraction was potentiated by 0.6 mM Mg, while that on the K-contracture was not affected. 6. Forskolin shortened the action potential at 0.3 microM, and hyperpolarized the membrane with a decrease in membrane resistance at 3.0 microM. The membrane effects were augmented by 0.6 and 1.2 mM Mg, respectively. 7. It was hypothesized that external Mg ions could affect at least two processes involved in actions at beta-adrenoceptors on rat myometrium; receptor-agonist interaction and cyclic AMP-mediated inhibition of membrane excitability.
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PMID:Augmentation by external Mg ions of beta-adrenoceptor-mediated actions in the longitudinal muscle of rat uterus. 254 49

The effect of adrenaline (Ad) on muscarinic transmission was examined in B neurones of bullfrog sympathetic ganglia by using intracellular and voltage-clamp recording methods. Bath-application of Ad (5-500 microM) caused a depression of the slow excitatory postsynaptic potential (EPSP) elicited by repetitive stimulations of preganglionic nerve fibres in the presence of curare (30 microM). Ad also depressed the 'muscarinic' ACh potential induced by ionophoretic application of ACh directly to curarized sympathetic neurones in a concentration-dependent manner. Isoprenaline mimicked the effect of Ad in producing the inhibition of the 'muscarinic' ACh potential. Propranolol antagonized the inhibitory action of Ad. Dibutyryl adenosine 3',5'-monophosphate had no significant effect on the 'muscarinic' ACh potential. Under voltage-clamp conditions, Ad caused an inward current associated with inhibition of the M-current (Brown and Adams 1980). Ad depressed the amplitude of slow postsynaptic currents produced by applications of ACh and muscarinic. At a concentration of 100 microM, Ad produced a 68 +/- 8% (n = 12) depression of the amplitude of the muscarinic ACh current. The inhibition of muscarinic transmission induced by Ad is due to a direct suppression of the muscarinic current at the postsynaptic membrane in bullfrog sympathetic ganglia.
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PMID:Adrenaline inhibits muscarinic transmission in bullfrog sympathetic ganglia. 254 82

The value of exercise thallium scintigraphy in detecting coronary artery disease is well established. However, there are at times situations in which the exercise test cannot be readily used. Isoproterenol (ISP) stress ECG (ISP-ECG) is reportedly a useful method in diagnosing coronary artery disease. In the present study, we assessed the diagnostic value of ISP thallium scintigraphy, comparing it with those of ISP-ECG and exercise thallium scintigraphy. The study population consisted of 24 patients who had histories of chest pain without previous myocardial infarction. ISP was given at increasing doses of 0.02, 0.04, 0.08 micrograms/kg/min at 3-minute intervals, and was terminated for any of the following reasons: angina, significant arrhythmia, significant ST segment depression (greater than or equal to 0.1 mV) or target heart rate. Thallium scintigrams were obtained immediately after terminating ISP infusion, and after a 3-hour delay, redistribution scans were obtained. Scintigrams were considered positive when a reversible defect was present. In nine patients who underwent exercise tests, exercise thallium scintigraphy was also performed. After the stress tests, coronary angiography was performed. According to the presence or absence of significant coronary artery stenosis (greater than or equal to 75%), all subjects were divided into two groups: coronary artery disease (CAD) group (n = 12) and so-called normal coronary (NC) group (n = 12). 1. Among 12 patients in the CAD group, ISP induced anginal pain in six (50%), and ISP-ECG and ISP thallium scintigraphy were positive in 10 (83%) and in 11 (92%), compared with four (33%), four (33%) and two (17%) in the NC group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Isoproterenol stress thallium scintigraphy for detecting coronary artery disease. 264 60

Isoproterenol, as an exercise simulating agent, was evaluated in twenty subjects, ten normal volunteers and ten with Coronary Artery Disease (CAD). Both groups were evaluated using 0.5 ug increments of intravenous infusion of isoproterenol every 3 minutes with computerised ECG (Marquette Electronics--MAC PC) monitoring. The normal volunteers did not have significant ST segment depression even at heart rates of 130 BPM. The CAD groups showed diagnostic ischaemic ST segment depression at heart rates below 130 BPM. None of the subjects had any serious complications during or after the test. Isoproterenol infusion is a better alternative to exercise testing.
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PMID:Isoproterenol infusion--an alternative to exercise testing. 274 6

1. The effects of cholinergic and purinergic stimulation on action potential, force of contraction and 86Rb efflux were investigated in human atrial and ventricular heart muscle. 2. In atrial heart muscle, carbachol and (-)-N6-(R-phenyl-isopropyl)-adenosine (R-PIA) and 5'-(N-ethyl)-carboxamido-adenosine (NECA) evoked transient decreases of action potential duration and force of contraction; the steady-state effects on force of contraction were virtually identical to control values. In the presence of propranolol, steady-state values after carbachol, R-PIA or NECA amounted to about 50% of control values. 3. In ventricular heart muscle, carbachol, NECA and R-PIA did not significantly affect the action potential configuration or force of contraction. 4. Carbachol, NECA and R-PIA induced a maintained depression of the positive inotropic response to isoprenaline in both atrial and ventricular heart muscle. 5. The rate constant of 86Rb efflux was slightly increased by carbachol, NECA and R-PIA in atrial (10-20%) but not in ventricular heart muscle. 6. In the presence of isoprenaline, carbachol, NECA and R-PIA did not significantly affect the rate constant of 86Rb efflux in both atrial and ventricular heart muscle. Isoprenaline alone increased the rate constant of 86Rb by about 25% in both tissues.
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PMID:Functional role of cholinoceptors and purinoceptors in human isolated atrial and ventricular heart muscle. 279 Mar 82

The clearance function of complement receptors on Kupffer cells is depressed after several forms of experimental injury. In vitro studies have shown that stimulation of beta-receptors on macrophages causes a depression of several aspects of macrophage function. The present study evaluated the possibility that the increase in sympathetic activity associated with injury contributes to the depression of Kupffer cell complement receptor function. Complement receptor function was assessed in rats from the hepatic uptake of rat erythrocytes coated with IgM. Isoproterenol caused a depression of receptor function when infused at a rate of 5.0 and 0.5 micrograms/kg/min for 15 min but not after infusion of 0.05 micrograms/kg/min. Infusion of isoproterenol, norepinephrine, and epinephrine at 0.5 micrograms/kg/min depressed receptor function by 41%, 38%, and 29%, respectively. Beta-receptor blockade with propranolol prevented the depression of receptor function caused by isoproterenol and norepinephrine. Thermal injury depressed receptor function by 65%, and this depression was reduced to 35% by beta-receptor blockade. Therefore, stimulation of beta-receptors on macrophages by increased circulating levels of catecholamines after injury could contribute to the depression of Kupffer cell function caused by injury.
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PMID:Effect of beta-receptor stimulation on Kupffer cell complement receptor clearance function. 284 35


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