UMLS:C0011570 - FACTA Search

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

There have been few reports concerning facilitation and depression in sympathetic ganglia9,17,40. In the present investigation, pairs of excitatory postsynaptic potentials (EPSPs) were recorded intracellularly from bullfrog paravertebral sympathetic ganglia for an analysis of the site and mechanism responsible for the phenomena of facilitation and depression of ganglionic transmission. The ratio of the amplitude of the second of a depression of ganglionic transmission. The ratio of the amplitude of the second of a pair of EPSPs divided by the first was compared to the time interval between each pair of EPSPs divided by the first was compared to the time interval between each pulse. These ratios demonstrated two phases: an earlier phase of facilitation (20-500 msec pulse intervals) and a later phase of depression (500 msec-10 sec). Additional parameters-rate of rise of synaptic potentials (dV/dt), synaptic currents (EPSCs), and synaptic conductances (Gtr)-were determined and all confirmed the results obtained with EPSPs. Furthermore, the degree of facilitation or depression could be modulated by altering the extracellular concentration of calcium. On the other hand, comparison of the amplitude of pairs of presynaptic terminal spikes did not show any variability over similar stimulus intervals, nor were the amplitudes of miniature EPSPs significantly different before or after an evoked EPSP. Therefore, the processes of facilitation and depression of ganglionic transmission occur as a result of normal nerve terminal activity. The processes are occurring simultaneously, such that one or the other may predominate depending upon the interval between pulses, as well as the relative concentration of extracellular calcium.
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PMID:Facilitation and depression of synaptic transmission in amphibian sympathetic ganglia. 18 60

The release of endogenous taurine, GABA, glycine, aspartate, glutamate, glutamine and alanine from the rat visual cortex was measured using a cortical cup technique. The electrocorticogram (ECoG) was monitored throughout most experiments. 2. Spreading depression, evoked by the dropwise placement of 10% KCl solution on to the brain outside the cup was associated with a significant increase in the release of GABA and glutamine but a marked fall in that of glutamate. The evoked release of GABA and glutamate but not of glutamine was Ca2+ dependent. 3. A solution containing 50 mM-K+ placed within the cup elicited a significant increase in the release of taurine and GABA, whereas 100 mM-K+ additionally released aspartate and glutamate. The K+-evoked release of these amino acids with the exceptions of taurine and glutamine was Ca2+-dependent. 4. Three series of experiments were carried out in which the preparations were stimulated electrically. Bipolar stimulation (100 Hz, 1 msec pulse width, 2-5 mA for 5 min) with the electrode within the cup was followed by significant increases in taurine, GABA and glutamate release; using a 5 mA current, there was an additional release of aspartate and alanine. Only the evoked release of GABA and glutamate was Ca2+ dependent. 5. In the second and third series of experiments, the electrode was sited adjacent to the cup or on the contralateral cortex respectively. Following stimulation (100 Hz, 1 msec pulse width, 2-5 mA for 5 min) there was a significant increase in taurine and GABA release and a significant fall in the release of aspartate and glutamate. With the exception of taurine, these changes in release were Ca2+ dependent. Reducing the stimulus current to 1-5 mA or the period of stimulation to 2-5 min initiated similar but statistically insignificant changes in release. A range (10-100 Hz) of stimulation frequencies was examined: the evoked release of GABA was linearly related to frequency whereas that of taurine was frequency-independent. The fall in aspartate and glutamate release was maximal at a frequency of about 50 Hz. 6. The results are discussed in relation to (a) the possible sites of release of the amino acids and (b) the proposed neurotransmitter roles of the physiologically active amino acids.
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PMID:The release of endogenous amino acids from the rat visual cortex. 18 88

Two siblings, female 10 years old, and male 15 years old, with the diagnosis of vitamin D-dependent rickets were studied. Another sibling, also with the same diagnosis, died of bronchopnemonia at about 7 months of age. Both patients developed rachitic manifestations since the first year of life, which persisted despite the administration of massive doses of vitamin D intermitently. Severe hypocalcemia, moderate hypophosphatemia and elevated serum alkaline phosphatase were the most characteristic biochemical findings. Both patients showed diminished renal tubular reabsorption of amino acids and phosphates. These alterations were reversible during I.V. calcium gluconate administration. The clinical biochemical and X-ray manifestations disappeared completely after one year of treatment with dihydrotaquisterol. Vitamin D-dependent rickets is an autosomal recessive disease, characterized by a hydroxylation defect of 25 hydroxycholecalciferol at the carbon 1 level, due to abscence of 25 hydroxy-D1-hydroxylase. Thus 1-25 Dihydroxycholecalciferol, the active form of vitamin D3 is not formed, resulting in depression of intestinal calcium absorption and reabsorption from the bones.
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PMID:[Hypocalcemic vitamin D-dependent renal rickets]. 18 33

1. Responses of cerebral cortical neurones to the microiontophoretic application of acetylcholine, noradrenaline, cyclic adenosine 3',5'-monophosphate (cyclic AMP) and cyclic guanosine 3',5'-monophosphate (cyclic GMP) were examined.2. The application of acetylcholine and cyclic GMP to identified pyramidal tract neurones resulted in an increased frequency of firing in a large number of cells. Upon application of both substances to cells which could not be identified as pyramidal tract cells, a reduction in the frequency of spontaneous firing was sometimes observed.3. Careful current controls had no effect on the cells discussed here, indicating that the observed responses were not due to the iontophoretic currents. Also, the electro-osmotic ejection of cyclic GMP (outward current) produced similar changes of cell firing to those which followed iontophoretic application (inward current).4. The microiontophoretic application of atropine resulted in a blockade of acetylcholine responses while leaving responses to cyclic GMP unaffected. This suggests that cyclic GMP was not acting indirectly by releasing acetylcholine from presynaptic endings.5. Ejection of cyclic GMP from solutions containing calcium ions produced responses comparable to those produced by cyclic GMP alone. It is unlikely therefore that cyclic GMP was causing excitation by chelating calcium.6. Applications of noradrenaline and cyclic AMP produced a reduction in the spontaneous discharge rate of most neurones tested.7. Phosphodiesterase inhibitors such as ICI 63,197 caused a potentiation of the noradrenaline responses of pyramidal tract neurones.8. 5'-adenosine monophosphate produced a powerful depression of all cells to which it was applied. This action was blocked by aminophylline, suggesting the effect was mediated through an adenosine receptor. Responses to cyclic AMP were usually not abolished, but were reduced by about 50% in amplitude.9. These results are consistent with the hypothesis that cyclic AMP may mediate some neuronal effects of noradrenaline and cyclic GMP may mediate some effects of acetylcholine. The results are also consistent with the suggestion that the two nucleotides may sometimes mediate opposite cellular responses to humoral stimuli.
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PMID:Microiontophoretic studies of the effects of cylic nucleotides on excitability of neurones in the rat cerebral cortex. 19 28

Adenosine depressed norepinephrine contractions of dogs' saphenous vein strips in both the presence and the absence of Ca2+ and after inhibition of calcium influx by verapamil. It antagonized noncompetitively contractions induced by Ca2+ in depolarized strips after alpha-adrenergic blockade. Contractions obtained with acetylcholine were also depressed by adenosine. This depression was not accompanied by an increase in cAMP or a decrease in the elevated cGMP level. Thus the depression of the smooth muscle cell reactivity still occurs in the absence of calcium influx and is not mediated by the cyclic 3',5'-nucleotide system. Adenosine diphosphate and triphosphate, but not adenosine (10(-6) to 10(-4) M), increased the basal tension of resting saphenous strips. This was prevented by removal of calcium from the bath. In contracted strips, lower concentrations of both nucleotides (10(-6) to 10(-5) M) caused relaxation whereas with high concentrations (10(-4) to 10(-3) M) further contraction occurred. Thus, unlike adenosine, the adenine nucleotides facilitate calcium influx.
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PMID:Action of adenosine and adenine nucleotides on dogs' isolated veins. 19 78

1.beta-Bungarotoxin, crotoxin and taipoxin, presynaptic neurotoxins of snake venom origin, have about the same phospholipid-splitting activities as a much less toxic cobra phospholipase A2 in the presence of Ca2+ and deoxycholate. 2. Sr2+ was a much less effective activator of the enzymes than is Ca2+, the activation by Sr2+ being only 3-6% for beta-bungarotoxin and crotoxin and 12% for taipoxin. 3. Sr2+ also inhibited the Ca2+ -activated enzymes by 80% in the cases of beta-bungarotoxin and crotoxin, but only 16% in the case of taipoxin. 4. Mg2" had no significant effect on beta-bungarotoxin or crotoxin, but activated taipoxin in the presence or absence of Ca2". 5. In Sr2+ -Tyrode lacking Ca2+ all three toxins exhibited the same immediate depression followed by facilitation in the rat and mouse diaphragms, but the final blocking activity was only 3-10% with beta-bungarotoxin and crotoxin and was 30% with taipoxin. 6. In Sr2+ -Tyrode, increasing in the rate of nerve stimulation had less accelerating effect on the development of neuromuscular block than in Ca2+ -Tyrode for any of the toxins. 7. Removal of Mg2+ from Sr2+ -Tyrode did not diminish the potency of taipoxin in blocking neuromuscular transmission, suggesting that enzyme activity at the outer surface of the axolemma does not contribute to the neuromuscular blocking action. 8. All of the results indicate that there are close correlations between the presynaptic activities of these toxins and their phospholipid-splitting activities in the cationic environment prevailing in the axoplasm. Apparently the final blocking effect of these toxins is due to phospholipase A action within the nerve terminal.
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PMID:Effects of Sr2+ and Mg2+ on the phospholipase A and the presynaptic neuromuscular blocking actions of beta-bungarotoxin, crotoxin and taipoxin. 19 83

Short term in vitro experiments showed that, added alone, verapamil inhibited both glycolysis and Ca uptake in embryonic chicken and rat bone cells. Added together with PTH, verapamil (0.02 MM) enhanced cAMP production, had no effect on lactate production, but significantly inhibited citrate, calcium and phosphate release from embryonic rat and mouse calvaria incubated under hypocalcemic conditions. The depression by verapamil of PTH-stimulated demineralization was confirmed histologically. It is concluded that in addition to cAMP, Ca plays a key role in the action of PTH on bone.
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PMID:The effect of verapamil on the action of parathyroid hormone on embryonic bone in vitro. 20 Apr 41

1 The report of the depression by indomethacin of vasoconstrictor responses to noradrenaline and their partial restoration by prostaglandin E(2) (PGE(2)) and PGE(1) in rat isolated perfused mesenteric blood vessels was investigated. The further suggestion that prostaglandins may be necessary for the combination of noradrenaline with the alpha-adrenoceptor in this tissue was also studied.2 The reported depression by indomethacin was confirmed and was further shown to be in the form of a concentration-dependent flattening of the noradrenaline concentration-effect curve.3 A concentration-dependent restorative effect was observed for all prostaglandins studied. The decreasing order of potency for the restoration towards normal of the indomethacin-depressed responses to noradrenaline was: PGE(2), PGE(1), PGA(1), PGF(2alpha), PGA(2).4 The prostaglandins studied were not uniform in their restorative actions and could be separated into two groups. PGE(2) and PGE(1) restored responses towards the control level whereas PGA(1), PGA(2) and PGF(2alpha) increased responses to an above control level and did so over a smaller concentration range. The possibility of several prostaglandin receptors is discussed.5 At concentrations equi-effective in restoring depressed responses to control levels PGA(1) but not PGE(2), caused a parallel shift of the noradrenaline concentration-effect curve to the left and a small, gradual rise in the basal perfusion pressure.6 The reason for the differing effects remains obscure but does not seem to involve a change in the alpha-adrenoceptor as indicated by the pA(2) of phentolamine. Furthermore, the restorative and potentiating effect of PGA(1) is not mediated by blockade of neuronal uptake of noradrenaline.7 It appears that prostaglandins are required for the vasoconstrictor action of noradrenaline in rat mesenteric blood vessels and that this effect is distal to the drug-receptor interaction. The possible involvement of prostaglandins with intracellular calcium ions is discussed.
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PMID:The influence of prostaglandins on noradrenaline-induced vasoconstriction isolated perfused mesenteric blood vessels of the rat. 20 65

In a retrospective analysis to determine whether secondary hyperparathyroidism in uremia has a role in uremic peripheral neuropathy, we simultaneously measured motor-nerve conduction velocity and serum parathormone level in 42 uremic patients. We compared age-matched groups of nondiabetic uremic patients, divided into three groups according to serum parathyroid hormone, for degree of impairment of motor-nerve conduction velocity, and 12 diabetic patients with uremia. The group with highest levels had a significantly (P less than 0.01) lower conduction velocity (25.3 +/- 4.9 m per second) than the group with normal or slightly elevated parathyroid hormone, who had only mild depression of nerve conduction (45.1 +/- 1.3 m per second). Mean serum calcium and creatinine were not significantly different between groups. Nerve conduction velocity was similarly depressed in 17 patients on additional dialysis studied prospectively and divided into groups according to parathyroid hormone levels. These results suggest a relation between high parathormone levels and uremic neuropathy and implicate parathyroid hormone as a uremic toxin.
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PMID:Search for the uremic toxin. Decreased motor-nerve conduction velocity and elevated parathyroid hormone in uremia. 20 86

When retinas from dark-adapted C57BL/6 mice were incubated in the dark for 5 min at 37 degrees C in Earle's medium, they contained 80-120 pmol/mg protein of cGMP and about 13 pmol/mg protein of cAMP. When the incubation in darkness was in calcium-deficient Earle's medium with 3 mM EGTA, a 10-20 fold increase occurred in the cGMP level, peaking at 2-3 min, but no change occurred in cAMP. This elevated level fell in 3 min to normal dark levels on return to normal Earle's medium, but was still about three times that of control levels after 15 min in EGTA-containing solution. Bright light after 2 min of dark incubation of dark-adapted retinas resulted in a 40-50% fall in cGMP, and bright light sharply reduced the elevated dark cGMP level of retinas in calcium-deficient media with 3 mM EDTA. However, no depression of normal dark levels of cGMP has thus far been obtained by increasing external calcium levels, even in the presence of the ionophore A23187. All the above phenomena involving dark cGMP levels and calcium are similar in Earle's medium with 100 mM of K+ substituted for Na+. Congenic rodless (rd/rd) mouse retinas have less than 5% of control cGMP and show only traces of calcium sensitivity. Thus, the above phenomena in controls are likely to be largely occurring in rods. The data suggest a dependency of the dark cGMP level on the calcium level, but that the light-induced fall in cGMP may largely be calcium insensitive.
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PMID:Calcium and cyclic nucleotide regulation in incubated mouse retinas. 20 16

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