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)

The Mauthner fiber giant fiber synapses of the hatchetfish are chemically transmitting axo-axionic synapses in the medulla. Tetanic stimulation at room temperature depletes the presynaptic Mauthner terminal of vesicles and leads to the appearance of large numbers of irregular membraneous compartments in the terminal. Stimulation during cooling to 12 degrees C depletes the terminal of vesicles and greatly increases the external surface, which forms large whorls of invaginating double membranes. Many coated vesicles are attached to the surface and the invaginating whorls. It is concluded that vesicles are discharged by exocytosis and fusion of their membrane with the external surface, and that at room temperature, membrane is reinternalized by coated vesicles and formed into irregular compartments. In completion of the cycle, these compartments disappear, and the vesicle population recovers over an hour or two of rest. When the Mauthner fibers are stimulated at low rates, the p.s.p.'s in the giant fibers are large and suprathreshold. Minature p.s.p.'s are generated spontaneously or can be evoked by subthreshold depolarization or tetanic stimulation of the Mauthner fiber. Stimulation of the Mauthner fibers at gradually increasing frequencies depresses p.s.p. amplitude to or below the level of miniature p.s.p.'s, but no failures are observed. Small p.s.p.'s without failures suggest that the quantum number remains high but that quantal size is greatly reduced, either by partial filling, as is supported by the morphological observation of vesicle depletion, or by desensitization. When stimulation is stopped, recovery of p.s.p. amplitude occurs in 1 or 2 seconds, but if tetanic stimulation is resumed immediately, p.s.p. amplitude decreases again and much more rapidly than in the initial rundown. This result suggests that depression of p.s.p. amplitude is not due to desensitization and leaves partial filling as the most likely explanation of small quanta. Calculated quantal size following a tetanus recovers in 200-500 ms, which probably largely reflects the time for filling since enough vesicles can be supplied to prevent failures with much shorter intervals between stimuli. Because quantal size appears to decrease gradually as stimulation frequency increases, it appears that release of vesicles can interrupt filling, leading to the conclusion that filling and release sites are very close together. This conlusion is consistent with other data in the literature obtained by different techniques.
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PMID:Stimulation-induced depletion of vesicles, fatigue of transmission and recovery processes at a vertebrate central synapse. 18 Nov 97

The effects of soman, sarin and VX were examined on ganglionic transmission through paravertebral chain ganglia of the bullfrog, Rana catesbeiana. Low frequency (0.1 Hz), short (2 sec) and long (10 sec) trains of preganglionic stimulation, after exposure to the agents, induced repetitive activity in the extracellularly recorded compound action potential. An irreversible transient depression was observed after exposure to the agents during the first second of short and long stimulus trains. Long stimulus trains of high frequency were required to produce a rundown in the amplitude of the compound action potential, whether recorded in the presence of each agent (10 microM) or following a wash with agent-free solution. The rundown of the compound action potential was use-dependent and not blocked or reversed by atropine (10 microM). Intracellular recordings, in the presence of either soman or VX, demonstrated (1) an increase in the amplitude of the residual excitatory postsynaptic potential or current evoked by synaptic stimulation, (2) an increase in the amplitude and duration of the acetylcholine-induced potential, (3) no increase in either the amplitude or duration of the carbachol-induced potential, (4) repetitive firing with orthodromic but not antidromic stimulation and (5) a concentration- and frequency-dependent depolarization of individual ganglion neurons with orthodromic stimulation which resulted in a decrease in the generation of action potentials. These results suggest that the agent-induced decrease in the compound action potential occurred as a consequence of activity-dependent depolarization of ganglion neurons, which occurs after inhibition of cholinesterase.
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PMID:The effects of irreversible acetylcholinesterase inhibitors on transmission through sympathetic ganglia of the bullfrog. 166 71

Effects of a novel antiarrhythmic agent, 5-hydroxydecanoate (5-HD), were investigated on the electrical activity of the guinea pig ventricular myocytes. The shortening of action potential duration induced by applying iodoacetate (IAA) for 5 to 10 min was reversed completely by 5-HD (100 microM) in the papillary muscle. The single channel current recording in the cell-attached configuration revealed both activation of the ATP-sensitive K+ channel during the treatment with IAA and after depression of the channel by the additional application of 100 microM 5-HD. The quick rundown of the ATP-sensitive K+ channel activity interfered the analysis of the drug effect in the usual inside-out patch configuration. The channel activity in the isolated patch was partially recovered and stabilized by applying a tissue extract, which was prepared from guinea pig ventricle. Under this condition relationship between the 5-HD concentration and the K+ channel open probability was characterized with a K1/2 of 0.16 microM and a Hill coefficient of 0.88. The open- and close-time analysis revealed a decrease of the mean duration of the bursting channel opening and an increase of the interburst time under the effect of 5-HD. The inward-rectifier K+ channel, responsible for the resting K+ conductance, was not affected by 5-HD. It was concluded that the curative effect of 5-HD on the shortened action potential in the IAA-treated myocytes is mediated by the depression of the ATP-sensitive K+ channel.
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PMID:Blockade of the ATP-sensitive K+ channel by 5-hydroxydecanoate in guinea pig ventricular myocytes. 173 18

The action potential configuration, developed tension, and resting tension were monitored in normoxic and hypoxic guinea pig papillary muscles superfused with solutions containing no substrate, glucose, or acetate (1-10 mM). In normoxic muscle, acetate provoked a concentration-dependent transient depression of the action potential duration and force of contraction, depression was maximal after 10-30 min, and recovery was complete after 90-120 min. In hypoxic muscle, acetate accelerated functional rundown (action potential shortening, decline of developed tension, increase in resting tension). Because rundown in hypoxic muscle was sensitive to factors affecting glycolysis (moderated by external glucose; accentuated by 2-deoxyglucose), the accentuated rundown with acetate may be accounted for by a partial block of glycolysis. However, block of glycolysis cannot explain the acetate-induced transient depression in normoxic muscle, since the depression was enhanced in normoxic muscle with 2-deoxyglucose-blocked glycolysis. We suggest that the transient depression is due to a transient depression of high energy nucleotides with consequent effects on ionic currents.
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PMID:Acetate-induced depression of electrical and contractile activity in normoxic and hypoxic guinea pig papillary muscle. 276 5

A majority of transmitter quanta in the nerve terminal is in a large pool of store (S), which can be utilized for release only after transformation into activated quanta (n) via two intermediate states called available quanta (A) and releasable quanta (N). Mobilization is a collective term applicable for aggregates of S----A, A----N and N----n conversions. In the present article, various electrophysiological procedures for kinetic analyses of the transmitter release in neuromuscular transmission were discussed to elucidate this not well understood process of mobilization. Especially, frequency augmentation, tetanic rundown and depression, and recovery from depression experiments were proposed to be very useful tools in identifying the drug effect on the mobilization process. Since d-tubocurarine, 2-(4-phenylpiperidino)cyclohexanol (AH5183) and Ba ions satisfied the above three criteria of drug action on mobilization, these were concluded to affect the mobilization of transmitter in neuromuscular transmission.
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PMID:Kinetic analyses of transmitter release in neuromuscular transmission. 290 13

Clonazepam (0.5 mg/kg, i.v.) changed the characteristic pattern of the exponential decline of the monosynaptic responses, the early tetanic rundown, evoked by trains of 10 stimuli (2, 5 or 10 Hz) applied to either the biceps-semitendinosus or triceps surae nerve, and recorded from the ventral root in spinal cats. In the case of the biceps-semitendinosus, clonazepam did not affect the first monosynaptic response or the last five monosynaptic responses forming the plateau, while the second monosynaptic response was markedly depressed, especially at the higher frequencies tested. The triceps surae reacted differently to the administration of clonazepam, in that the first response was increased and the amount of depression of the second response was lessened, with no change of the plateau. All the effects of clonazepam were reversed by the benzodiazepine antagonist, ethyl 8-fluoro-5,6-dihydro-5-methyl-6-oxo-4H-imidazo[1,5-a] [1,4]benzodiazepine-3-carboxylate (Ro15-1788; 5 mg/kg, i.v.), which alone had no effect of its own on any parameters, suggesting that the effects of clonazepam were mediated by central benzodiazepine receptors. Diazepam (1.0 mg/kg, i.v.), caused the same changes in the homosynaptic depression of the biceps-semitendinosus pathway as did clonazepam, but increased the plateau instead of the second response in that of the triceps surae pathway.
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PMID:The effects of benzodiazepines on spinal homosynaptic depression. 298 24

In a representative sample of 401 adults in Illinois in 1984, the authors found that increased participation in exercise, sports, and physical activities is associated with improved psychologic well-being. Part of this association is through improved subjective physical health. The authors controlled for potentially confounding factors, including sociodemographic characteristics, instrumentalism, and overweight. They concluded that exercise is associated with decreased symptoms of depression (feelings that life is not worthwhile, low spirits, etc.), anxiety (restlessness, tension, etc.), and malaise (rundown feeling, trouble sleeping, etc.) in the general population, most of which is not severely depressed, and in which many persons are engaged in moderate, nonaerobic exercise.
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PMID:Exercise and psychologic well-being in the community. 325 71

The kinetics of the direct action of 4-aminopyridine (4AP) and streptomycin (SM) on the mechanism of transmitter release were studied by recording the endplate potentials from curarized frog muscles using conventional microelectrode techniques, and by calculating the fractional release from the store of available acetylcholine quanta from the experiments with tetanic rundown during short train stimulations. To explain the tremendous facilitatory effect of 4AP on the fractional release and the antagonistic interaction of SM thereupon, it was postulated that 4AP and SM modify the transmitter output by combining with the Ca-dependent process X; i.e., 4AP and SM compete for the occupancy of the X site. A combination of 4AP or SM presumably modifies allosterically the action of the Ca-X complex, resulting in a profound augmentation of the evoked release of the available transmitter with the former and its depression with the latter. The theoretically derived equations from the above assumptions agreed reasonably well with the results obtained.
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PMID:Kinetic analysis of the action of chemical modulators on neuromuscular transmission. 612 Feb 54

Observations of the dynamic staining and destaining of FM1-43 in frog motor nerve terminals (Henkel and Betz, 1995) suggested that staurosporine might shorten the interval between exocytosis and endocytosis, inducing a "kiss and run" mode of exocytosis and endocytosis. We tested this hypothesis by using FM1-43 imaging (to measure the time course of FM1-43 endocytosis), intracellular recording of evoked synaptic potentials (to measure acetylcholine release), and electron microscopy (to examine synaptic vesicle distribution). Staurosporine reduced FM1-43 uptake during but not after a tetanus, increased the speed of end plate potential (EPP) amplitude rundown, and greatly slowed the recovery from synaptic depression. Ultrastructural observations showed pronounced vesicle depletion near active zones after tetanic stimulation in staurosporine-treated preparations. These results suggest that staurosporine acted primarily to impair mobilization of synaptic vesicles during tetanic stimulation.
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PMID:Effects of staurosporine on exocytosis and endocytosis at frog motor nerve terminals. 1115 64

The effect of the new antiepileptic drug levetiracetam (LEV; KEPPRA) on the neuronal high-voltage-activated (HVA) Ca(2+) current was investigated on pyramidal neurones, visually identified in the CA1 area of rat hippocampal slices. Nystatin-perforated patch clamp recordings were made under experimental conditions designed to study HVA Ca(2+) currents. The HVA current, activated by steadily increasing voltage-ramps, was reversibly eliminated by Cd(2+) and depressed by either nimodipine, or omega-Conotoxin GVIA. After 30 min perfusion of the slices with LEV 32 microM, the current decayed to 55+/-9% (mean+/-SEM; n=9) of the initial value, which is significantly (P<0.05, two-tailed t-test) lower than the rundown to 84+/-10% in a control group (n=10) of neurones. The limited, but significant depression of the neuronal HVA Ca(2+) current, produced by LEV at a clinically relevant concentration, might contribute to the antiepileptic action of the drug.
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PMID:Levetiracetam inhibits the high-voltage-activated Ca(2+) current in pyramidal neurones of rat hippocampal slices. 1140 44


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