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)

Morphine and morphine-related agents were applied by microiontophoresis in the lumbar spinal cord of spinal cats to single units classified on the basis of their responses to natural cutaneous or proprioceptive stimulation. Opiate application had a current-dependent depressant effect on the ongoing activities of about one-third of the units tested. This effect was observed in laminae I and IV--VI, but only with units responding to noxious cutaneous stimuli: the nociceptive responses were themselves depressed. Excitatory and inhibitory responses to glutamate and gamma-aminobutyric acid, respectively, were also depressed. Intravenous administration of the opiates at doses reported to produce analgesia in the cat also depressed only units responding to noxious cutaneous stimuli, including their nociceptive responses. This depression could be reversed by either the iontophoretic application (100 nA) or the intravenous administration (0.1--0.8 mg/kg) of naloxone. These results are interpreted as further evidence that the analgesic effects of opiates are at least partly due to an action at the spinal level.
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PMID:Action of narcotic analgesics and antagonists on spinal units responding to natural stimulation in the cat. 48 72

Mammalian spinal neurons grown in tissue culture were used to study the effects of the four convulsants-penicillin, pentylenetetrazol, picrotoxin, and bicuculline-on these neurons' responses to amino acids. Bath application of all four convulsants produced paroxysmal depolarizing events in the neurons; iontophoresis of the four convulsants selectively depressed responses produced by iontophoresis of the putative inhibitory transmitter GABA, and effected this depression without altering either inhibitory responses to beta-alanine or glycine, or excitation mediated by glutamate. These results support the hypothesis that the convulsant activity of these agents comes in part from selective antagonism of GABA-mediated postsynaptic inhibition.
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PMID:Specific antagonism of GABA-mediated postsynaptic inhibition in cultured mammalian spinal cord neurons: a common mode of convulsant action. 56 20

Commissural evoked potentials (EP) in hippocampal area CA1 were investigated during microiontophoretic application of sodium glutamate (SG) in experiments on unanesthetized rats immobilized with diplacin. EP were recorded by the central barrel of a five-barreled microiontophoretic microelectrode before and during application of SG. The effect of SG in the region of EP reversal was characterized by depression of the initial positive phase of the response and an increase in negativity. In the radial layer SG caused a substantial increase in the commissural response recorded at a depth. At a distance of 100 mu from the tip of the iontophoretic pipet no changes in EP were found. An increase in the intensity of transhippocampal stimulation was accompanied by a marked increase in the amplitude and a change in shape of the individual phases of EP and it abolished the effect of the microiontophoretically applied SG. During paired stimulation with an interval of 20--200 msec different effects of SG on the testing response were recorded depending on the length of the interval.
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PMID:Layer by layer analysis of commissural hippocampal evoked potentials during glutamate microiontophoresis. 61 91

1. The effects of microiontophoretically applied glutamate, ibotenate and other related amino acids on the spike activity of feline spinal interneurones were investigated. 2. Unlike the other amino acids, which evoked excitatory responses only, ibotenate evoked slow biphasic responses (excitation-depression) from the majority of these neurones. The depressant action was associated with an increase in spike height and was reversible. 3. The ibotenate depression could be observed as a temporary reduction in background firing rate, a loss of sensitivity to other amino acids, a progressive decrease in the excitatory responses to repetitive ibotenate applications or a fading of excitation following a prolonged administration of ibotenate. 4. The onset of the excitatory effects of glutamate, quisqualate and ibotenate was relatively well fitted by diffusion equations for a continuous point source. However, radial distances for diffusion in the case of ibotenate responses were comparatively greater than those for glutamate and quisqualate. 5. The depressant action of ibotenate was not antagonized by strychnine, picrotoxin or bicuculline. 6. Some methods of quantifying the responses to excitatory amino acids are described. The excitatory potency of quisqualate and N-methyl-D-aspartate was several times greater than that of glutamate. Aspartate and ibotenate were equipotent, while alpha-aminopimelate and alpha-methyl-DL-aspartate were much weaker. 7. It is suggested that the biphasic action of ibotenate on spinal interneurones might be the result of activation of excitatory and inhibitory sites fairly remote from the cell somata where extracellular recordings were probably made.
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PMID:A comparison of the action of glutamate, ibotenate and other related amino acids on feline spinal interneurones. 63 39

Stimulation of the intracerebral noradrenergic pathway causes a vasodilatation in the hypothalamus. We have investigated whether this vasodilatation is caused by a direct vascular innervation or whether it is secondary to an activation of hypothalamic neurons. Non-specific neuronal activation using glutamate increased the mean hypothalamic blood flow. Depression of neuronal activity using barbiturate reduced hypothalamic blood flow and blocked the glutamate and the intracerebral noradrenergic pathway-induced vasodilatation. These results suggest that stimulation of the intracerebral noradrenergic pathway increases hypothalamic neuronal activity which indirectly causes a vasodilatation.
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PMID:Vasodilator mechanism of the intracerebral (non-sympathetic) adrenergic pathway. 63 79

We have assessed the vitamin B6 status of 40 nonpregnant women of reproductive age, 30 pregnant women, 20 postpartum, not depressed, women and 24 postpartum, depressed women by means of the erythrocyte glutamate-oxaloacetate transaminase activation test (alpha EGOT). The level of mental depression was evaluated in the nonpregnant controls, the postpartum controls and the postpartum, depressed patients by the Beck Depression Inventory and the Depression Adjective Check Lists. The results of the alpha EGOT did not indicate any significant differences between the postpartum, depressed patients and any of the control groups. The Beck and Depression Adjective Check Lists scores were significantly higher in the postpartum depressed patients than in the postpartum controls or nonpregnant controls. On the basis of this study, there is no evidence for vitamin B6 deficiency in women suffering from postpartum depression.
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PMID:Vitamin B6 status in women with postpartum depression. 64 33

1. The influx of a number of amino acids into squid giant axons has been studied. Particular emphasis has been placed on glycine and to a lesser extent glutamate. 2. To facilitate the study of the uptake of 14C-labelled amino acids a technique was devised in which the 14C taken up was measured directly in the intact axon with a glass scintillator fibre. This technique gave results similar to the usual technique in which the axoplasm was extruded for the assay of radioactivity. 3. The changes in glycine influx with extracellular glycine concentration suggests that two saturating components are present, one with high affinity and one with low affinity. 4. The glycine influx does not seem normally to be sensitive to the removal of extracellular sodium by replacement with choline. A Na-sensitive component appeared, however, after a period of immersion in artificial sea water. There was also some depression of glycine influx if Na were replaced by Li. 5. Glutamate uptake was greatly reduced by removal of extracellular Na in confirmation of work by Baker & Potashner (1973). Orthophosphate uptake was also greatly reduced by removal of extracellular Na. 6. CN reversibly inhibited glycine uptake after a delay, indicating that part of the uptake mechanism may require ATP. 7. 14C-labelled glycine injected into squid axons was found not to exchange to any serious extent with other compounds over periods of a few hours. The glycine efflux could therefore be studied. This was found to be markedly increased by extracellular glycine and by certain other neutral amino acids applied extracellularly in the artificial sea water. 8. The enhanced glycine efflux in extracellular glycine was not affected by ouabain and CN. 9. It is suggested that glycine uptake in squid axons involves two components. One is sensitive to CN and ouabain and probably derives energy from ATP break-down. The other is probably an ATP independent exchange diffusion system in which other amino acids as well as glycine can exchange for glycine. Both these systems are independent of extracellular Na concentration. A third Na-dependent system may appear under certain conditions.
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PMID:Glycine fluxes in squid giant axons. 67 Dec 72

1. The effects of the barbiturate anaesthetic pentobarbitone on the membrane properties and amino acid pharmacology of mammalian C.N.S. neurones grown in tissue culture were studied using intracellular recording coupled with bath application, extracellular ionophoresis, or focal diffusion. 2. The addition of an anaesthetic concentration of pentobarbitone to the bathing medium abolished all spontaneous synaptic activity, but did not render individual cells electrically inexcitable nor prevent evoked synaptic acitivity. 3. Focal ionophoresis of pentobarbitone or diffusion from blunt micropipettes reversibly increased membrane conductance, effectively dampening excitability without directly affecting individual action potential characteristics. 4. Pentobarbitone-induced membrane conductance was reversibly blocked by picrotoxin. The inversion potential of the pentobarbitone voltage response depended on Cl- ion gradients and was similar to that of GABA. 5. Pentobarbitone reversibly enhanced the conductance increase produced by GABA with a variable slowing of response kinetics, shifting GABA dose-response curves to the left. Responses to glycine and beta-alanine were not affected. 6. Higher ionophoretic currents of pentobarbitone, which measurably increased membrane conductance, attenuated and markedly slowed GABA responses. Similar effects on GABA responses were observed by superimposing GABA pulses on low level GABA currents. 7. Pentobarbitone, in the absence of an increase in membrane conductance, reversibly depressed depolarizing responses to glutamate without changing response kinetics. Slower responses to acetylcholine which were associated with an apparent decrease in membrane conductance were not affected by the drug. 8. Analysis of double-reciprocal plot data suggested a non-competitive type of antagonism between pentobarbitone and glutamate. Pentobarbitone depression of glutamate was not affected by picrotoxin. 9. Both GABA and glutamate responses appeared to be equally sensitive to pentobarbitone. Specific interaction of the drug with amino acid receptor-coupled events is indicated by the requirement for pentobarbitone pipette placement close to the amino acid response site. 10. The results suggest that pentobarbitone depresses neuronal excitability by (1) directly activating post-synaptic GABA-receptor coupled Cl- conductance, (2) potentiating post-synaptic GABA-induced conductance events, probably at the level of the GABA receptor, and (3) depressing post-synaptic glutamate-induced excitation, probably at the level of the conductance mechanism.
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PMID:Pentobarbitone pharmacology of mammalian central neurones grown in tissue culture. 69 Aug 85

Veratridine, ouabain, glutamate and high concentrations of K+, agents which cause depolarization of excitable cells, markedly elevate levels of adenosine 3':5'-monophosphate (cyclic AMP) and guanosine 3':5'-monophosphate (cyclic GMP) in brain tissue, in vitro. Phenytoin inhibits veratridine (5 micron)- and ouabain (100 micron)-induced accumulations of both cyclic nucleotides in slices of mouse cerebral cortex. As little as 10 to 30 micron phenytoin produces a statistically significant depression, and 100 to 400 micron inhibits more than 90%. In contrast, at concentrations up to 400 micron, the drug has little or no effect on elevations of cyclic AMP or cyclic GMP caused by glutamate (10 mM) or K+ (64 mM). The inhibitory action of phenytoin on ouabain-induced elevations of cyclic nucleotides appears to be noncompetitive; inhibition of the veratridine effects probably is also noncompetitive. Tetrodotoxin also inhibits ouabain- and veratridine-induced elevations of cyclic nucleotides in brain slices, but it is 3 orders of magnitude more potent than phenytoin. Like phenytoin, tetrodotoxin does not inhibit the effects of glutamate or K+ on cyclic nucleotide regulation. These data suggest that, similar to tetrodotoxin phenytoin blocks sodium channels in excitable membranes. Possibly this mechanism is responsible for the antiepileptic action of phenytoin.
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PMID:Similar effects of phenytoin and tetrodotoxin on cyclic nucleotid regulation in depolarized brain tissue. 73 31

Two mechanisms have been proposed to explain spreading depression (SD): one based on a release of glutamate (Van Harreveld, 1959), and the other on a release of potassium (Grafstein 1956) from neuronal elements. Both glutamate and KCl cause transparency changes in the retina, comparable to those occurring in this tissue during SD. The glutamate effect is inhibited by MgCl2 (10mM), in contrast to the transparency change due to KCl which is not affected by Mg++. Also SD is usually inhibited by MgCl2 which suggests that such SDs are based on a glutamate release. Impairment of the tissue metabolism promotes SDs which are insensitive to MgCl2. The resulting failure of the mechanisms that transport K+ and glutamate which leak out of the intracellular compartment back into the cells and fibers, seems to be involved in the generation of Mg++ insensitive SDs. This may facilitate either K-based SDs or glutamate-based SDs since the inhibitory effect of Mg++ is counteracted by an enhanced glutamate concentration. Both proposed mechanisms for SD seem to be possible under special circumstances.
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PMID:Two mechanisms for spreading depression in the chicken retina. 73 64


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