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

Development of the effect of glycine and gamma-aminobutyric acid [GABA] on spontaneous motility was studied in 11- to 19-day-old chick embryos under normal conditions and after acute and chronic decapitation. Chronic decapitation was performed on the 2nd day of incubation. Glycine (100 mg/kg egg weight) and GABA (103 mg/kg egg weight) (applied onto the shell membrane) demonstrably inhibited spontaneous motility only from the 15th day of incubation, the inhibitory effect increasing with the embryo's age. When administered together in half doses, glycine and GABA completely inhibited spontaneous motility for the first time in 19-day-old embryos. Neither amino acid influenced depression of motility immediately after decapitation, but 24 and 48 hours after, in 17- and 19-day-old embryos, they had a paradoxical effect, i.e. they transiently activated motor activity and even caused motor paroxysms. After chronic decapitation, both glycine and GABA again had a mild, protracted inhibitory effect. A comparison of spontaneous motility in normal and chronically decapitated embryos showed that the role of supraspinal factors in spinal motor output increases significantly with development of the chick embryo from the 15th day of incubation and that inhibition of these supraspinal factors plays the decisive role in the effect of glycine and GABA.
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PMID:Development of spontaneous motility in chick embryos. The spinal and supraspinal component of the inhibitory effect of glycine and GABA. 14 12

Major inhalational anesthetics cause inhibition in the electron transport chain in the region of Complex I resulting in decreased oxygen utilization, inhibition of metabolism of NAD-linked substrates, but not of succinate, inhibition of mitochondrial calcium uptake, and depression of synaptic transmission because of postulated changes in ACh sensitivity or GABA inhibition. Many cellular metabolic effects in CNS and other tissues are secondary to the above. Many metabolic changes noted with anesthetics occur subsequent to activation of the sympathetic nervous system either directly by the anesthetic or by surgical stimulation in the presence of light anesthesia. Many important studies remain to be done.
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PMID:Effects of anesthesia on intermediary metabolism. 16 50

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

Three kinds of the cholinoceptive neurons, nicotinic depolarizing (D)-, nicotinic hyperpolarizing (H)-, and muscarinic H-tyes, as well as two other kinds of neurons, GABA H- and dopamine H-types, were identified in Aplysia abdominal ganglion, and the effects of disulfide bond reduction and reoxidation on their postsynape acetylcholine-induced responses of both nicotinic types (D- and H-) were depressed by reducing the disulfide bonds with dithiothreitol (DTT) and restored by reoxidizing with 5, 5' -dithiobis-(2-nitrobenzoic acid): (DTNB), whereas the responses of the muscarinic H-, GABA H-, and dopamine H-cells were not affected at all by either DTT or DTNB. In contrast to the results obtained from the electroplax, the cholinergic receptors in our preparation showed neither the activation by hexamethonium nor the augmentation of decamethonium-induced responses after reduction of disulfide bonds. In addition, our preparation did not demonstrate the long-lasting responses to bromoaTT-induced depression of the nicotinic responses was studied on the dose-response curves; the mode of receptor inhibition was rather complexed, being neither type of competitive nor non-competitive. We concluded that the disulfide bond is a crucial element in both types of nicotinic receptors (D and H), and that this bond is related to the activation process of the receptors regardless of their ionic specificities.
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PMID:Effects of disulfide bond reduction on the excitatory and inhibitory postsynaptic responses of Aplysia ganglion cells. 18 9

The data obtained from this study suggest that the nonionizable anesthetic benzyl alcohol has two prominent actions on GABA- and glutamate-mediated synaptic transmission at the lobster neuromuscular junction. They are as follows: (1) depression of the excitatory end-plate potential and the postsynaptic membrane response to applied glutamate, and (2) a hyperpolarization of the postsynaptic resting membrane potential associated with a decrease in effective membrane resistance. No change in amplitude of the inhibitory end-plate potential or inhibitory reversal potential was seen. Excitatory miniature end-plate potential frequency was also unaffected. The depression of excitatory synaptic transmission appears to be due to a decreased responsiveness of the postsynaptic receptor-ionophore complex.
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PMID:Depression of glutamate-mediated synaptic transmission by benzyl alcohol. 19 78

The microiontophoretic application of taurine and GABA was studied in the cerebellar cortex of the rat. Both taurine and GABA produced a dose-dependent depression of spike frequency of cerebellar neurons. GABA (2-42 nA, mean 27 nA) induced an inhibition of spike discharge on all 138 cells tested, including 29 Purkinje cells. Taurine (60-200 nA, mean 108 nA) induced an inhibition of spike discharge on 93 of the 106 cerebellar neurons tested, including inhibition on 22 of 25 Purkinje cells. Iontophoretic application of bicuculline and picrotoxin antagonized the inhibitory effects of both GABA and taurine on Purkinje cells as well as on cerebellar neurons in general. Strychnine did not antagonize the inhibition of either GABA or taurine. Simultaneous application of taurine and GABA produced a synergistic inhibitory effect on the firing rate of Purkinje cells. Taurine, in contrast to GABA, appeared to be more depressant when applied in the Purkinje cell dendritic zone than when applied near the soma. The data are discussed in terms of taurine functioning as a neurotransmitter in the cerebellum of the rat and having receptor sites distinct from those for GABA.
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PMID:A comparison of the inhibitory effects of taurine and GABA on identified Purkinje cells and other neurons in the cerebellar cortex of the rat. 20 21

The effects of several benzodiazepines on a variety of nervous activities known or presumed to depend on GABA are presented and compared with those of agents that deplete or increase the level of endogenous GABA: antagonism of various convulsant agents in mice, enhancement of presynaptic inhibition in the spinal cord and the cuneate nucleus of cats, decrease of the spontaneous firing rate of cerebellar Purkinje cells in cats and rats, antagonism of bicuculine-induced depression of the strio-nigral-evoked potential in the cat, potentiation of haloperidol-induced catalepsy in rats, GABA-mimetic actions on drug-induced PGO-waves in cats and on eserine-induced circling in guinea pigs. Diazepam slightly increased the GABA level in the cat spinal cord and in the total brain of mice and rats; this increase does not seem to be due to an increase of GABA synthesis. It is concluded that benzodiazepines probably enhance presynaptic inhibition at all levels of the neuraxis and that this effect requires not only the presence of GABA but is also dependent on an activity of GABA-ergic neurons. Benzodiazepines also appear to enhance postsynaptic inhibition where this is mediated by GABA. Many actions of benzodiazepines can be tentatively explained by a stimulus-bound enhancement of GABA effects.
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PMID:Possible involvement of GABA in the central actions of benzodiazepines. 24 99

The effects of some central depressant drugs on amino acid-induced depolarization of motoneurons have been determined in the isolate hemisected frog spinal cord. Motoneuron depolarization was recorded from ventral roots and measurements were made in the presence or absence of procaine or tetrodotoxin to minimize indirect effects of both drugs and amino acids. Chlorpromazine (0.05-0.1 mM) and diazepam (0.5 mM) produced a similar differential pattern of depression of amino acid-induced depolarizations. Responses induced by L-homocysteate were markedly antagonized by these drugs, while responses to quisqualate were unaffected. L-Aspartate-induced responses were antagonized more than L-glutamate-induced responses. This pattern of antagonism resembles that previously described for Mg2+. In contrast, pentobarbital (0.1 or 0.3 mM), and the inhibitory amino acids GABA and beta-alanine (0.5-1.0 mM), depressed amino acid-induced responses in a more uniform manner. The differential effects observed with chlorpromazine and diazepam provide further support for the possibility that responses to excitant amino acids structurally related to L-glutamate may have different underlying mechanisms.
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PMID:Differential antagonism by chlorpromazine and diazepam of frog motoneurone depolarization induced by glutamate-related amino acids. 30 13

The effects of chemicals on visual activity was investigated by recording the proximal negative response (PNR) in the perfused eyecup of frogs. Various amino acids reversibly decrease or abolish the PNR over an equivalent concentration range but differ in this depressive action in the presence of convulsant alkaloids. Depression produced by GABA was antagonized by picrotoxin or bicuculline; while glycine-produced depression was selectively antagonized by strychnine. In addition to selective antagonism of amino acids, the convulsants produced differential enhancement of sustained and transient phases of the PNR. In this respect, the effects of picrotoxin and bicuculline are similar to those of semicarbazide and chloride-free solutions which may also inactivate GABA pathways. The effects of these chemicals on the time course and input-output relation of the PNR suggest that processes involving GABA may regulate the transformation from sustained to transient signals which occurs in the inner retina.
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PMID:GABA-mediated control of transient signals in the inner retina. 30 12

The hereditary hepatic porphyrias, PV, AIP and HC, are characterized biochemically by increased excretion of porphyrins and the porphyrin precursors ALA and PBG. They are characterized clinically by episodes of acute neurological involvement. The increased production of porphyrins and porphyrin precursors has been shown to be due to partial enzyme blocks along the heme biosynthetic pathway which results in secondary depression of the key enzyme ALA-synthetase. The neurological manifestations could therefore be related to either a decrease in essential heme-proteins or other heme-containing compounds within the nervous system, or to a toxic effect of the over-production of the porphyrin precursors ALA and PBG. There is evidence for and against both theories. Recent work from a number of research groups has shown the porphyrin precursors to have potent pharmacological effects on the nervous system, and these are possibly related to the GABA receptor and binding site-porphyrin precursor interactions. Current studies on therapy of the acute attack have concentrated on suppression of ALA-synthetase activity, and consequently, on reduced ALA and PBG production. A number of such methods of therapy have met with remarkable success and hold promise for the future treatment of the acute attack.
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PMID:The neurological manifestations of porphyria: a review. 32 53


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