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

The effect of intracisternal (i.c.m.) injection of clonidine, noradrenaline, and piperoxane on the pressor response to electrical stimulation of a peripheral somatic afferent nerve was investigated using anaesthetized cats. It was found that noradrenaline caused a depression of the magnitude of the pressor response and this effect was antagonized by subsequent injection of piperoxane i.c.m. In contrast, clonidine had no significant effect on the magnitude of the somatic pressor reflex but caused a dose-dependent prolongation of the reflex after cessation of nerve stimulation. This prolongation was antagonized by piperoxane which also caused an increase in the magnitude of the reflex. Piperoxane alone had no significant effect on the magnitude or duration of the reflex. Neither magnitude nor duration of the somatic pressor reflex was influenced significantly by a reduction in resting blood pressure. It is suggested that clonidine and noradrenaline act at different sites within the central nervous system to produce qualitatively different changes in the efferent sympathetic discharge pattern modulating the somatic pressor reflex.
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PMID:Effects of alpha-agonists on circulatory responses to somatic afferent nerve stimulation. 3 Jun 38

The actions of three intravenous anaesthetics, Althesin, thiopentone and ketamine have been compared on the rat isolated atria and portal vein. Although the three anaesthetics had grossly similar actions on the two preparations. i.e. depression of atrial rate and depression of the amplitude of myogenic activity in the portal vein, there were enough differences to suggest that they produced their effects by different mechanisms. These differences were particularly obvious in interactions with noradrenaline and the effects of changes in calcium ion concentration on the concentration effect relationships for the agents on the atria and portal vein. Generally Althesin was unaffected by changes, but in qualitatively different ways.
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PMID:An in vitro study of the effects of calcium on the cardiovascular actions of thiopentone, althesin and ketamine in the rat. 3 16

Chronic administration of the pre-synaptic alpha-adrenoreceptor agonist clonidine decreases the concentration of the extra-neuronal metabolite of noradrenaline normetanephrine in the amygdaloid cortex and increases it in the mid-brain. Conversely, blockade of these pre-synaptic receptors by yohimbine increases the normetanephrine concentration in the amygdaloid cortex and decreases it in the mid-brain. Mianserin had a qualitatively similar action to that of yohimbine. When given clinically to rats in combination with clonidine, mianserin antagonizes both the depression of behaviour of the rats in the 'open field' apparatus and also the effects of the alpha-agonist in reducing the concentration of normetanephrine in the amygdaloid cortex. It thus appears that the chronic effects of mianserin are due to an increase in noradrenaline release as a consequence of the inhibitation of pre-synaptic alpha-adrenoreceptors.
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PMID:Chronic effects of mianserin on noradrenaline metabolism in the rat brain: evidence for a pre-synaptic alpha-adrenolytic action in vivo. 4 Dec 80

Rats were maintained on ad lib food and a forced-intake regimen of ehtanol for up to 270 days. The ethanol treatment induced alterations in the metabolism of central catecholamines seen as increased endogenous concentrations of dopamine concomitantly with decreased concentrations of noradrenaline in the limbic forebrain. The synthesis of catecholamines, measured as the accumulation of dopa following inhibition of aromatic amino acid decarboxylase, was unchanged during chronic ethanol treatment. Local application of dopamine into the nucleus accumbens caused a greater increase in locomotor activity in chronic ethanol rats than in controls thus indicating that chronic ethanol treatment increased the sensitivity at or beyond central dopamine receptors. This phenomenon of functional dopamine receptor supersensitivity was first observed after 5 months of ethanol treatment and lasted for about 4 weeks after cessation of the ethanol treatment. The sensitivity of noradrenergic and cholinergic receptor mechanisms appeared to be unchanged after chronic exposure to ethanol. The effect of the GABAergic drug, gamma-butyrolactone (GBL) on the accumulation of dopa after inhibition of aromatic amino acid decarboxylase was studied in chronic ethanol rats. The enhancement of the dopa formation in dopaminergic neurons induced by GBL was markedly attenuated after chronic ethanol treatment. The gross behavioural depression by GBL was also weakened. This may indicate that chronic ethanol treatment causes subsensitivity of GABA receptors.
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PMID:The effect of chronic ethanol administration on central neurotransmitter mechanisms. 4 85

The antidepressants can be classified chemically. The standard division is between the tricyclic antidepressants and the chemically heterogeneous MAOIs. Many other compounds can be included among the antidepressants, e.g. the bicyclics and possibly also the beta-stimulants, the alpha-blockers and ions such as rubidium. As regards the mechanisms of action, we have the antidepressants which act selectively upon serotonin and those which act more particularly upon noradrenaline. This notion must be extended. Dopamine may be involved in certain depressive syndromes and also other systems may have a role, such as electrolyte systems, cell permeability and the multiple influences which have a bearing upon the monoamines. Finally, the effect upon receptors and their nature are discussed. A third type of classification refers to the therapeutic spectrum of the drug. We have the sedative antidepressants, active in agitated depression and the stimulant antidepressants which are active in retarded depression. However, the two categories of antidepressants have the same global antidepressant action.
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PMID:[Classification of the antidepressants (author's transl)]. 4 66

Previous studies had suggested that the epileptic bursts of feline generalized penicillin epilepsy represent the response of hyperexcitable cortex to thalamocortical volleys normally evoking spindles. If this were the case, it should be possible to convert the epileptic bursts of generalized penicillin epilepsy into spindles by decreasing the excitability of cortical neurons. In cats exhibiting the EEG signs of feline generalized penicillin epilepsy cortical excitability was decreased by hypoxia, by the topical application to the cortex of KCl (inducing spreading depression), barbiturates, GABA, AMP or noradrenaline. During generalized penicillin epilepsy, hypoxia and KCl-induced spreading depression abolished epileptic bursts which were replaced by spindles. When spindles and epileptic complexes occurring in the same animal were compared, a direct correlation between the frequencies of these two rhythms could be demonstrated, that of the epileptic complexes being about half that of the spindle waves. These observations support the hypothesis that the epileptic bursts of feline generalized penicillin epilepsy are induced by thalamocortical volleys normally involved in spindle genesis. Topical cortical applications of barbiturates, GABA, AMP and noradrenaline reduced or inverted the negative spikes of the spike and wave complexes, while augmenting the negative slow waves, or revealing them clearly in instances in which they had been poorly developed. This effect is interpreted as being due to a selective inactivation of the superficial cortical layers. That topical cortical application of barbiturates, GABA, AMP and noradrenaline was capable of transforming into typical spike and wave complex epileptic bursts, which had not previously conformed to this pattern, indicates that the intracortical electrophysiological events of typical and atypical epileptic bursts in feline generalized penicillin epilepsy are fundamentally the same and reflect an alternation between excitatory and inhibitory sequences.
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PMID:Effects of changes in cortical excitability upon the epileptic bursts in generalized penicillin epilepsy of the cat. 8 21

Rats given quipazine (5 mg/kg) or LSD (0.05 mg/kg), were decapitated at the time of maximum of behavioral effect of drugs (head twitches), resp. 30 and 15 min, or when the behavioral effects disappeared (resp. 60 and 30 min), and concentrations of dopamine (DA), noradrenaline (NA), serotonin (5HT) and 5-hydroxyindole-3-acetic acid (5-HIAA) were assayed in the striatum. Quipazine significantly elevated the DA level at both periods tested. LSD at the peak of its action depressed the level of 5-HIAA, and in the next period produced a significant depression of striatal levels of NA, 5HT and 5-HIAA.
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PMID:The effect of quipazine and LSD on monoamines in the rat striatum. 9 44

1. Electrical stimulation of the guinea-pig or rat vas deferens (pre- or post-ganglionically) at frequencies from 2-5 to 40 Hz with trains of stimuli of 30 sec duration induced a biphasic response. A rapid contraction (component A) was followed after a brief relaxation by a slower contraction (component B); the two phases were seen most clearly with stimulation frequencies of less than 10 Hz. 2. The responses to post-ganglionic stimulation were always larger than those to preganglionic stimulation. In general, at low frequencies component A exceeded component B whilst at high frequencies component B was the larger. Separation of the two components on the basis of their frequency response characteristics was better for rat than for guinea-pig vasa. 3. Log. frequency-response curves to transmural (post-ganglionic) electrical stimulation and log dose-response curves to noradrenaline were recorded for guinea-pig and rat vasa deferentia at 32 degrees, 22 degrees and 12 degrees C. For the guinea-pig reduction of bath temperature to 12 degrees C increased the amplitude of component A at 2-5 and 5 Hz; component B could not confidently be distinguished at this temperature. At 22 degrees C there was potentiation of B at lower frequencies and depression of B at higher frequencies. There was no response to noradrenaline at 12 degrees C. At 22 degrees C the response to noradrenaline was increased except to doses at or near the maximum to which the response was reduced. 4. For the rat was deferens component A was little changed by reduction of temperature. Component B at 12 degrees C was greatly depressed at higher frequencies. The response to noradreanaline was increased to lower doses and decreased to higher doses as the temperature was lowered. 5. The B component of the response of guinea-pig vasa at 22 degrees C and rat vasa at 32 degrees C was more sensitive than the A component to inhibition by thymoxamine. 6. Further analysis of the mechanisms underlying the A and B components of the biphasic response may be facilitated by relative isolation of each component by the appropriate selection of parameters of electrical stimulation and of temperature for the species being investigated. The contractions of the B component are similar to, if not identical with, those produced by exogenously applied noradrenaline.
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PMID:The relation between stimulus frequency and the relative size of the components of the biphasic response of the vas deferens to electrical stimulation at different temperatures. 13 53

The effects of iontophoretically applied Na+-, K+-dependent adenosinetriphosphatase (Na+,K+-ATPase) (EC 3.6.1.3) inhibitors (ouabain, digitoxin, digitoxigenin, strophanthin K, strophanthidin, thevetin A and B, ethacrynate, and harmaline) on the depression of rat cerebral cortical neurones by noradrenaline, 5-hydroxytryptamine, and histamine have been studied. The inhibitors antagonized depressions of spontaneously active neurones evoked by these amines, but not those evoked by gamma-aminobutyric acid, adenosine, adenosine 5'-monophosphate, or calcium. The antagonistic potencies of the various inhibitors appeared to be proportional to their known potencies as inhibitors of Na+, K+-ATPase. The data therefore support the hypothesis that amines depress central neurones by activating an electrogenic sodium pump.
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PMID:Antagonism of biogenic amine-induced depression of cerebral cortical neurones by Na+, K+-ATPase in inhibitors. 14 20

In experiments on isolated gallbladders (GB) of frogs it was established that noradrenaline in concentration of 6.10(-9)--3.10(-4) M acting on the organ from the serosalsurface causes firstly a short increase and then -- a prolonged inhibition of the absorption rate of NaCl -- isotonic fluid from the gall bladder cavity. While the concentration of the mediator increases in the inculation medium, its inhibiting effect increases too. Depression, and at high concentration in the medium, full inhibition of the process of fluid absorption is accompanied with distinct decrease of Na--, K--ATPase activity of gall bladder epithelial cells. Mediator in concentration of 3.10(-8) M caused an increase of membrane potential of the epithelial cells, while its increasing in the inculation medium to 3.10(-6) M caused a decrease of the transmembrane potential difference. Under the noradrenaline influence the increase of the osmotic permeability of the gall bladder's wall for the water flow directed from the mucosa to the serosalsurface of the organ took place, and also the decrease of the wall's permeability for the water flow in the opposite direction was seen. It was concluded that the noradrenaline inhibitory action on the process of absorption of NaCl--isotonic fluid from the gall bladder cavity was observed because of the decrease of the Na--K--ATPase activity, and also because of the change of the permeability of epithelium for the passive ion and water transport.
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PMID:[Effect of noradrenaline on ion and water transport through frog gall bladder epithelium]. 15 53


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