UMLS:C0011570 - FACTA Search

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Query: UMLS:C0011570 (depression)
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1. The carotid body and the carotid nerve were removed from anaesthetized cats and placed in a small Perspex channel through which Locke solution (at various pH values and usually equilibrated with 50% O(2) in N(2)) was allowed to flow. The glomus was immersed in the flowing solution while the nerve was lifted into oil covering the saline. Sensory discharges were recorded from the nerve and their frequency was used as an index of receptor activity. At times, a small segment of carotid artery, containing pressoreceptor endings, was removed together with the glomus. In this case, pressoreceptor discharges were recorded from the nerve.2. The amplitude of either chemo- or pressoreceptor discharges was not changed by strong acid solutions. Acid decreased the frequency of the baroreceptor discharges only when pH fell to less than 4.0. Solutions at low pH increased the chemosensory discharge, but acid depressed the increased chemoreceptor discharge elicited by KCl. These experiments indicated that H(+) ions probably acted as membrane ;stabilizers' without depolarizing either the nerve fibres or endings.3. Acid solutions increased the action of acetylcholine chloride (AChCl) (100-200 mug) on chemoreceptors. This effect probably was due either to inactivation of tissue cholinesterase or to enhanced sensitivity of the sensory endings to ACh.4. Choline chloride (10(-3)M), which favours ACh synthesis, protected the preparation against decay during prolonged experimentation. Hemicholinium-3 (HC-3), which blocks ACh synthesis in low concentrations (10(-5)M), depressed the chemosensory response to acid and to hypoxia when such stimuli were applied repeatedly. This concentration of HC-3 did not change effects of applied ACh.5. Substances which affect ACh release markedly changed the chemoreceptor discharge increase induced by acidity and other forms of stimulation. In the absence of Ca(2+), acid, anoxia, and interruption of flow provoked receptor depression while receptor excitation induced by ACh and KCl persisted. All stimuli excited and showed increased effectiveness as the Ca(2+) concentration was raised, but their effects declined as Ca(2+) was increased above normal values. Mg(2+) ions depressed the chemoreceptor effects induced by all these stimuli. The action of Mg(2+) was not due entirely to nerve ending block. Morphine sulphate (which decreases ACh release in other structures) also depressed the receptor response to acid and flow interruption.6. Cholinergic blocking agents such as mecamylamine, hexamethonium, atropine, dihydro-beta-erithroidine (DHE), HC-3 (10(-4)M), choline and acetylcholine (in combination with choline) depressed the effects of acid and ACh on the chemoreceptors. The effect induced by interruption of flow was depressed only by mecamylamine and DHE.7. Agents which affect the fate of released ACh, such as acetylcholinesterase and eserine salicylate, did not affect clearly the response of chemoreceptors to acid.8. The results suggest that acid stimulates chemoreceptor fibres through an indirect mechanism, viz. through increased release and/or decreased destruction of a presynaptic transmitter from the glomus cell. This transmitter is probably ACh (see following paper, Eyzaguirre & Zapata, 1968).
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PMID:Pharmacology of pH effects on carotid body chemoreceptors in vitro. 429 75

1. Studies involving the electrophoretic administration of antagonists of ACh (atropine, DHbetaE) and cholinesterase inhibitors (neostigmine, physostigmine) to MGN neurones indicate that ACh is an excitatory transmitter in the feline MGN, most probably released from fibres which originate in or traverse the mesencephalon.2. Auditory afferents to the MGN, cortico-geniculate fibres and the excitatory fibres which mediate ;spontaneous' firing of MGN neurones are unlikely to be cholinergic.3. Almost all geniculo-cortical relay cells are excited by ACh, this excitation being mediated by receptors which have both muscarinic and nicotinic properties. The excitation of relay cells by ACh is sometimes preceded or followed by a depression of firing which is resistant to atropine and DHbetaE, but the significance of this depression is unknown.4. The firing of many unidentified MGN neurones is depressed by ACh in the absence of any excitation, and this depression is blocked by both atropine and DHbetaE, and potentiated by anticholinesterases. This type of depression by ACh may be related to cholinergic inhibition, but this possibility has yet to be investigated.
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PMID:Cholinergic and non-cholinergic transmission in the medial geniculate nucleus of the cat. 434 15

The neuromuscular depolarizing block induced by intra-arterially injected ACh was studied to determine the variability in the same subject and in different subjects without disorders at the motor end-plate. Amplitude of action potentials of the opponens pollicis muscle evoked by intermittent repetitive supramaximal stimulation of the median nerve at the wrist were recorded for one hour from the beginning of ACh injection. The features of prompt and late depression stages after the injection were analysed statistically. Re-testing of the same subjects after a while shows that, in spite of all efforts to maintain the same experimental conditions, variations do occur in late depression. Time course and duration are particularly affected, while the degree of depression is altered but slightly. The presence of such variations limits this test to evaluation of the influence of other factors only within their already established statistical limits.
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PMID:Neuromuscular block after intra-arterially injected acetylcholine. 1. Introduction, methods, and technique. 435 Jul 3

Adrenergic and cholinergic agonists and antagonists were applied microelectrophoretically to over 700 neurons in the cat supraoptic nucleus, 20 percent of which were antidromically identified as neurosecretory cells. Norepinephrine uniformly depressed all sensitive cells. Acetylcholine caused both muscarinic depression and nicotinic excitation which were antagonized by atropine and dihydro-beta-erythroidine, respectively. These results support the hypothesis that norepinephrine and acetylcholine are directly involved in controlling the release of antidiuretic hormone.
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PMID:Supraoptic neurosecretory cells: adrenergic and cholinergic sensitivity. 439 31

1. Neurones in the supraoptic nucleus were examined for their responsiveness to microiontophoretically applied monoamines and cholinomimetic agents. One hundred and sixty-one of the 749 neurones recorded were antidromically identified as neurosecretory cells.2. The monoamines, dopamine, noradrenaline and serotonin, reduced the activity of all cells which responded.3. Reduction in activity following noradrenaline administration was antagonized by the beta-adrenergic blocking agent MJ-1999 and potentiated by desmethylimipramine.4. Acetylcholine produced either a decrease or an increase in activity of responsive cells with depression the predominant result. Both the depressant and the excitatory response to acetylcholine were seen in individual neurosecretory cells which were depressed by noradrenaline.5. Application of acetyl-beta-methylcholine and carbaminoylcholine consistently resulted in depression of all responsive cells, while nicotine excited the majority of responsive cells. Both types of response were observed on the same neurosecretory cell.6. The depressant response was antagonized by the muscarinic blocking agent atropine while the excitatory response was antagonized by the nicotinic blocking agent dihydro-beta-erythroidine. Responses to acetylcholine were potentiated by the acetylcholinesterase inhibitor physostigmine.7. The data indicate that noradrenaline-containing terminals on these neurosecretory cells are likely to inhibit their discharge rate, while the presumed cholinergic terminals might function as either excitatory or inhibitory, depending on the receptor activated.8. These results support the hypothesis that ADH release is related to the neuronal activity of the supraoptic neurosecretory cell.
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PMID:Noradrenaline and acetylcholine responses of supraoptic neurosecretory cells. 439 77

1. In cats, rabbits and monkeys, single cortical shocks can reduce the excitability of cortical neurones for 100-300 msec; the inhibitory effect is readily demonstrated, even in previously quiescent cells, against a background of activity evoked with small amounts of L-glutamate, released from an extracellular recording micropipette by iontophoresis.2. Other forms of cortical activity are also inhibited in a similar way by direct or indirect cortical stimulation; they include single unit discharges produced by iontophoretic applications of ACh or by a cathodal current, spontaneous discharges, and slow wave activity, both spontaneous and evoked.3. Most stimuli which elicit cortical activity also evoke some inhibition in the cortex, for instance, transcallosal volleys, and thalamic or peripheral shocks. In each case, a characteristic, prolonged depression is produced by single shocks.4. The most effective stimuli are direct cortical shocks, especially when applied within the cortex, below a depth of 0.6 mm; surface cathodal shocks are more effective than anodal shocks. These stimuli do not first excite the cells which are inhibited and they are not strong enough to cause appreciable local injury.5. Because of its long duration, the inhibition is often readily maintained by repetitive stimulation at frequencies of 5-7/sec. A cumulative effect leads to a further silent period after the end of stimulation; this increases with the strength, frequency and duration of the tetanus, so that after stimulation at 50-100/sec, the silent period may last for over 1 min. During this time, a stronger depolarizing stimulus can initiate firing.6. The inhibitory effect is often preceded and followed by phases of increased excitability; these may also show cumulative enhancement during repetitive stimulation, and a high frequency tetanus often leads to a short after-discharge, which is then followed by a long silent period, as above. Comparable changes take place in rabbits during spreading depression.7. The inhibitory effect of a direct shock can spread over an area covering 1 cm of cortical surface, affecting the cells through all cortical layers; but the spread is uneven in different directions, being particularly poor under most sulci.8. This type of inhibition can be elicited in all areas of the neocortex, and it is evident in kittens within a week of birth.9. Antidromic pyramidal stimulation is very much less effective in evoking inhibition of Betz cells, and other cortical neurones, than direct cortical stimulation; the inhibition by direct shocks is therefore not likely to be mediated through pyramidal excitation.
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PMID:An inhibitory process in the cerebral cortex. 495 15

1. In cats anaesthetized with pentobarbitone, the fluid spaces in and around the brain stem were perfused from the third ventricle to the foramen magnum with artificial cerebrospinal fluid (c.s.f.) flowing usually at the rate of 5 ml/minute. Test solutions were substituted for the artificial c.s.f. without switching artifact for periods varying from 5 to 60 seconds. Observations were made on respiratory excursions, end-expiratory% CO(2) and arterial blood pressure.2. Perfusion with sucrose solution equiosmolar with the c.s.f. produced no respiratory or cardiovascular response. Replacement of sodium with potassium (60 to 133 mM) resulted in a prompt but mild respiratory stimulation and a delayed fall in blood pressure associated with a slowing of the heart beat. Replacement of sodium with magnesium (40 to 131 mM) resulted in a late prolonged apneustic depression of breathing and in an early but slight reduction in blood pressure.3. Procaine (1 to 50 mg/ml) elicited a respiratory response similar to that of excess magnesium; however, an initial rise in blood pressure to as high as 200 mmHg was evoked with procaine. Nicotine (0.05 to 0.5 mg/ml) produced an immediate brief bradypnea followed by a vigorous and slowly reversing hyperpnea accompanied most often by a fall in blood pressure. Tachyphylaxis was observed in the response to nicotine. Noradrenaline (0.001 and 0.1 mg/ml) did not produce any effect, and it did not alter the responses elicited by procaine and nicotine given by perfusion either simultaneous with or subsequent to the noradrenaline. Acetylcholine (0.5 mg/ml) produced weak transient respiratory stimulation and a small fluctuation in blood pressure which disappeared in repeated tests. Methacholine (1 mg/ml) caused a brief hyperpnea and a fall in blood pressure both of which were abolished after atropine (0.2 mg) was injected into the third ventricle. Pilocarpine (10 mg/ml) elicited no change in respiration or blood pressure. Respiratory and cardiovascular effects produced by strychnine (1 mg/ml) were attributable non-specifically to convulsive movements of the animal. Ethamivan (1 mg/ml) produced a single deep breath and a slowly reversing rise in blood pressure. Cyanide (0.5 mg/ml) barely stimulated the respiration but it produced a long lasting rise in blood pressure. Ethyl alcohol (0.1 ml/ml) elicited brisk though brief respiratory stimulation and a short lasting fall in blood pressure.4. It was shown that the effects of procaine and nicotine were not qualitatively altered when the perfusion effluent was collected through a ventral craniotomy instead of the cisterna magna.
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PMID:Respiratory responses to chemical pulses in the cerebrospinal fluid of cats. 506 7

1. The responses of identified cells in the rat cerebral cortex to cholinomimetic and anticholinergic substances has been investigated.2. Acetylcholine and muscarinic agonists have an excitatory action on 80% of pyramidal tract cells. This response is found especially on cells responding to specific thalamic stimulation and the burst of spikes evoked from this site can sometimes be blocked by the iontophoresis of atropine. This strongly suggests an excitatory transmitter function for acetylcholine in a specific thalamocortical pathway.3. Experiments on non-pyramidal tract cells have detected a muscarinic depression of some cells, and a nicotinic excitation of some cells above a depth of 600 mu in the cortex.4. It is suggested that the increased release of acetylcholine from the cortex produced by atropine administration may be due to an excess of muscarinic inhibitory over excitatory synapses in the cortex.
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PMID:Cholinergic mechanisms in the rat somatosensory cerebral cortex. 507 8

1. Some spontaneously firing cells in the cerebral cortex of cats can be depressed by iontophoretically applied acetylcholine or acetyl-beta-methylcholine, and this depression is antagonized by atropine. Thirteen per cent of 101 spontaneously active neurones tested were depressed by cholinergic agents and 64% were excited.2. Single stimuli applied to the adjacent cortical surface excited 132 neurones orthodromically. Acetylcholine or acetyl-beta-methylcholine depressed this synaptic firing in 18% of the cells. The depression was blocked by atropine.3. The population of neurones in which cholinergic agents depressed spontaneous or synaptic firing was located within the superficial half of the cortex.4. Glutamate-induced firing was depressed by cholinergic agents in 41% of 211 cells tested; atropine and strychnine strongly antagonized this depressant action, while dihydro-beta-erythroidine was a weaker antagonist.5. Long duration inhibition of glutamate-induced firing evoked by repetitive stimulation of the cortical surface could be blocked by atropine or strychnine in both the intact and chronically isolated cortex. This provides strong evidence for a system of intracortical cholinergic neurones which make direct inhibitory contacts with neurones in the superficial layers of the cortex.
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PMID:Acetylcholine inhibition in the intact and chronically isolated cerebral cortex. 508 32

1. Acetylcholine (ACh), other cholinomimetics, cholinesterase inhibitors and cholinergic antagonists were administered iontophoretically to medial geniculate (MG) neurones and their effects on chemically or neurally evoked responses recorded extracellularly.2. Acetylcholine had excitant actions on 45% of the neurones tested. Most of these were of a slow time course. Desensitization to the excitant effects was frequently observed.3. Acetylcholine excited 91% of neurones activated antidromically by stimulation of the auditory cortex, 71% of neurones activated synaptically from the auditory cortex, 74% of neurones activated from the inferior colliculus and 100% of geniculo-cortical relay neurones.4. Acetylcholine had depressant effects, which were generally of a rapid time course, on 29% of MG neurones. No desensitization to the depressant effects was observed.5. On 4% of neurones, ACh had both excitant and depressant effects. Such "dual" effects were manifested either as an initial excitation followed by a depression, or as a depression followed by an excitation.6. Eserine, neostigmine and edrophonium potentiated both excitant and depressant actions of ACh on many cells. Neostigmine and edrophonium occasionally antagonized the effects of ACh.7. Atropine, hyoscine, dihydro-beta-erythroidine, hexamethonium and (+)-tubocurarine antagonized both excitant and depressant effects of ACh. The muscarinic blocking agents were usually more effective than the nicotinic agents.8. Carbamylcholine, acetyl-beta-methylcholine, nicotine, butyrylcholine, arecoline and pilocarpine had excitant, depressant or no effects on MG neurones. Generally, carbamylcholine was more potent than acetyl-beta-methylcholine and ACh, which were more potent than nicotine. Butyrylcholine, arecoline and pilocarpine were even less potent, often having no effect.9. The cholinomimetics generally had similar effects to those of ACh on the same neurones, but sometimes were quite different. Carbamylcholine, acetyl-beta-methylcholine and nicotine antagonized the effects of ACh on some neurones.10. The results suggest that cholinoceptive receptors on MG neurones are not homogeneous. Although there are possibly some purely muscarinic and purely nicotinic receptors, the majority appear to be of intermediate muscarinic-nicotinic type. These mediate either excitation or inhibition.
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PMID:Properties of cholinoceptive neurones in the medial geniculate nucleus. 541 82

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