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)

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

1. In anaesthetized cats, stimulation of efferent components of the carotid sinus or aortic nerves depressed chemoreceptor discharge from the relevant chemoreceptor afferents. The local application of 2% procaine hydrochloride to the sinus nerve trunk, peripheral to the site of the stimulating electrodes and proximal to that of the afferent nerve twig, abolished the depression of afferent chemoreceptor discharge caused by electrical stimulation; on washing the procaine away electrical stimulation once more induced depression of chemoreceptor discharge.2. The depressant effect of efferent stimulation on carotid chemoreceptor activity was still seen during complete carotid glomeral ischaemia. Atropine given by close intra-arterial injection to the carotid body did not affect the depressant influence of efferent sinus nerve stimulation on carotid body chemoreceptor discharge.3. Stimulation of the sinus nerve efferents usually increased carotid body blood flow. Close arterial injection of atropine abolished this effect.4. The responses of glomeral blood flow and carotid chemoreceptor activity to efferent stimulation of the cut sinus nerve were not temporally related. It seems improbable that the depressant effect of such stimulation on chemoreceptor discharge was due to alterations of glomeral blood flow.5. Stimulation of the peripheral end of the cervical vagus in atropinized cats reduced chemoreceptor activity recorded in the ipsilateral aortic nerve.
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PMID:The effects of electrical stimulation of the distal end of the cut sinus and aortic nerves on peripheral arterial chemoreceptor activity in the cat. 557 48

1. Drugs have been applied micro-electrophoretically to units in the hippocampal cortex of the anaesthetized cat, and their effects on cell firing were recorded simultaneously.2. L-Glutamate rapidly and powerfully excited hippocampal units, an effect which was quickly reversed on stopping the expelling current. The local application of L-glutamate also excited a fast seizure discharge at 15-50/sec. Both these effects of L-glutamate were strongly depressed by fimbrial stimulation.3. gamma-Aminobutyric acid had a strong depressant action on all the units on which it was tested; the time course of this effect was rapid.4. ACh excited half the units to which it was applied. Characteristically this excitation developed slowly over many seconds and persisted after stopping the expelling current. Most cholinoceptive units were found to be concentrated in the superficial layer of the cortex corresponding to the hippocampal pyramidal cells and their main dendritic processes.5. Atropine selectively blocked the excitation of cholinoceptive units by ACh, but not the excitation by L-glutamate. No cholinoceptive units were blocked by dihydro-beta-erythroidine, though several were selectively blocked by dimethyl (+)-tubocurarine.6. The most usual effect seen with 5-HT was depression, though several units were found to be excited. Some of the units tested with 3-hydroxytyramine (dopamine) or noradrenaline were found to be depressed.
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PMID:Micro-electrophoretic studies of neurones in the cat hippocampus. 594 16

Sucrose gap recording technique was employed to record surface potentials from superior cervical ganglia (SCGs) of several species. Repetitive preganglionic stimulation (30 Hz, 1-2 sec) elicited in curarized rabbit, rat and cat SCGs, a biphasic response as the initial slow positive (P) potential, was followed by a late negative (LN) potential. In curarized guinea-pig SCG, a LN response with no detectable P potential was observed. Neostigmine (0.5-1 microM) increased the amplitude and duration of the P and LN responses in the majority of the rabbit, rat and cat SCGs. LN response of guinea-pig SCG was first enhanced by neostigmine; subsequently, it was converted into a hyperpolarizing potential. Alpha receptor antagonists, phenoxybenzamine, phentolamine and dihydroergotamine, and a beta receptor antagonist, propranolol, did not appreciably alter the P and LN responses of the rabbit, cat and rat SCG or neostigmine-induced hyperpolarization of the guinea-pig SCG. Dopaminergic receptor antagonists, haloperidol, chlorpromazine and metoclopramide, caused no significant depression of the P and LN responses in the rabbit SCG. Atropine (1 microM) consistently abolished the P and/or LN of all these ganglia, as well as the neostigmine-induced hyperpolarization of the guinea-pig SCG. These results demonstrate that muscarinic receptors are involved in the generation of P and LN potentials of mammalian sympathetic ganglia, while the adrenergic and disynaptic nature of P response remains to be clarified. Furthermore, there appears to be no correlation between the generation of P potential and elevation of cyclic AMP in the SCG.
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PMID:A comparative study of the pharmacological properties of the positive potential recorded from the superior cervical ganglia of several species. 610 60

The effect of somatostatin on lateral hypothalamic self-stimulation was investigated in atropine- and methysergide-pretreated rats. Somatostatin markedly decreased the self-stimulation rate of the animals. Atropine in a dose which had no action on self-stimulation partly antagonized the effect of somatostatin. Methysergide potentiated the somatostatin-induced depression of self-stimulation behavior. These results suggest that the central cholinergic and serotoninergic systems may play a role in the somatostatin-induced inhibition of self-stimulation.
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PMID:The effect of somatostatin on self-stimulation behavior in atropine- and methysergide-pretreated rats. 613 93

Six cases of toxic ingestion of clonidine hydrochloride are reviewed. Apnea, respiratory depression, and rhythm disturbances were more frequent in our patients than in those previously reported; hypotension and bradycardia occurred at a similar frequency. Satisfactory management consisted of close attention to vital signs and judicious treatment of specific physiologic abnormalities. Atropine effectively corrected bradycardia. Tolazoline was found to be ineffective in reversing symptoms and signs of clonidine overdosage. Hypotension was managed by volume expansion, and if necessary, by a continuous infusion of dopamine. Naloxone, although not used in our patients, may be of both diagnostic and therapeutic value in treating clonidine overdosage.
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PMID:Management of clonidine ingestion in children. 613 26

Two cases of severe beta-blocker overdose are presented that were treated successfully with glucagon therapy. The effects of glucagon in reversing the cardiovascular depression of profound beta-blockade, including its mechanism of action, onset and duration of action, dosage and administration, cost and availability, and side effects are reviewed. Medical complications of beta-blocker overdose include hypotension, bradycardia, heart failure, impaired atrioventricular conduction, bronchospasm and, occasionally, seizures. Atropine and isoproterenol have been inconsistent in reversing the bradycardia and hypotension of beta-blocker overdose. Glucagon increases heart rate and myocardial contractility, and improves atrioventricular conduction. These effects are unchanged by the presence of beta-receptor blocking drugs. This suggests that glucagon's mechanism of action may bypass the beta-adrenergic receptor site. Because it may bypass the beta-receptor site, glucagon can be considered as an alternative therapy for profound beta-blocker intoxications. The doses of glucagon required to reverse severe beta-blockade are 50 micrograms/kg iv loading dose, followed by a continuous infusion of 1-15 mg/h, titrated to patient response. Glucagon-treated patients should be monitored for side effects of nausea, vomiting, hypokalemia, and hyperglycemia. The high cost and limited availability of glucagon may be the only factors precluding its future clinical acceptance.
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PMID:Glucagon therapy for beta-blocker overdose. 614 98

The acetylcholine (ACh) stores of cholinergic neurons of the myenteric plexus of guinea-pig ileum were labelled by preincubation with 3H-(methyl)-choline. The secretion of labelled transmitter evoked by electrical field stimulation at 1 Hz in the presence of eserine increased by 55% after addition of 0.5 mM 8-Br adenosine 3', 5'-cyclic monophosphate (8-Br cAMP). Atropine further enhanced the secretory response, but not more than in the absence of 8-Br cAMP. 8-Br guanosine 3', 5'-cyclic monophosphate (8-Br cGMP, 0.5 mM) did not change the secretory response to 0.5 or 1 Hz stimulation, either at 1.8 mM or at 0.6 mM calcium, in the absence of eserine. Nor did 1 mM 8-Br cGMP alter the effects of atropine or of oxotremorine. Activation of guanylate cyclase by 0.1 mM N-methyl-N'-nit-ro-N-nitroso guanidine failed to alter the secretory response to 0.5 Hz stimulation in the absence of eserine, or to influence the depression of the secretion caused by oxotremorine. The phosphodiesterase inhibitor 3-isobutyl-l-methylxanthine (a mM) neither altered the secretory response in the presence of eserine, nor the enhancing effect of atropine. The results suggest that cyclic nucleotides are probably not critically involved as "second messengers" in the muscarinic "autoinhibition" of ACh secretion from cholinergic myenteric neurons of guinea-pig ileum.
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PMID:Secretion of 3H-acetylcholine from guinea-pig ileum myenteric plexus is enhanced by 8-Br adenosine 3', 5'-cyclic monophosphate but not changed by 8-Br guanosine 3', 5'-cyclic monophosphate. 618 55

The possibility that acetylcholine (ACh) may inhibit its own release from nerve terminals by acting on presynaptic receptors has been investigated using the electric organ of Torpedo marmorata. ACh release was analysed by electrophysiological and biochemical methods conjointly. Oxotremorine, at micromolar concentrations, depressed nerve-electroplaque transmission by reducing the amount of ACh released by nerve impulses. This effect was competitively antagonised by nanomolar concentrations of atropine or methylatropine. Other muscarinic agonists, betanechol, pilocarpine and muscarine, however, failed to depress transmission but choline was effective at high concentrations. Anticholinesterase drugs, physostigmine, neostigmine or fluostigmine (diisopropylfluorophosphate, given as pretreatment and subsequently washed out) markedly depressed evoked ACh release. When cholinesterase was inhibited, the addition of oxotremorine or exogenous ACh caused a further depression of ACh release. Atropine was found to be very effective in reversing the depression of transmitter release produced by anticholinesterases. Looking for the mechanism of these presynaptic changes, we found that oxotremorine had little, if any, effect on the size of the ACh store of the tissue, on the compartmentation of ACh inside and outside synaptic vesicles, or on the rate of ACh turnover. The changes induced by oxotremorine cannot be explained by a reduction in calcium entry, since the presence of oxotremorine did not change the uptake of 45Ca observed after repetitive stimulation. Electrophysiological techniques were used to test for an effect of atropine in experiments where transmission of one impulse was expected to depress ACh release by subsequent impulses. This depression was not affected atropine, making it unlikely that the 'muscarinic' inhibition of ACh release has a role as a short-term feedback regulation of transmission. A second possibility is that oxotremorine (and external non-hydrolysed ACh) can enter the presynaptic membrane and interfere with the mechanism of transmitter release.
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PMID:Cholinergic inhibition of acetylcholine release in the electric organ of Torpedo. 628 Oct 33

1 Drug actions on electrical and mechanical properties of smooth muscle cells and neuromuscular transmission in the canine cerebral arteries were investigated by use of microelectrode and isometric tension recording methods. 2 In the basilar and middle cerebral arteries, the resting membrane potentials were--49.4 mV and -51.7 mV, respectively, the length constants 0.57 mm and 0.45 mm, respectively and the time constants 142 ms and 118 ms, respectively. 3 Outward current pulses did not evoke the spike in either artery but did evoke the spike under conditions of pretreatment with 10 mM tetraethylammonium (TEA). 4 The maximum slope of depolarization produced by a ten fold increase in [K]o plotted on a log scale was 40.1 mV in the basilar artery and 42.2 mV in the middle cerebral artery. 2-Nicotinamidoethyl nitrate, the K-permeability accelerator, had no effect on the membrane potential. 5 K-free or ouabain [10(-5)M] treatment slightly depolarized the membrane. Re-addition of K [5.9 mM] hyperpolarized the membrane by several mV. Thus, the contribution of an active Na-K pump in the membrane potential seems to be small. 6 In both arteries, acetylcholine, adenosine, noradrenaline and isoprenaline in concentrations up to 10(-5)M did not modify the membrane potential and resistance, while 5-hydroxytryptamine (over 10(-8)M) and ATP (over 10(-5)M) depolarized the membrane, decreased the membrane resistance and produced a dose-dependent contraction. Adenosine suppressed the contraction evoked by excess [K]o (39.8 mM). 7 Perivascular nerve stimulation produced excitatory junction potentials (e.j.ps). Often e.j.ps were followed by a hyperpolarization. Repetitive stimulation produced facilitation after several stimuli and depression followed. In some cells, this depression appeared without facilitation. 8 The e.j.ps ceased with pretreatment with guanethidine (10(-6)M) or tetrodotoxin (3 X 10(-7)M), while phentolamine (10(-7)M) and yohimbine (10(-7)M) enhanced the amplitude of e.j.ps. ATP (10(-5)M) and noradrenaline (10(-6)M) suppressed and prazosin had little effect on the e.j.ps. Atropine (10(-6)M) also had no effect on the e.j.ps. 9 Specific features of the cerebral artery and systemic vascular beds were compared, and the features of adrenoceptors on the smooth muscle membrane were compared with findings in other vascular beds.
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PMID:Membrane properties and excitatory neuromuscular transmission in the smooth muscle of dog cerebral arteries. 629 82


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