bluuebunny/crossref_metadata_2025_split huggingface dataset:
Modification of the responses of brain stem neurones to transmitter substances by anaesthetic agents
Authors: BRADLEY P. B. , DRAY A. 
Published: July 2012

Summary
. The effects of microiontophoretic applications of acetylcholine (ACh), (—)‐noradrenaline ((—)‐NA) and 5‐hydroxytryptamine (5‐HT) have been investigated on spontaneously active brain stem neurones in decerebrate unanaesthetized rats and in rats anaesthetized wih either tribromoethanol, urethane or pentobarbitone.
. Four types of responses to both (—)‐NA and 5‐HT were seen. These were: simple excitation; excitation preceded by a short‐lasting inhibition; short‐lasting inhibition and prolonged inhibition. Three types of responses to ACh were seen: an excitation with long latency of onset; excitation with short latency of onset, resembling the response to an excitant amino acid, and a short‐lasting inhibitory response.
. The types of responses to microiontophoretically applied ACh, (—)‐NA or 5‐HT in anaesthetized and unanaesthetized animals were similar.
. The number of ACh excitatory responses with short latency of onset were significantly reduced in the pentobarbitone‐anaesthetized group and a small but significant increase in the number of 5‐HT inhibitory effects were observed in each anaesthetized group of animals.
. A significantly greater proportion of slower firing neurones (less than 10 spikes/s) were found in the pentobarbitone‐anaesthetized animals.
. The effects of microiontophoretically applied and i.v. administered pentobarbitone were studied on spontaneously active neurones which responded consistently to ACh and a control agonist.
. Pentobarbitone administered by either route reduced the firing rate of most neurones studied and was shown to antagonize specifically the excitation of neurones by exogenously applied ACh.
. It is suggested that postsynaptic antagonism of endogenously released ACh may be a contributing factor in the mechanism of action of pentobarbitone.
Acetylcholine release from the rabbit isolated superior cervical ganglion preparation
Authors: DAWES P. M. , VIZI E. S. 
Published: July 2012

Summary
. The rabbit isolated superior cervical ganglion preparation has been used to measure the release of acetylcholine from the tissue at rest and during preganglionic nerve stimulation.
. In the presence of physostigmine, the resting release of acetylcholine was 013+001 (nmol/g)/min (10 experiments) and that during stimulation with 300 shocks at 10 Hz was 3·1 ± 0·4 (pmol/g)/volley in 4 experiments (means ± s.e.m.). The volley output was independent of the frequency of stimulation over the range 1 to 10 Hz but was higher at 0·3 Hz.
. Tetrodotoxin, 0·8 μm, had no effect on the resting release of acetylcholine but reduced the stimulated release below detectable levels (2 pmol). Lowering the temperature of the bathing fluid to 5° C reduced to below detectable levels both the resting release and that produced by nerve stimulation.
. The resting release of acetylcholine was increased by a potassium‐rich (49·4 mm K+) bathing solution and by replacing the sodium chloride in the solution with lithium chloride (113 mM Li+).
. (—)‐Noradrenaline bitartrate, 3 μm, and (±)‐adrenaline bitartrate, 1·5 μm, reduced by 70% the output of acetylcholine induced by stimulation at 0–3 Hz, but failed to reduce the resting release or that evoked by stimulation at 10 Hz. The inhibition was reversed by phentolamine.
. It is concluded that the rabbit superior cervical ganglion in vitro is a suitable preparation for studying transmitter release and that the ganglion blocking effect of catecholamines is due to a reduction in transmitter release.
The effect of salicylate on the biliary excretion of 14C‐bishydroxycoumarin in rat
Authors: BUTTAR H. S. , COLDWELL B. B. , THOMAS B. H. 
Published: July 2012

Summary
. The effect of intravenous sodium salicylate on the biliary excretion of 14C‐bishydroxycoumarin (14C‐BHC) was studied in rats.
. Salicylate (88·9 mg/kg) increased the biliary excretion of 14C‐radioactivity from a control value of 12·3±2·7% to 29·3±2·5% of the administered dose in 6 h after injection.
. During the 6 h period, 11% of the dose of radioactivity underwent biliary recycling in the salicylate‐treated rats compared to only 6% in the absence of salicylate.
. About 15·3% of the radioactivity excreted in the bile of rats given BHC alone was detected as unchanged BHC, 8·6% was present as BHC‐conjugate, conjugates of BHC metabolites accounted for 30·9%, and the remainder consisted of unidentified metabolites.
. Salicylate treatment did not significantly alter the excretory pattern of unchanged BHC and its metabolites.
Effects of prostaglandin E1 on acid secretion, mucosal histamine content and histidine decarboxylase activity in rat stomach
Authors: HÅKANSON R. , LIEDBERG G. , OSCARSON J. 
Published: July 2012

Summary
Prostaglandin E1 inhibits basal and pentagastrin‐stimulated gastric acid secretion. The mechanism of this action is not clear. One possible explanation might be that prostaglandin E1 interferes with the local release or synthesis of histamine which has been proposed as the mediator of the effects of gastrin on the parietal cell.
A single injection of prostaglandin E1 did not affect mucosal histamine content or histidine decarboxylase activity in the rat stomach. Pentagastrin lowered the histamine content and activated the histidine decarboxylase to the same extent in prostaglandin E1‐pretreated and in control rats. We conclude therefore that the inhibitory effect of prostaglandin E1 on basal and pentagastrin‐stimulated acid secretion is not caused by inhibition of histamine release or histamine synthesis.
Repeated injections of prostaglandin E1 resulted in a significant elevation of the gastric histidine decarboxylase activity in normal but not in antrectomized rats. Conceivably, this increase in enzyme activity is secondary to prostaglandin E1‐induced inhibition of acid secretion, which will stimulate release of gastrin due to the rise in intragastric pH.
The uptake of 3H‐γ‐aminobutyric acid by the retina
Authors: GOODCHILD MARGARET , NEAL M. J. 
Published: July 2012

Summary
The accumulation of 3H‐γ‐aminobutyric acid (GABA) by the isolated rat retina has been measured.
When retinae were incubated at 37° C in a medium containing 3H‐GABA, tissue:medium ratios of about 25:1 were attained after a 30 min incubation.
After incubations of 40 min at 37° C, almost all (98%) the radioactivity in the tissue was present as unchanged 3H‐GABA.
The process responsible for 3H‐GABA uptake showed many of the properties of an active uptake system: it was temperature‐sensitive, required the presence of sodium ions in the external medium, was inhibited by anoxia, dinitrophenol and ouabain, and showed saturation kinetics.
The estimated Km value of GABA was 4·0 × 10−5M, and Vmax was 0·167 (μmoles/min)/g retina.
The uptake of 3H‐GABA was not affected by the presence of large molar excesses of glycine, l‐glutamate, l‐aspartate, l‐alanine, l‐proline, or l‐histidine, but was inhibited by dl‐γ‐amino‐β‐hydroxybutyrate, β‐guanidinopropionate, and l‐2,4‐diaminobutyrate.
The retina was capable of achieving a large net uptake of GABA, indicating that the accumulation of 3H‐GABA by the tissue was not due only to an exchange process with the endogenous GABA pool.
The uptake of 3H‐GABA occurred only in tissue from the central nervous system. Thus, retina and cerebral cortex rapidly accumulated radioactivity, but slices of cornea, posterior wall of the eye, and liver achieved tissue: medium ratios of approximately one.
There was a rapid efflux of radioactivity from retinae placed in fresh medium and after 60 min, 90% of the radioactivity was lost from the tissue. The radioactivity released into the medium was present largely as 3H‐acidic and neutral metabolites. When the metabolism of GABA was inhibited by the presence of amino‐oxyacetic acid in the medium, only about 10% of the radioactivity was lost from the tissue during a similar 60 min incubation, and the radioactivity released was present largely as unchanged 3H‐GABA.
It is suggested that the GABA uptake process may represent a possible mechanism for the inactivation of GABA if this amino acid is released at inhibitory synapses in the retina.
Uptake kinetics and ion requirements for extraneuronal uptake of noradrenaline by arterial smooth muscle and collagen
Authors: GILLESPIE J. S. , TOWART R. 
Published: July 2012

Summary
The ionic requirements for noradrenaline uptake into vascular smooth muscle cells were studied by perfusing rabbit isolated ear arteries with noradrenaline (10−3M) either in Krebs solution or in Krebs solution modified by altering the concentration of one or more ion. Noradrenaline uptake was measured by quantitative microphotometry.
Some uptake into smooth muscle continued in isotonic sucrose in the absence of all ions. Omission of Na+ from the Krebs solution partially inhibited uptake as did high (100 mm) K+. Omission of K+, Ca++ or Mg++ had no effect on uptake. Lithium was able completely to substitute for Na+.
Alteration in ion concentration did not affect the binding of noradrenaline to collagen.
The kinetics of uptake of noradrenaline into smooth muscle were analysed and found to be saturable with a Km of 4·9 × 10−4M.
It is concluded that the ionic requirements of the transport mechanism for the uptake of noradrenaline by vascular smooth muscle show a relatively low specificity.
The accumulation and metabolism of (—)‐noradrenaline by cells in culture
Authors: POWIS G. 
Published: July 2012

Summary
Cultured bovine embryonic tracheal cells, EbTr (NBL‐4) possess a process for the intracellular accumulation of (—)‐noradrenaline with the characteristics generally ascribed to extraneuronal uptake by cardiac and smooth muscle cells in the body. It has a Km of 2·6 × 10−4M.
The accumulation process is inhibited competitively by normetanephrine, but only at relatively high concentrations, IC50 = 2·1 × 10−4M. Inhibition also occurs with 17‐β‐oestradiol, IC50 = 1·3 × 10−5M.
The noradrenaline metabolites, 3,4‐dihydroxy‐mandelic acid and 3,4‐dihydroxy‐phenylglycol potentiate accumulation and reduce intracellular levels of normetanephrine in a similar manner to known inhibitors of catechol‐O‐methyl transferase.
It is suggested that intracellular, rather than extracellular, normetanephrine may exert feedback inhibition upon noradrenaline accumulation by combining with the transport process at the inner surface of the cell membrane.
The effects of pargyline on overflow of transmitter and uptake of noradrenaline in the cat spleen
Authors: BLAKELEY A. G. H. , POWIS G. , SUMMERS R. J. 
Published: July 2012

Summary
Twenty minutes after the addition of pargyline (5 × 10−4M) to blood perfusing the isolated spleen of the cat, the overflow of transmitter resulting from stimulation of the sympathetic nerves increased 2–3–3‐fold. Lower doses of pargyline did not significantly affect overflow.
Monoamine oxidase activity, measured with either radioactively labelled tyramine or noradrenaline as substrate, was almost completely inhibited by doses of pargyline in the range of 10−4M to 5 × 10−4M. Inhibition of enzyme activity was not correlated with the effect on overflow. Pargyline had only a slight inhibitory effect on catechol‐O‐methyl transferase.
Uptake of a 1 μg injection (pulse) of labelled noradrenaline, following pargyline (5×10−4M), was increased to 199·1% of that found in control experiments.
Pargyline significantly reduced the vascular responses to nerve stimulation but had no significant effect on capsular responses.
The inhibitor had no effect on resting overflow of labelled noradrenaline from the spleen but doubled the overflow of labelled noradrenaline following nerve stimulation.
It is suggested that the effect of pargyline on overflow is due to increased release of transmitter during nerve stimulation.
The possible clinical significance of these findings is discussed.
Acetylcholine release from guinea‐pig ileum by parasympathetic ganglion stimulants and gastrin‐like polypeptides
Authors: VIZI E. S. 
Published: July 2012

Summary
The release of acetylcholine by parasympathetic ganglion stimulants from the nerve terminals of the guinea‐pig longitudinal muscle strip was studied. The acetylcholine released was collected in the presence of physostigmine sulphate.
Nicotine and 1,1‐dimethyl‐4′‐phenylpiperazinium iodide (DMPP) released acetylcholine. Tetrodotoxin (50 ng/ml) and hexamethonium completely prevented their action on acetylcholine release, indicating that their effect is on nicotinic receptors of cell bodies. Noradrenaline (1 μg/ml), excess magnesium, and calcium withdrawal inhibited the acetylcholine release induced by nicotine or by DMPP.
There was rapid tachyphylaxis to the acetylcholine releasing action of both nicotine and DMPP.
The octapeptide amide of cholecystokinin and caerulein (10−9M) enhanced the acetylcholine release without producing tachyphylaxis. Tetrodotoxin completely inhibited acetylcholine release. However, hexamethonium or desensitization with 5‐hydroxytryptamine did not prevent their action. In the early phase of nicotine action the polypeptides studied failed to increase acetylcholine release. However, a few minutes later the tissue became sensitive to polypeptides despite the fact that the tissue was still exposed to nicotine. These data suggest the presence in the parasympathetic ganglion cells of separate gastrointestinal hormone‐sensitive receptors.
Noradrenaline inhibited the acetylcholine releasing action of polypeptides. This effect was mediated via α‐adrenoceptors since phentolamine prevented its action.
Excess magnesium (9·3 mm) also reduced the acetylcholine release in response to the polypeptides.
Effect of phospholipase C on calcium release from epithelia treated with antidiuretic hormone
Authors: CUTHBERT A. W. , WONG P. Y. D. 
Published: July 2012

Summary
Addition of antidiuretic hormone (ADH) to the bladders of toads (Bufo marinus) preloaded with 45Ca causes an increase in the rate of calcium efflux.
Pretreatment of the serosal surfaces of bladders with phospholipase C prevents the action of ADH on calcium efflux.
Structure‐activity relationships in some series of 2‐alkyl‐1,2,3,‐benzotriazinium compounds
Authors: CULL GERALDINE A. G. , SCOTT N. C. 
Published: July 2012

Summary
The potencies of four series of N‐alkyl‐1,2,3‐benzotriazinium iodides have been estimated on the frog rectus abdominis and chick biventer cervicis preparations.
The partition coefficients between chloroform and water were measured for all of the compounds, as well as the ionization constants for some members of two of the series.
The potencies of the compounds increased with the number of carbon atoms in the N‐alkyl side chain up to a maximum at the n‐butyl homologue while partition coefficients increased up to the n‐pentyl homologue, and there may be some association between the lipid solubilities of the compounds and their biological activity.
The responses of the tissues to the benzotriaziniums were not abolished by tubocurarine, indicating that the site of action was not at acetylcholine receptors.
The similarity between the actions of the benzotriaziniums and those of quinine and quinidine is discussed.
Effect of chronic l‐DOPA administration on catecholamine metabolism in the rat
Authors: LANCASTER JULIE , SAWYER P. R. , SHEPHERD D. M. , TURNBULL M. J. 
Published: July 2012

Summary
l‐DOPA was administered to rats by twice daily intraperitoneal injection for a period of eleven days. The daily dose was gradually increased from 250 mg/kg to 1 g/kg. The animals were killed 12 h after the last injection and tissue catechol‐O‐methyl transferase, DOPA‐decarboxylase and monoamine oxidase activity determined.
Catechol‐O‐methyl transferase activity was reduced in the liver (46%) and red blood cells (38%) but was approximately doubled in the heart.
Liver DOPA‐decarboxylase activity was reduced by approximately 25%.
l‐DOPA administration did not significantly affect the activity of any of the enzymes studied in brain tissue.
Role of brain monoamines in the fatal hyperthermia induced by pethidine or imipramine in rabbits pretreated with a monoamine oxidase inhibitor
Authors: GONG S. N. C. , ROGERS K. J. 
Published: July 2012

Summary
The intravenous infusion of pethidine or imipramine, in doses of 5 mg/kg, caused fatal hyperpyrexia in rabbits premedicated with pargyline.
The drug interaction was not antagonized when either reserpine or α‐methyl‐p‐tyrosine were administered with pargyline. Neither reserpine nor α‐methyl‐p‐tyrosine prevented the rise in brain stem 5‐hydroxytryptamine content following monoamine oxidase inhibition, although the increase in catecholamines normally produced by pargyline was prevented.
The development of fatal hyperthermia was completely prevented when rabbits were treated with p‐chlorophenylalanine prior to pargyline premedication. In these animals, the concentration of brain stem catecholamines, but not 5‐hydroxytryptamine, was increased.
The results indicate that the hyperthermia evoked by pethidine or imipramine in combination with monoamine oxidase inhibitors can take place only in the presence of raised concentrations of 5‐hydroxytryptamine in the brain stem.
Effect of depletion of cerebral monoamines on the concentration of glycogen and on amphetamine‐induced glycogenolysis in the brain
Authors: HUTCHINS D. A. , ROGERS K. J. 
Published: July 2012

Summary
An increase in the concentration of glycogen occurs in the mouse brain after depletion of cerebral catecholamines by alpha methyl‐p‐tyrosine methylester (H44/68), diethyldithiocarbamate, or reserpine.
Depletion of cerebral 5‐hydroxytryptamine with parachlorophenylalanine (PCPA) does not result in a change in the concentration of brain glycogen.
When H44/68 is administered together with reserpine to inhibit the synthesis and storage of cerebral catecholamines, and thus bring about their total depletion from the brain, the cerebral glycogenolytic effect of amphetamine is abolished.
Amphetamine‐inducing glycogenolysis is only partially antagonized if only one of the catecholamine‐depleting agents H44/68, diethyldithiocarbamate, or reserpine is injected prior to the amphetamine. The persistence of this glycogenolytic effect of amphetamine is possibly due to the presence of residual stores of catecholamines available for release by the stimulant drug.
Depletion of cerebral 5‐hydroxytryptamine by PCPA does not result in any antagonism of amphetamine‐induced glycogenolysis.
The results suggest that amphetamine depletes brain glycogen by the release of central catecholamines rather than by a direct action at receptors.
Action of drugs on denervated myoepithelial cells of salivary glands
Authors: EMMELIN N. , THULIN A. 
Published: July 2012

Summary
The pressure in the ducts of the two submaxillary glands was recorded in anaesthetized dogs in which either the superior cervical ganglion had been removed or the chorda‐lingual nerve had been cut on one side, 17–30 days earlier. Noradrenaline, adrenaline, phenylephrine, acetylcholine and methacholine were injected to produce pressure rises attributed to contraction of myoepithelial cells.
After sympathectomy increased pressure responses were obtained with all the drugs, but particularly with noradrenaline. Cocaine increased the effect of noradrenaline on the normal gland but slightly less than sympathectomy.
Parasympathetic decentralization increased the pressure effects of acetylcholine and methacholine, and in most cases also increased those of the sympathomimetic drugs.
It is concluded that the myoepithelial cells of this gland normally receive motor impulses from both divisions of the autonomic nervous system, and that many, if not all, of the cells are innervated by both. Disconnecting the gland from the central nervous system by either pathway causes supersensitivity of the classical post‐junctional type, and sympathetic ganglionectomy causes in addition a pre‐junctional sensitization.
Prostaglandin E1 causes sedation and increases 5‐hydroxytryptamine turnover in rat brain
Authors: HAUBRICH D. R. , PEREZ‐CRUET J. , REID W. D. 
Published: July 2012

Summary
Administration of prostaglandin E1 (1 mg/kg, i.p.) to rats induced sedation and a decrease in muscular tone. Prostaglandin E1‐induced sedation was accompanied by the low voltage—high frequency E.E.G. pattern characteristic of the waking animal.
Administration of prostaglandin E1 also increased the turnover rate of 5‐hydroxytryptamine and raised the concentration of acetylcholine in brain.
The behavioural effects of prostaglandin were blocked by prior administration of p‐chlorophenylalanine or pargyline, drugs which lowered the brain concentration of 5‐hydroxyindoleacetic acid (5‐HIAA), and was potentiated by pretreatment with probenecid, which elevated the 5‐HIAA concentration. Pretreatment with atropine sulphate failed to alter prostaglandin E1‐induced sedation.
The results are compatible with the possibility that prostaglandin E1 induces a state resembling paradoxical sleep through an action on 5‐hydroxytryptamine metabolism in brain.
Effects of vinblastine on catecholamine‐biosynthetic enzymes in heart, sympathetic ganglion and adrenal glands of rats
Authors: HANBAUER I. , KOPIN I. J. , MAENGWYN‐DAVIES GERTRUDE D. , THOA N. B. , WEISE VIRGINIA K. 
Published: July 2012

Summary
The effect of vinblastine on the activities of dopamine‐β‐hydroxylase (DBH) in heart, superior cervical ganglion and adrenal glands of rats and tyrosine hydroxylase (TH) and phenylethanolamine‐N‐methyl transferase (PNMT) in adrenal glands was examined.
In the superior cervical ganglion and heart, DBH activity decreased within hours, reached a minimum in 3 to 5 days and slowly returned towards normal over the next 2 weeks.
There was an increase in the activities of TH, DBH and PNMT in adrenal glands which was prevented by adrenal denervation.
When the same total dose of vinblastine was administered subdivided over a period of 5 days, enzyme activities in heart, superior cervical ganglion or adrenal glands remained unchanged.
Interaction of benzilylcholine mustard, benzilylcholine and lachesine with the histamine receptor in the longitudinal muscle of guinea‐pig ileum
Authors: REASBECK P. G. , YOUNG J. M. 
Published: July 2012

Summary
The histamine receptors of longitudinal muscle strips from guinea‐pig ileum were inactivated on extended exposure to concentrations of benzilylcholine mustard (BCM) above 10−6M. These concentrations are 3 orders of magnitude greater than those required for inactivation of the muscarinic receptors. Mepyramine (3 × 10−8M) afforded complete protection for the histamine receptor against the effects of BCM.
Recovery from block at 30° C was very slow with a first‐order rate constant of approximately 10−7 s−1.
The rate constant, k2, for the alkylation reaction in which the reversible BCM‐receptor complex is converted into an irreversible complex is much greater than the rate constant, k–1, for dissociation of the reversible complex. The value of the rate constant, k1, for formation of the reversible complex was 1·1 ± 0·2 × 103 M−1 s−1.
These observations suggested that k1 was probably not much greater than for BCM acting on the muscarinic receptor, even though the value of k1 was reduced by more than 2 orders of magnitude. This effect has been established for benzilylcholine and lachesine, reversible analogues of BCM. For both drugs k1 for the histamine receptor was approximately 3 orders of magnitude less than for the muscarinic receptor, whereas k‐1 was greater by a factor of only 6.