bluuebunny/crossref_metadata_2025_split huggingface dataset:
Amphetamine and conditioned ‘anxiety’
Authors: CAPPELL HOWARD , GINSBERG RONALD , WEBSTER C. D. 
Published: July 2012

Summary
Rats pressed a bar for milk reward at a steady rate, but this baseline responding was suppressed in the presence of an auditory stimulus associated with electric shock (conditioned suppression). The effects of (+)‐amphetamine sulphate on this conditioned suppression were studied in two experiments.
(+)‐Amphetamine sulphate (0·5, 1·0 or 2·0 mg/kg) reduced the baseline rate of responding and also reduced the conditioned suppression, i.e. responding in the presence of the auditory stimulus was partially restored. Both these effects were dose related.
In a further experiment the effects of 1·0 mg/kg on two levels of conditioned suppression were studied. Regardless of its degree, (+)‐amphetamine attenuated suppression.
The results were compared to previous research which found that amphetamine increased baseline responding and exaggerated conditioned suppression. It was concluded that the conditioned suppression procedure should be used with caution as an animal model of anxiety in psychopharmacological investigations.
An analysis of central adrenoceptors for control of cardiovascular function
Authors: BHARGAVA K. P. , MISHRA N. , TANGRI K. K. 
Published: July 2012

Summary
In dogs anaesthetized with pentobarbitone sodium, bradycardia with hypotension occurred on intracerebroventricular (i.c.v.) injection of noradrenaline (50–200 μg) or phenylephrine (100–400 μg), but tachycardia with hypotension occurred on i.c.v. injection of isoprenaline (100–200 μg).
These cardiovascular responses were central effects, and from the results obtained after bilateral vagotomy, removal of both stellate ganglia and transection of the upper cervical cord, it was evident that the efferent nervous pathway for all these effects was the sympathetic nervous system.
An i.c.v. injection of the α‐adrenoceptor blocking agent phenoxybenzamine (10 mg) blocked the bradycardia and hypotension produced by noradrenaline or phenylephrine, and an i.c.v. injection of a β‐adrenoceptor blocking agent, either propranolol (2 mg) or N‐isopropyl‐p‐nitrophenyl‐ethanolamine (INPEA) (10 mg), blocked the tachycardia and hypotension produced by isoprenaline.
The cardiovascular effects produced by i.c.v. injection of the three sympathomimetic amines could be reproduced in cross‐circulation experiments in the recipient dog when the amines were injected into its head circulation, and the effects of noradrenaline and phenylephrine, but not those of isoprenaline, were abolished by the α‐adrenoceptor blocking agent yohimbine (1 mg/kg) injected intravenously into the donor dog.
It is concluded that the central α‐adrenoceptors are concerned with bradycardia and the central β‐adrenoceptors with tachycardia, but that both receptors are concerned with hypotension.
Effects of perivascular nerve stimulation on the contraction and automaticity of the blood‐perfused canine papillary muscle
Authors: ENDOH M. , HASHIMOTO K. , KIMURA T. 
Published: July 2012

Summary
Effects of ventricular perivascular nerve stimulation (p.n.s.) on the ventricular contractility and idioventricular rate were investigated with the blood‐perfused papillary muscle of the canine right ventricle.
Perivascular nerve stimulation of supramaximal voltage and 1 msec pulse‐duration caused a definite positive inotropic response at a frequency of 1 Hz, which gradually reached a maximum at 15 to 20 Hz when the papillary muscle was electrically driven at 120 beats/min at a constant temperature of 38–39° C. The frequency—response curve was sigmoid.
The spontaneous regular idioventricular rate of 46 ± 4 beats/min was accelerated to at most 60 ± 4 beats/min (n = 11) by p.n.s. The stimulus frequency—response relations between chronotropic and inotropic responses to p.n.s. were almost the same.
Tetrodotoxin blocked completely the responses to p.n.s. while it had little or no effect on the inotropic response to exogenous noradrenaline.
Positive inotropic responses to p.n.s. were diminished by β‐adrenoceptor blocking agents (alprenolol, propranolol and pindolol) and were enhanced during infusion of cocaine.
In reserpine‐ or guanethidine‐pretreated muscles, p.n.s. as well as field stimulation produced negative inotropic responses, which were enhanced by physostigmine and were blocked by atropine.
Hexamethonium enhanced slightly the positive inotropic responses to p.n.s. as well as field stimulation.
It was concluded that the perivascular nerves of the coronary artery of the canine ventricle are mainly composed of postganglionic adrenergic fibres but there are also pre‐ and postganglionic cholinergic nerve fibres.
Effects of several muscarinic agonists on cardiac performance and the release of noradrenaline from sympathetic nerves of the perfused rabbit heart
Authors: FOZARD J. R. , MUSCHOLL E. 
Published: July 2012

Summary
The effects of several muscarinic agonists on atrial tension development, ventricular rate and noradrenaline release from terminal sympathetic fibres evoked by electrical nerve stimulation (SNS) and 1,1‐dimethyl‐4‐phenylpiperazinium (DMPP) were measured in isolated perfused rabbit hearts.
Hexamethonium, in a concentration which almost abolished the release of noradrenaline by DMPP, had no effect on the release produced by SNS, confirming that the stimulation was postganglionic.
The order of potency for inhibition of atrial tension development was N‐methyl‐1,2,5,6, tetrahydro‐nicotinic acid prop‐2‐yne ester (MH‐1)>oxotremorine > acetylcholine > methacholine > carbachol > furtrethonium > pilocarpine>4‐(m‐chlorophenylcarbamoyloxy)‐2‐butynyltrimethylammonium chloride (McN‐A‐343)>N‐benzyl‐3‐pyrrolidyl acetate methobromide (AHR 602). All effects were abolished by atropine (1·4 × 10−6M).
Each compound was more potent relative to acetylcholine in inhibiting ventricular rate than atrial tension. With the exception of carbachol, the order of potency was the same.
Both AHR 602 and McN‐A‐343 facilitated the release of noradrenaline by SNS and inhibited that by DMPP. The effects were atropine‐resistant and hence non‐muscarinic.
The muscarinic compounds (except AHR 602 and McN‐A‐343) each produce atropine‐sensitive inhibition of noradrenaline release evoked both by SNS and DMPP although it is likely that furtrethonium and pilocarpine have additional non‐muscarinic inhibitory activity against DMPP. The order of potency on both parameters and the potencies relative to acetylcholine were in good agreement with those for inhibition of atrial tension.
The results suggest that similar muscarinic receptors mediate inhibition of atrial tension development, ventricular rate and neuronal noradrenaline release caused by SNS and DMPP.
In terms of the two muscarinic sites known to be present in the superior cervical ganglion, the receptors of the terminal fibres mediating inhibition of noradrenaline release are more likely to correspond to those mediating hyper‐polarization than to those mediating depolarization, for which AHR 602 and McN‐A‐343 show specificity.
Apparent differences between the effects of hyoscine in vivo and in vitro on the responses of chicken oesophagus to nerve stimulation
Authors: BARTLET A. L. 
Published: July 2012

Summary
In chickens anaesthetized with sodium pentobarbitone, stimulation of a vagus nerve produced contractions in the muscles in the pre‐crop oesophagus which were only partly antagonized by hyoscine.
The effect of hyoscine in an isolated preparation of chicken oesophagus responding to nerve stimulation was shown previously to be similar to that now found in the in vivo preparation.
The effects of indomethacin on calcium, sodium, potassium and magnesium fluxes in various tissues of the guinea‐pig
Authors: NORTHOVER B. J. 
Published: July 2012

Summary
Isolated tissues of the guinea‐pig were bathed with Krebs solution at 37° C and subjected to 100 ms pulses of electrical stimulation for 30 min at a frequency of 0·1 or 1·0 Hz. The tissues were then dried, ashed, and the ash analysed for calcium, sodium, potassium and magnesium.
Gastric smooth muscle, cardiac and skeletal muscles and brain all showed a gain of sodium and calcium and a loss of potassium in response to electrical stimulation, but there was no significant change in the magnesium content of any of these tissues.
Indomethacin (0·5 mm) reduced the calcium content of unstimulated gastric smooth muscle and reduced the gain of calcium and sodium in response to electrical stimulation, but slightly increased the net loss of potassium in response to electrical stimulation.
Gastric smooth muscle which had gained calcium as a result of electrical stimulation, gradually lost it again when stimulation ceased. Indomethacin (0·5 mm) hastened the net loss of calcium from previously stimulated muscle.
Indomethacin (0·5 mm) failed to alter the calcium, sodium, potassium and magnesium contents of unstimulated cardiac muscle, skeletal muscle and brain. In these tissues indomethacin (0·5 mm) also failed to prevent the changes in the content of these minerals which occurred in response to electrical stimulation.
A study of clofazimine in the rat
Authors: CURREY H. L. F. , FOWLER P. D. 
Published: July 2012

Summary
Clofazimine, an anti‐mycobacterial agent used in the treatment of leprosy, has been reported to be particularly effective in the treatment of acute erythema nodosum leprosum reactions.
The present experiments were designed to study in the rat this apparent anti‐inflammatory activity.
In doses relatively non‐toxic to the animals clofazimine inhibited both rat adjuvant arthritis and the inflammatory paw swelling following an adjuvant injection.
Clofamizine failed to inhibit both the primary antibody response to sheep erythrocytes and the tuberculin skin response.
It is concluded that clofazimine exhibits definite anti‐inflammatory (but not immunosuppressive) activity, and that it should be tested in patients with rheumatoid arthritis.
Pharmacological actions of a new β‐adrenoceptor agonist, MJ‐9184–1, in anaesthetized cats
Authors: GWEE M. C. E. , NOTT M. W. , RAPER C. , RODGER I. W. 
Published: July 2012

Summary
The effects of (–)‐isoprenaline and the new β‐adrenoceptor agonist, MJ‐9184–1, on the lungs, on the cardiovascular system, and on slow contracting skeletal muscle have been compared in cats under chloralose anaesthesia.
Both amines reduced the increases in airways resistance produced by 5‐HT, depressed incomplete tetanic contractions of the soleus muscle, lowered the blood pressure and produced an increase in heart rate. In comparison with (‐)‐isoprenaline, MJ‐9184–1 had a long duration of action.
The effects of MJ‐9184–1 and (–)‐isoprenaline were antagonized by the β‐adrenoceptor antagonist, propranolol.
MJ‐9184–1 was approximately half as potent as (–)‐isoprenaline in its effects on pulmonary resistance and soleus muscle contractility, and one seventh as potent in producing chronotropic effects in the heart.
These results suggest that MJ‐9184–1 possesses some specificity as a β2 receptor stimulant.
The effect of sodium γ‐hydroxybutyrate on the metabolism of dopamine in the brain
Authors: HUTCHINS D. A. , RAYEVSKY K. S. , SHARMAN D. F. 
Published: July 2012

Summary
Sodium gamma hydroxybutyrate (GHB‐Na), when given to rats and mice, caused a sleep‐like state and a fall in body temperature of about 10° C.
GHB‐Na produced a dose‐dependent increase in the concentration of dopamine (DA) in the brains of mice kept at an environmental temperature of 18–20° C or 30–32° C.
The concentrations of 3,4‐dihydroxyphenylacetic acid (DOPAC) and 4‐hydroxy‐3‐methoxyphenylacetic acid (HVA), the metabolites of DA, were increased in the striatal tissues of rats and mice, after the administration of GHB‐Na. However there was a delay of 60 min before the concentration of HVA increased whereas there appeared to be little delay before the concentration of DOPAC increased.
When GHB‐Na was administered to reserpine‐treated animals, no increase occurred in the concentration of dopamine in the brains of mice or rats, or of DOPAC in the rat brain.
Reserpine did not prevent the induction of the sleep‐like state by GHB‐Na.
The results presented suggest that the effect of GHB‐Na in increasing the concentration of DA requires unimpaired storage mechanisms for the amine.
Effects of some centrally acting drugs on acetylcholine synthesis by rat cerebral cortex slices
Authors: SHARKAWI M. 
Published: July 2012

Summary
Brain cortex slices from rats injected i.p. with urethane (1 g/kg), chloral hydrate (350 mg/kg) or physostigmine (0·75 mg/kg) were examined for acetylcholine (ACh) content, cholinesterase (total enzyme) activity and formation of 14C‐ACh from carbon 14‐uniformly labelled glucose (U‐14C‐d‐glucose) in the presence of 0·01 mm physostigmine.
Slices from rats treated with urethane, chloral hydrate, or physostigmine contained significantly higher concentrations of ACh than slices from untreated animals.
Only slices from physostigmine‐treated rats had a significantly lower cholinesterase activity.
Slices from urethane‐ or chloral hydrate‐treated animals formed significantly less 14C‐ACh than slices from untreated or physostigmine‐treated rats when incubated in 4 mm K+ medium. In an ACh‐releasing medium (31 mm K+) slices from rats treated with urethane or chloral hydrate and slices from untreated rats formed similar amounts of 14C‐ACh.
Slices from rats treated with atropine (25 mg/kg) or pentylenetetrazol (75 mg/kg) had a similar ability to form 14C‐ACh as slices from untreated animals when incubated in either 4 or 31 mm K+ medium.
These findings suggest that the intraneuronal ACh concentration is a limiting factor in the regulation of ACh synthesis.
The mechanism of the facilitatory action of edrophonium in cat skeletal muscle
Authors: BLABER L. C. 
Published: July 2012

Summary
The effects of edrophonium have been observed in the transversely cut tenuissimus muscle of the cat.
Concentrations of edrophonium 10−7M to 10−5M increased the amplitude of the end‐plate potential (e.p.p.) but produced no greater increase in time course than previously observed in curarized muscle.
When the e.p.p. and gross nerve action potential were recorded simultaneously, antidromic discharges were observed in the motor nerve concomitantly with repetitive e.p.ps in the presence of edrophonium.
Edrophonium produced no effect on the input resistance or equilibrium potential of the end‐plate.
The fractional release of transmitter was significantly increased by edrophonium but there was no increase in the quantal release of transmitter in the transversely cut muscle preparation.
In curarized muscle edrophonium also increased the quantal release, the size of the available store of transmitter and the rate of refilling of the available store.
It is concluded that edrophonium facilitates transmission to skeletal muscle by inducing a repetitive antidromic discharge in the nerve, following orthodromic stimulation. The antidromic discharge propagates by axon reflex to other nerve terminals of the same motor unit producing repetitive e.p.ps. It is also suggested that edrophonium antagonizes tubocurarine by acting as a partial agonist at the motor nerve terminal.
Effects of caffeine and isoprenaline on mammalian ventricular muscle
Authors: CLARK ANNE , OLSON CAMILLE B. 
Published: July 2012

Summary
Caffeine, 0·6–20·0 mm, altered the duration of the action potential recorded from kitten papillary muscles; low concentrations shortened and high concentrations prolonged the action potential.
Caffeine, 20 mm, prolonged the action potential by delaying the final phase of repolarization.
Caffeine, 2·0–20·0 mm increased the tension developed and the duration of the isometric contraction.
When large stimulating electrodes were used, all concentrations of caffeine increased the duration of the action potential; this effect was probably due to the interactions of caffeine and released endogenous catecholamines.
Concentrations of caffeine and isoprenaline, which separately caused little change in the duration of the action potential, greatly prolonged the action potential when used together.
The effects of caffeine may be due to an increase in membrane calcium current in addition to an action on intracellular calcium stores.
Behavioural studies of the actions of cocaine, monoamine oxidase inhibitors and iminodibenzyl compounds on central dopamine neurones
Authors: CHRISTIE JANICE E. , CROW T. J. 
Published: July 2012

Summary
Turning behaviour after unilateral lesions of the nigro‐striatal dopamine pathway in rats has been used to compare the actions of cocaine and desipramine on central dopamine‐containing neurones.
Administration of cocaine alone (5–20 mg/kg) resulted in no turning or minimal turning towards the lesioned side; the monoamine oxidase inhibitors nialamide and pargyline administered alone were also ineffective.
After pre‐treatment with nialamide (100 mg/kg) or pargyline (25 mg/kg) cocaine evoked high rates of turning towards the lesioned side.
Desipramine (1–100 mg/kg), either alone or in combination with nialamide did not evoke turning.
Turning evoked by the cocaine‐nialamide combination was abolished by pre‐treatment with α‐methyl‐p‐tyrosine (150 mg/kg).
Pre‐treatment with reserpine (5 mg/kg, 24 h previously) substantially diminished turning evoked by the cocaine‐nialamide combination but potentiated turning resulting from administration of methylamphetamine (5 mg/kg).
Cocaine (20 mg/kg) administered 15 min prior to (+)‐methylamphetamine (5 mg/kg) reduced the turning behaviour in the first hour after administration of the latter drug but prolonged the total duration of the effect.
Some effects of inhibiting endogenous prostaglandin formation on the responses of the cat spleen
Authors: FERREIRA S. H. , MONCADA S. , VANE J. R. 
Published: July 2012

Summary
Cat isolated spleens release prostaglandins into the venous effluent in response to stimuli such as nerve stimulation, noradrenaline and angiotensin II.
The release of prostaglandins is abolished by pre‐treatment of the spleen with indomethacin (0·3–5 μg/ml).
The capsular and vascular responses to the different stimuli are augmented after inhibition of prostaglandin release.
The prevention of prostaglandin release, as well as the augmentation of vascular and capsular responses, are reversible after indomethacin treatment is stopped.
The role of prostaglandins as modulators of the responses to several stimuli is discussed.
Effect of single dose administration of diuretics on the blood sugar of alloxan‐diabetic mice or mice made hyperglycaemic by the acute administration of diazoxide
Authors: FOY J. M. , FURMAN B. L. 
Published: July 2012

Summary
Frusemide produced hyperglycaemia in mice when administered together with diazoxide. The interaction between the drugs in elevating the blood sugar was shown to be additive.
The diuretic, natriuretic and kaliuretic effects of frusemide were very markedly attenuated by diazoxide.
Neither ethacrynic acid nor hydrochlorothiazide exerted any effect upon blood sugar when administered together with diazoxide.
Bilateral nephrectomy completely prevented the hyperglycaemic effect of frusemide in normal mice and in mice treated with diazoxide. Diazoxide itself still produced hyperglycaemia in nephrectomized mice.
Frusemide, ethacrynic acid and diazoxide, but not hydrochlorothiazide, each produced hyperglycaemia in alloxan‐diabetic mice, this being prevented by bilateral nephrectomy.
Further studies of binding of bromosulphthalein sodium by human serum albumin: effects of albumin concentration and buffer composition
Authors: THOMPSON J. M. 
Published: July 2012

Summary
Binding isotherms of equilibrium solution concentration of bromosulphthalein (BSP) determined on the number of moles of BSP bound per mole of human serum albumin (HSA) in 310 ideal milliosmolar pH 7·4, Krebs—Henseleit and Krebs improved mammalian Ringer number 1 buffers at 37° C were determined using continuous diafiltration. The albumin concentration range was from about 10 to 30 g/litre.
The results indicate a competition between HSA polymerization and HSA binding BSP, confirming in more physiological conditions, the findings of Crawford, Jones, Thompson & Wells (1972) with pH 7·4 phosphate buffer.
The results in Krebs—Henseleit buffer were markedly different from those in Krebs mammalian Ringer buffer and it is suggested that the differences in ionic composition influence the HSA conformation and so affect the competition between HSA polymerization and HSA binding BSP.
Concentration of histamine in different parts of the brain and hypophysis of rabbit: effect of treatment with histidine, certain other amino acids and histamine
Authors: ABOU Y. Z. , ADAM H. M. , STEPHEN W. R. G. 
Published: July 2012

Summary
Estimates have been obtained by biological assay of the histamine concentration in different parts of the rabbit brain and hypophysis.
Mean values (ng/g) for the brain were: hypothalamus, 660; central grey matter and medial thalamus, 275; tegmental region of mid‐brain, the hind‐brain and caudate nucleus, 140 to 170; hippocampus and cerebral cortex, 90 to 110; cerebellum (vermis), 60.
The mean value (ng/g) for the anterior lobe of the hypophysis was 650; for the posterior lobe, 400.
In conscious rabbits, intravenous infusion of histidine in the dose range 62 to 1,500 mg/kg, raised significantly (P < 0·01) the concentration of histamine in all regions of the brain examined, the pattern of distribution remaining unchanged. The largest increases occurred in the mid brain (90 to 320%) and in the hypothalamus (50 to 250%); in these areas the higher doses produced higher concentrations. Elsewhere in the brain the concentration rose in response to the lowest dose of histidine, but was not increased when higher doses were given. Concentrations in the anterior lobe of the hypophysis were unaltered.
The infusion of histidine, unlike that of amino acid precursors, of the monoamines, produced no obvious disturbance in the animals.
The rise in brain histamine after dosage with histidine persisted for several hours, depending on the dose; with 500 mg/kg, the rise was virtually unchanged after 16 hours.
Histamine (5 mg/kg by intravenous infusion) raised the concentration of histamine in the hypophysis but not in the brain.
After the infusion of DOPA, α‐methyldopa or 5‐hydroxytryptophan, the histamine concentration rose in the mid‐brain but not in other parts of the brain.
These amino acids, when infused singly with histidine, did not interfere with the histidine‐induced rise of brain histamine.