bluuebunny/crossref_metadata_2025_split huggingface dataset:
TRYPTAMINES AND SOME OTHER SUBSTANCES AFFECTING WAKING AND SLEEP IN FOWLS
Authors: MARLEY E. , NISTICO G. 
Published: July 2012

Adult fowls (Gallus domesticus) with cannulae chronically implanted in the IIIrd cerebral ventricle and various other sites of the brain, received infusions or injections of tryptamines and catecholamines into the brain; effects of and interactions between these substances on behaviour, electrocortical activity and body temperature were studied. Reserpine‐induced arousal, was investigated in young and adult fowls.
Tryptamine and α‐methyltryptamine, given intraventricularly or into the hypothalamus of intact fowls evoked behavioural and bilateral electrocortical arousal, postural changes, elevation of body temperature and tachypnoea; behavioural and bilateral electrocortical arousal were obtained with infusions into the mesencephalon. Ipsilateral electrocortical arousal only, resulted from infusion of α‐methyltryptamine into the hypothalamus or mesencephalon of fowl encéphale isolé preparations. The above effects in intact fowls were reduced or replaced by sleep following administration of noradrenaline or α‐methylnoradrenaline into the IIIrd ventricle or hypothalamus. Pretreatment of intact fowls with an amine oxidase inhibitor surprisingly attenuated or reversed the excitant effects of intraventricular tryptamine.
5‐Hydroxytryptamine (hydrogen maleinate, creatinine sulphate or oxalate) given intraventricularly or infused into the hypothalamus, elevated body temperature; tachypnoea and postural changes developed at some stage during the elevation of body temperature. Sleep also was induced, although with the oxalate this was succeeded by marked arousal.
Behavioural and electrocortical sleep induced by 5‐hydroxytryptamine infused into the hypothalamus were replaced by arousal on infusing tryptamine into the hypothalamus, and vice versa.
Dexamphetamine infused into the hypothalamus induced drowsiness or sleep which even reversed arousal elicited by systemically administered dexamphetamine.
Reserpine‐induced arousal was achieved in young and adult fowls pretreated with mebanazine; this arousal was attenuated or replaced by sleep following intraventricular noradrenaline or dopamine but not by 5‐hydroxytryptamine nor by noradrenaline or dopamine applied to the hypothalamus. Prenylamine also induced arousal following pretreatment of chicks with mebanazine.
SOME PHARMACOLOGICAL PROPERTIES OF THE CREMASTER MUSCLE OF THE GUINEA‐PIG
Authors: NINOMIYA J.G. 
Published: July 2012

The tension developed in the guinea‐pig cremaster was recorded during spontaneous activity and electrical stimulation. Spontaneous rhythmic contraction was observed in many preparations, particularly in the tip of the cremaster. These contractions were very slow, lasting about 20 s and occurring at about 2 min intervals, but different preparations varied greatly. Twitches produced by electrical stimulation were similar to those in other skeletal muscles, being reduced by (+)‐tubocurarine and abolished by tetrodotoxin.
A slow contraction could be initiated by electrical stimulation using a pulse longer than 10 ms in spontaneously active preparations and in some quiescent preparations. Spontaneous and evoked slow contractions were not suppressed by tetrodotoxin, but were selectively abolished by verapamil. Histamine increased the basal tension and generated spontaneous contractions in quiescent preparations. Hypertonic solutions also had excitatory effects.
Contractions produced by acetylcholine and carbachol were blocked by atropine. Those produced by adrenaline and noradrenaline were stronger than those due to histamine, acetylcholine and carbachol and were abolished by an α‐adrenoceptor blocking agent, phentolamine. In the preparations in which the slow contraction was not observed, histamine, acetylcholine or adrenaline had very little effect.
It is suggested that the cremaster muscle consists of striated muscle together with some smooth muscle having properties similar to that in the vas deferens.
THE EFFECTS OF TETRAPHENYLBORON ON NEUROMUSCULAR TRANSMISSION IN THE FROG
Authors: MARSHALL I.G. , PARSONS R.L. 
Published: July 2012

The effects of tetraphenylboron (TPB) were studied on the frog sciatic nerve‐sartorius muscle preparation.
TPB (0.01–1 mM) blocked indirectly elicited twitches of the preparation.
TPB (0.01–0.1 mM) produced no depolarization but lowered membrane resistance. TPB increased miniature endplate potential (m.e.p.p.) frequency, the rate of rise of the endplate potential (e.p.p.), and slowed the rate of rise and rate of fall of the muscle action potential.
In Mg2+ solutions the quantal content of e.p.ps was initially increased by TPB (0.01 mM). This was followed by a decrease of e.p.p. and m.e.p.p. amplitudes, accompanied by a lack of e.p.p. failures.
Larger concentrations of TPB (0.1 mM) produced an increase in e.p.p. amplitude followed by the sudden abolition of e.p.ps. This effect was associated with abolition of the nerve terminal spike.
TPB (0.1 mM) exhibited no postjunctional blocking action.
The results indicate that TPB acts prejunctionally, initially causing an increased release of acetylcholine. Subsequently, transmitter output is reduced by a reduction of quantal size.
EFFECTS OF NARCOTIC ANALGESIC DRUGS ON THE CYCLIC ADENOSINE 3′, 5′‐MONOPHOSPHATE‐ADENYLATE CYCLASE SYSTEM IN RAT BRAIN
Authors: CLOUET DORIS H. , GOLD G.J. , IWATSUBO K. 
Published: July 2012

The concentrations of cyclic adenosine 3′, 5′‐monophosphate (cyclic AMP), measured in discrete brain areas removed from rats killed by microwave irradiation, rose transiently in most areas after the administration of morphine. The most pronounced changes, however, were found 2 h after doses of either 10 or 60 mg/kg morphine when cyclic AMP levels declined significantly in the hypothalamus, medulla and cerebellum. In morphine‐tolerant rat brains there were no decreases in cyclic AMP levels.
Basal adenylate cyclase activity in crude nerve‐ending fractions from discrete areas of rat brain was unaffected by the addition of active analgesic agonists, antagonists or inactive isomers to the assay medium in vitro, except for a nonspecific inhibition at drug concentrations of 1 mM.
The acute administration of morphine or levorphanol, but not dextrorphan produced transient increases in basal cyclase activity of crude nerve‐ending preparations from midbrain and striatum. In morphine‐tolerant rats, these changes in basal adenylate cyclase activity were no longer seen.
RELATIVE POTENCY OF BOMBESIN‐LIKE PEPTIDES
Authors: BROCCARDO M. , ERSPAMER G. FALCONIERI , MELCHIORRI P. , NEGRI L. , DE CASTIGLIONE R. 
Published: July 2012

The pharmacological activity of two natural bombesin‐like peptides, alytesin and litorin, and 25 related synthetic peptides has been compared to that of bombesin.
The minimum length of the amino acid chain required for the first appearance of bombesin‐like effects was represented by the C‐terminal heptapeptide, and the minimum length for maximal effects by the C‐terminal nonapeptide. The latter possessed approximately the same activity as bombesin and may be considered a good substitute.
Both the tryptophan and histidine residues seemed to be essential for bombesin‐like activity.
The C‐terminal octapeptide was less active than either bombesin or the C‐terminal nonapeptide and its action was more rapid in onset and less sustained.
Litorin apparently has an intermediate position between bombesin octapeptide and bombesin nonapeptide in the speed and duration of its effects. The relationship between structure and activity is discussed.
EFFECTS OF ANTICONVULSANT AND CONVULSANT DRUGS ON THE ATPASE ACTIVITIES OF SYNAPTOSOMES AND THEIR COMPONENTS
Authors: GILBERT J.C. , WYLLIE M.G. 
Published: July 2012

The effects of anticonvulsants, and other drugs on the Na+, K+‐adenosine triphosphatase (ATPase) (ouabain‐sensitive) and Mg++‐ATPase activities of synaptosomes and their components have been determined.
The Mg++‐ATPase activity of synaptosomes was not affected by the drugs but the Na+, K+‐ATPase activity was inhibited by phenytoin (diphenylhydantoin), ethosuximide and diazepam.
Fractions containing mainly membranes, mitochondria or synaptic vesicles, were prepared from synaptosomes by osmotic shock and subsequent density gradient centrifugation. Inhibition of Na+, K+‐ATPase activity by phenytoin, ethosuximide and diazepam was apparent only in the membrane fraction.
The fraction containing synaptic vesicles exhibited pronounced Mg++‐ATPase but no Na+, K+‐ATPase activity. In contrast to the enzymes of the membranes and mitochondria, the Mg++‐ATPase of the vesicles was inhibited by diazepam and all of the anticonvulsants tested.
IMPAIRMENT IN THE HEPATIC CLEARANCE OF [35S]‐BROMOSULPHO‐PHTHALEIN IN PARACETAMOL‐INTOXICATED RATS
Authors: BUTTAR H.S. 
Published: July 2012

The overall functional capacity of the liver was evaluated using [35S]‐bromosulphophthalein (BSP, 100 mg/kg, i.v.) in biliary fistulated adult rats pretreated orally with different doses of paracetamol (APAP) for varying time intervals.
The maximal hepatic damage occurred between 12–18 h after single doses of APAP (0.5 or 1 g/kg); hepatic excretory function returned to control levels by 48–72 hours.
Administration of either 0.5 or 1 g/kg APAP 18 h before BSP caused a dose‐dependent inhibition of the choleretic effect of BSP and of the 60 min cumulative excretion of the dye, but conversely, produced a significant increase in the liver and plasma concentrations of 35S.
Following acute (0.25 g/kg), or subacute (0.5 g/kg, twice daily for 7 days) treatment with APAP, the total excretion of 35S in bile and the retention of 35S in the liver or plasma remained essentially the same as that for the controls.
In rats given single doses of 1 g/kg APAP, the hepatic uptake of the dye was significantly increased during the early stages of intoxication, while the opposite effect was observed at late periods.
The bile flow appeared to be inversely related to the excretion of unchanged BSP, and directly related to the excretion of the major BSP conjugate in bile.
The hepatic clearance of BSP was more rapid in rats treated subacutely with 0.5 or 1 g/kg APAP, than in those treated acutely with equal doses, suggesting that the intensity of APAP‐induced hepatotoxicity became less severe after the repeated administration of this drug.
It is concluded that the hepatic uptake, metabolism and excretion of BSP are reversibly impaired following APAP‐induced liver injury.
BRAIN CONCENTRATIONS OF BIOGENIC AMINE METABOLITES IN ACUTELY TREATED AND ETHANOL‐DEPENDENT RATS
Authors: KAROUM F. , WYATT R.J. , MAJCHROWICZ E. 
Published: July 2012

Mass fragmentography was used to measure whole brain concentrations of some of the major metabolites of tyramine, octopamine, dopamine and noradrenaline in acutely treated and in ethanoldependent rats.
Treatments with ethanol, either acutely or chronically, failed to alter significantly brain concentration of p‐hydroxyphenylacetic and p‐hydroxymandelic acid (metabolites derived from tyramine and octopamine respectively). The effect on catecholamine metabolites was marked and therefore suggests that ethanol is selective in its effect on central metabolism of biogenic amines.
Acute ethanol treatment significantly increased brain concentration of homovanillic acid (HVA), 3,4‐dihydroxyphenylacetic acid (DOPAC) and 3‐methoxy‐4‐hydroxyphenylglycol (MHPG). Vanilmandelic acid (VMA) was not affected. All four metabolites (HVA, DOPAC, MHPG and VMA) were increased in the brains of rats rendered dependent on ethanol while still intoxicated (blood ethanol levels above 200 mg/dl). In ethanol‐dependent rats undergoing ethanol withdrawal syndrome (no ethanol present in blood), the brain concentrations of HVA and DOPAC were normal while those of MHPG and VMA continued to be elevated.
From the decline in the concentrations of HVA and DOPAC after 50 mg pargyline/kg in control rats and rats acutely treated with ethanol, it was concluded that ethanol has no effect on the transport of phenolic acids across the blood brain barrier.
No reversal in the metabolism of catecholamines from an oxidative to a reductive pathway, analogous to that produced by ethanol in the periphery, could be established in the brain.
The increase in catecholamine metabolite concentrations after ethanol treatment, either acute or chronic, were interpreted as manifestations of increases catecholamine turnover.
NATURE OF HISTAMINE RECEPTORS IN THE EMETIC CHEMORECEPTOR TRIGGER ZONE
Authors: BHARGAVA K.P. , DIXIT K.S. , PALIT G. 
Published: July 2012

The protective effects of the intracerebroventricular (i.c.v.) administration of the H1‐receptor antagonist, mepyramine and the H2‐receptor antagonists, burimamide and metiamide on centrally induced histamine‐emesis were studied in unanaesthetized dogs.
The PD50 values of intraventricular mepyramine, burimamide and metiamide against the 100% emetic dose of histamine (3.0 mg i.c.v.) were found to be approximately 200 μg, 20 μg and 20 μg respectively.
Although burimamide (i.c.v. or i.v.) afforded protection against histamine‐induced emesis, there was no protection against intravenous apomorphine‐or oral copper sulphate‐induced emesis.
The results suggest that both H1‐ and H2‐histamine receptors in the emetic chemoreceptor trigger zone of the area postrema are concerned in histamine‐induced emesis.
BLOCKADE BY BURIMAMIDE OF THE RESTORATIVE EFFECT OF HISTAMINE IN TETRODOTOXIN‐TREATED HEART PREPARATIONS
Authors: LEDDA F. , MANTELLI LAURA , MUGELLI A. 
Published: July 2012

In isolated heart preparations in which fast sodium channels were blocked by tetrodotoxin (2–4 × 10−5 m), excitability was restored by histamine (6 × 10−6 M to 10−5 m).
This effect was antagonized by EDTA (2 × 10−6 m), D600 compound (0.5 μg/ml) and the H2‐receptor antagonist, burimamide (2 × 10−4 m).
INVESTIGATIONS TO CHARACTERIZE A NEW ANTI‐ARRHYTHMIC DRUG, ORG 6001, INCLUDING A SIMPLE TEST FOR CALCIUM ANTAGONISM
Authors: SALAKO L.A. , WILLIAMS E.M. VAUGHAN , WITTIG J.H. 
Published: July 2012

The compound Org 6001 (3α‐amino‐2β‐hydroxy‐5α‐androstan‐17‐one hydrochloride) was found in recent experiments to exhibit anti‐arrhythmic activity. Evidence is presented in this paper concerning its mode of action.
Org 6001 was 1.8 times more potent than procaine as a local anaesthetic on desheathed frog nerve.
Org 6001 had no effect on the resting potential of isolated cardiac muscle of rabbit, but greatly reduced the maximum rate of depolarization (MRD). The action potential duration (APD) was marginally prolonged in atrial and ventricular muscle.
Org 6001 preferentially shortened APD in that part of the Purkinje system in which APD is normally longer than elsewhere, so that APD became more uniform throughout the ventricular conducting system.
Org 6001 did not block chronotropic responses to isoprenaline in atrial muscle.
Org 6001 had only a small negative inotropic effect in atrial muscle, and did not reduce the positive inotropic effect of raised calcium concentrations.
The effect of Org 6001 on MRD was reduced by lowering the external K+ concentration.
It is concluded that Org 6001 is an anti‐arrhythmic drug of the first class (local anaesthetic type), and within this group is of a sub‐class more closely related to lignocaine than to quinidine.
EFFECT OF PROSTAGLANDIN E1 ON NEUROMUSCULAR TRANSMISSION IN THE RAT
Authors: GRIPENBERG J. , JANSSON S.‐E. , HEINÄNEN V. , HEINONEN E. , HYVÄRINEN J. , TOLPPANEN E.‐M. 
Published: July 2012

The effect of prostaglandin E1 on neuromuscular transmission in the phrenic nerve‐diaphragm muscle preparation of the rat was studied with intra‐ and extracellular recording techniques.
Prostaglandin E1, in concentrations from 10 nm, induced intermittent failures in the generation of the end‐plate potential in response to repeated indirect stimulation.
Failures appeared abruptly, the end‐plate potential behaving in an all‐or‐nothing fashion. The effect occurred only at 36–38°C when the nerve was stimulated at 30–80 Hz and was reversible upon washing with drug‐free solution.
Since miniature end‐plate potentials were not affected, such failures must be attributed to a presynaptic action of prostaglandin E1.
Extracellular recording suggested that prostaglandin E1 prevented the action potential from reaching the nerve terminal.
MAZINDOL ANOREXIA IS MEDIATED BY ACTIVATION OF DOPAMINERGIC MECHANISMS
Authors: KRUK Z.L. , ZARRINDAST M.R. 
Published: July 2012

Anorexia in rats following injections of mazindol (0.1–8 mg/kg i.p.) could be antagonized by pretreatment with a dopamine receptor blocker (pimozide) but not by pretreatment with an α‐adrenoceptor blocker (phenoxybenzamine), a β‐adrenoceptor blocker ((‐)‐propranolol), or a 5‐hydroxytryptamine receptor blocker (methergoline).
In rats with a unilateral lesion in the substantia nigra made by stereotaxic injection of 6‐hydroxydopamine, mazindol caused a dose‐dependent turning towards the lesioned side, indicating an indirect mechanism of action. This effect could be antagonized by pretreatment with a dopamine receptor blocker.
In rats pretreated with reserpine and α‐methyl‐p‐tyrosine, mazindol did not have any motor stimulant action.
In vitro studies with synaptosomes prepared from rat brain, indicated that mazindol blocks uptake and causes release of dopamine.
It is concluded that the anorectic action of mazindol is mediated by a dopaminergic mechanism.
A COMPARISON OF AFFINITY CONSTANTS FOR MUSCARINE‐SENSITIVE ACETYLCHOLINE RECEPTORS IN GUINEA‐PIG ATRIAL PACEMAKER CELLS AT 29°C AND IN ILEUM AT 29°C AND 37°C
Authors: BARLOW R.B. , BERRY K.J. , GLENTON P.A.M. , NIKOLAOU N.M. , SOH K.S. 
Published: July 2012

The affinity of 17 compounds for muscarine‐sensitive acetylcholine receptors in atrial pacemaker cells and ileum of the guinea‐pig has been measured at 29°C in Ringer‐Locke solution. Measurements were also made at 37°C with 7 of them.
Some of the compounds had much higher affinity for the receptors in the ileum than for those in the atria. For the most selective compound, 4‐dipnenylacetoxy‐N‐methylpiperidine methiodide, the difference was approximately 20‐fold. The receptors in the atria are therefore different in structure from those in the ileum.
The effects of temperature on affinity are not the same for all the compounds tested, indicating different enthalpies and entropies of adsorption and accounting for some of the difficulty experienced in predicting the affinity of new compounds.
CALCIUM DEPLETION OF SYNAPTOSOMES AFTER MORPHINE TREATMENT
Authors: CARDENAS H.L. , ROSS D.H. 
Published: July 2012

It was confirmed that morphine administration in vivo produced a selective decrease in the calcium content of synaptosomal fractions prepared from rat cerebral cortices. This effect was prevented by naloxone.
After morphine or naloxone, there were no changes in the sodium, potassium and magnesium contents of any of the seven subcellular fractions tested.
Since the selective calcium loss was found to occur from fractions similar to those reported to exhibit opiate receptor binding, it is concluded that calcium may play a role in the action of narcotic agonist drugs.
MYOCARDIAL DIGOXIN UPTAKE: DISSOCIATION BETWEEN DIGITALIS‐INDUCED INOTROPISM AND MYOCARDIAL LOSS OF POTASSIUM
Authors: STEINESS EVA , VALENTIN N. 
Published: July 2012

The time course of myocardial uptake of digoxin, of increase in inotropic effect and of changes in myocardial potassium content were studied following a single intravenous dose of digoxin.
Nineteen dogs with intact circulation were investigated by the use of a biopsy technique which allowed samplings before and 10, 30, 60, and 90 min after administration of digoxin.
The myocardial concentration of digoxin was 196 × 10−9 mol/kg 10 min after administration of digoxin. Uptake continued at a slower rate, maximum concentration being 293 × 10−9 mol/kg at 60 minutes.
The inotropic effect increased parallel with the uptake of digoxin; 10 min after digoxin, contractility was 127% of the control value and this increased to 139% at 90 minutes.
Myocardial potassium content was slightly increased 10 min after digoxin, suggesting an initial stimulation of membrane Na+‐K+ ATPase. A subsequent significant fall in the myocardial potassium content probably reflects ATPase inhibition.
The temporal dissociation between the early onset of the positive inotropic effect and the delayed inhibition of membrane Na+‐K+ ATPase indicates that inotropism of digitalis glycosides is not mediated by the same binding site as that responsible for inhibition of Na+‐K+ ATPase.
THE EFFECTS OF RESERPINE AND 6‐HYDROXYDOPAMINE ON THE CONCENTRATIONS OF SOME ARYLALKYLAMINES IN RAT BRAIN
Authors: BOULTON A.A. , JUORIO A.V. , PHILIPS S.R. , WU P.H. 
Published: July 2012

The concentrations of p‐ and m‐tyramine were measured in the caudate nucleus of the rat brain following subcutaneous injection of reserpine or intraventricular injection of 6‐hydroxydopamine. β‐Phenylethylamine was analysed in the hypothalamus after reserpine.
Endogenous levels of p‐tyramine and m‐tyramine in the caudate nucleus, and β‐phenylethylamine in the hypothalamus were 8.02, 2.25 and 2.52 ng/g respectively.
Tyramine concentrations were reduced to less than 20% of control values one day after a reserpine injection of 1 or 10 mg/kg. A single dose of reserpine (0.4 mg/kg) significantly decreased the content of both tyramines in the caudate nucleus. The effects became apparent as early as 45 min after drug administration and persisted for at least 6 h in the case of p‐tyramine and for at least 19 days in the case of m‐tyramine.
The hypothalamic content of β‐phenylethylamine was unaffected by reserpine.
Ten days after an intraventricular injection of 6‐hydroxydopamine (250 μg), p‐ and m‐tyramine concentrations in the caudate nucleus were significantly below control levels.
The results suggest that p‐ and m‐tyramine may be stored by an intraneuronal reserpine‐sensitive storage mechanism. Alternatively, the tyramines may replace some of the catecholamines from their storage granules and then be released as false transmitters by the nervous impulse. The observed changes in tyramine levels might also reflect the fact that these amines may be metabolically related to another amine which is stored in reserpine‐sensitive granules.
THE DISTRIBUTION AND METABOLISM OF ARACHIDONIC ACID IN RABBIT PLATELETS DURING AGGREGATION AND ITS MODIFICATION BY DRUGS
Authors: BLACKWELL G.J. , DUNCOMBE W.G. , FLOWER R.J. , PARSONS M.F. , VANE J.R. 
Published: July 2012

1Gas chromatographic and radio‐isotope labelling techniques have been used to establish the origin of the arachidonic acid used by the platelet cyclo‐oxygenase for the synthesis of pro‐aggregatory prostaglandin endoperoxide derivatives.2Measurements of total platelet arachidonate content indicated that more than 95% is esterified in the phosphatide fraction of the cells.3During aggregation by collagen or thrombin as much as 80% of the total platelet arachidonate may be liberated and transformed by the platelet enzymes into hydroxyacids and other more polar compounds.4The phosphatidylethanolamine, phosphatidylcholine and phosphatidylinositol fractions are major sources of the arachidonate thus used.5Indomethacin, which prevents platelet aggregation by inhibiting the cyclo‐oxygenase, did not affect this release of arachidonate from the phosphatides but did prevent the transformation of arachidonate to endoperoxide derivatives.6Mepacrine, a drug which possesses weak anti‐phospholipase activity in platelets, also prevents aggregation by collagen or thrombin, but seems to do so by preventing substrate release from the phosphatide fraction.7It is suggested that phospholipase A2 plays a key role in the initial events during platelet aggregation induced by collagen.