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Biomedical subjects

E Marley

Publications and source records attributed to E Marley.

At least 37 records · Page 2Linked to original sources
PubMed1976

Some pharmacological effects of p-chlorophenylalanine unrelated to tryptophan hydroxylase inhibition.

1 Experiments were performed on a variety of tissues from different species to establish whether or not the properties of p-chlorophenylalanine methyl ester (PCPA) included a 5-hydroxytryptamine (5-HT)-like action which might explain the soporific action of PCPA in chicks. 2 PCPA, like 5-HT, contracted the rat fundal preparation (as did PCPA base), and in cats enhanced twitch tension of a lower limb flexor reflex, evoked adrenal medullary secretion and attenuated histamine-induced gastric secretion; the effects on the rat fundal strip and the adrenal medulla were prevented by methysergide. 3 Like 5-HT, PCPA elicited bronchoconstriction of guinea-pig lungs, isolated or in vivo; this was not prevented by methysergide but reduced by polyphloretin and by indomethacin. Perfusate collected from the lungs during PCPA-induced bronchoconstriction and applied to superfused isolated tissues contained a substance with prostaglandin-like activity. 4 In contrast, the effect of PCPA on the guinea-pig isolated ileum differed from that of 5-HT, since it relaxed the ileum when contracted by transmural excitation, by acetylcholine, histamine of 5-HT and contracted the ileum on wash-out.

Animals↗
PubMed1975

Some central effects of 5-hydroxytryptamine in young chickens at and below thermoneutrality.

1 Three salts of 5-hydroxytryptamine, the hydrogen maleinate, the oxalate and the creatinine sulphate were infused into the hypothalamus of 10-18 day old chickens at ambient temperatures in and below the thermoneutral range. Body temperature was recorded and behaviour observed. Electrocortigrams were recorded in experiments in which 5-hydroxytryptamine hydrogen maleinate was used. The effects of a monoamine oxidase inhibitor and methysergide on these responses were similarly studied. 2 At thermoneutrality (31 degrees C) all 3 salts produced behavioural sleep. 5-Hydroxytryptamine oxalate had inconsistent effects on body temperature. 5-Hydroxytryptamine creatinine sulphate produced hypothermia at small doses and mild hyperthermia at higher doses. 5-Hydroxytryptamine hydrogen maleinate produced hypothermia at all doses tested; the falls in temperature induced by this salt were intensified in magnitude and duration by monoamine oxidase inhibition unlike the responses to the other 2 salts. 3 At temperatures below thermoneutrality (16 degrees C) all 3 salts produced behavioural sleep and electrocortical sleep was recorded with 5-hydroxytryptamine hydrogen maleinate. All 3 salts produced hypothermia, which was intensified in magnitude and duration by monoamine oxidase inhibition. 4 The hypothermia produced by 5-hydroxytryptamine hydrogen maleinate was prevented by equimolar doses of methysergide. 5 The position of the cannula in the hypothalamus was found to be crucial. 6 The results contrast with those found in the adult fowl. No conclusion is drawn as to the relationships of the actions of these salts when infused compared with the effects of endogenous 5-hydroxytryptamine release.

Animals↗
PubMed1975

Tryptamines and some other substances affecting waking and sleep in fowls.

1 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. 2 Tryptamine and alpha-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 alpha-methyltryptamine into the hypothalamus or mesencephalon of fowl encephale isole preparations. The above effects in intact fowls were reduced or replaced by sleep following administration of noradrenaline or alpha-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. 3 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. 4 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. 5 Dexamphetamine infused into the hypothalamus induced drowsiness or sleep which even reversed arousal elicited by systemically administered dexamphetamine. 6 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.

Animals↗
PubMed1975

Central effects of clonidine 2-(2,6-dichlorophenylamino)-2-imidazoline hydrochloride in fowls.

1 The effects of clonidine infused into the IIIrd cerebral ventricle, the hypothalamus or intravenously were studied on behaviour, electrocortical activity, body, comb and leg temperatures, respiration and carbon dioxide elimination in adult and young fowls (Gallus domesticus). 2 Behavioural and electrocortical slow wave sleep were induced by clonidine infused into IIIrd cerebral ventricle, the hypothalamus or intravenously. Suprisingly, sleep elicited by intravenous clonidine was much longer-lasting than that induced by an identical dose given intraventricularly. 3 Body temperature was lowered by clonidine given intraventricularly or infused into the hypothalamus. Depending on initial comb temperature and ambient temperature, comb temperature was elevated, unaffected or lowered as body temperature fell; temperature of the unfeathered legs also rose as body temperature declined after clonidine. 4 Following clonidine, but before any considerable decline of body temperature, tachypnoea and wing abduction developed; during recovery of body temperature, the wings were lowered and applied closely to the trunk and the feathers partly erected. 5 CO2 elimination fell more swiftly than body temperature following intrahypothalamic clonidine in young chicks; initial recovery developed sooner than that of body temperature, but eventual recovery was delayed compared to that for body temperature. The effects of clonidine were much more marked in young chicks studied at an ambient temperature below thermoneutrality as compared to thermoneutrality. 6 The soporific effects of clonidine were attenuated by intraventricular phentolamine; its hypothermic effects were prevented by phenoxybenzamine and prevented or attenuated by phentolamine. Intraventricular atropine, haloperidol, methysergide and propranolol were ineffective. 7 Larger doses of intraventricular phentolamine elicited shivering, tachypnoea and wing abduction; body temperature was elevated, to the extent even of lethal hyperthermia. Intraventricular atropine also elevated body temperature. 8 Clonidine infused intravenously, intraventricularly or into the hypothalamus, replaced the behavioural and electrocortical arousal evoked with dexamphetamine, by sleep associated with slow wave electrocortical activity.

Animals↗
PubMed1975

Effects of noradrenaline infused into the chick hypothalamus on thermoregulation below thermoneutrality.

1. Hypothermia induced by infusion of noradrenaline into the hypothalamus of 2-3 week old chicks, within their thermoneutral range, was considerably potentiated by lowering ambient temperature. 2. Noradrenaline-induced hypothermia was associated with reduced carbon dioxide elimination and reduced blood lactate concentrations whereas leg temperature, electromyographic activity, plasma NEFA and plasma glucose concentrations were increased. 3. Mechanisms postulated to explain the phenomenon are inhibitory and facilitatory effects of noradrenaline on some, but not all, heat production and heat loss mechanisms. Increased electromyographic activity after intrahypothalamic noradrenaline is assumed to be due to lack of effect of noradrenaline on spinal thermosensitive centres; increased plasma NEFA concentration may be due to inhibition of NEFA utilization.

Animals↗
PubMed1974

Effects of nicotine given into the brain of fowls.

1 The effects of nicotine, given into the IIIrd ventricle of adult conscious fowls (Gallus domesticus) or infused into various brain regions of conscious young chicks, were tested on behaviour, electrocortical activity, respiratory rate and body temperature. Its effects given intraventricularly or applied externally to the brain-stem of anaesthetized fowls were also examined.2 After intraventricular nicotine, fowls squatted for 3 to 5 min with eyes closed, electrocortical activity resembling that during sleep but with superimposed spike activity. Following this, fowls reawakened and tachypnoea developed, together with partial abduction of the wings from the trunk, the back becoming horizontal and the tail flexed. These effects were prevented by pempidine.3 Intraventricular nicotine suppressed or, less commonly, reduced operant key-pecking, an effect unrelated linearly to dose.4 Intraventricular nicotine given to fowls anaesthetized with chloralose produced brief apnoea, followed by increased amplitude of respiratory excursion for about 5 minutes. Respiratory rate accelerated slightly but tachypnoea did not develop. Nicotine applied directly to the ventral brain-stem increased respiratory amplitude in three out of seven fowls.5 In anaesthetized fowls, intraventricular nicotine raised blood pressure for 2 to 3 min, an effect prolonged up to 70 min by acute bilateral vagotomy, whereas pressor effects of intravenous nicotine were extended merely two to three fold. Dividing the spinal cord at C2 prevented pressor effects of intraventricular nicotine; those of intravenous nicotine were unaltered.6 In young chicks, nicotine infused into the diencephalon, telencephalon and myelencephalon induced effects similar to those observed immediately after intraventricular nicotine, i.e. chicks squatted with closed eyes but recovered within 3 to 5 minutes. Simultaneously, electrocortical activity changed from an alert to the sleep pattern, usually with superimposed ;spike' activity. Tachypnoea and associated postural changes did not develop. Pempidine prevented the behavioural and electrocortical effects of nicotine.

Aging↗
PubMed1974

Effects of cholinomimetic agents given into the brain of fowls.

1 Effects of cholinomimetic agents, given into the IIIrd ventricle of adult fowls (Gallus domesticus) or infused into the hypothalamus of young chicks, were tested on behaviour, respiratory rate and body temperature.2 Carbachol evoked behavioural and electrocortical arousal but lacked postural and respiratory effects. Contrariwise, pilocarpine increased respiratory rate and induced postural changes, i.e. abduction of the wings, but lacked other behavioural effects and did not alter electrocortical activity. Benzoylcholine induced tachypnoea, postural changes and brief electrocortical arousal. Acetylcholine was ineffective unless given with physostigmine, when electrocortical arousal, postural changes and tachypnoea developed. Methacholine induced tachypnoea and postural changes.3 Effects of carbachol and pilocarpine were prevented by hyoscine and those of benzoylcholine by pempidine; hyoscine and pempidine were required together to prevent the effects of methacholine and to attenuate those of acetylcholine with physostigmine.

Acetylcholine↗