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Biomedical subjects

J D Stephenson

Publications and source records attributed to J D Stephenson.

At least 73 records · Page 4Linked to original sources

Effects of spiperone on self-stimulation and other activities of the Mongolian gerbil.

1 Self-stimulation to lever pressing and capacitance probe touching was obtained in Mongolian gerbils (Meriones unguiculatus) from electrode placements within the medial forebrain bundle. 2 Lever pressing was more sensitive to the decremental effects of a central depressant, pentobarbitone, than capacitance probe touching, suggesting its greater responsiveness to disturbances of motor function. 3 Spiperone (0.005 to 0.05 mg/kg) attenuated capacitance probe touching and lever pressing equally, a finding explained by action on either reward pathways or on the ability to initiate responding. 4 This same dose range of spiperone (0.005 to 0.05 mg/kg) attenuated locomotor activity, whether spontaneous or evoked by non-contingent electrical stimulation, and produced catalepsy. 5 The spiperone-induced attentuation of self-stimulation was not necessarily a result of its action on dopaminergic reward pathways since the effects could equally well be explained by a failure to initiate responding.

Animals↗

Some effects of intravenous prostaglandin E, and endotoxin in young chickens.

1 The effects of intravenous prostaglandin E1 and endotoxin were studied in young chickens (11-17 days old). 2 At a thermoneutral ambient temperature (31 degrees C), intravenous prostaglandin E1, produced behavioural and electrocortical sleep, increased oxygen consumption and, after an initial fall, elevated body temperature. Below thermoneutrality (16 degrees C), the initial hypothermic effect was more marked and oxygen consumption was lowered. 3 The soporific actions of prostaglandin E1 were sufficient to counteract dexamphetamine-induced behavioural and electrocortical arousal and vocalization. 4 Intravenous injection of the O-somatic antigen of Shigella dysenteriae evoked, after a latent period, long lasting hyperthermia. This indicates that in young chicks the blood brain barrier is probably permeable to endotoxins.

Animals↗

Some effects of prostaglandins E1 and E2 and of endotoxin injected into the hypothalamus of young chicks: dissociation between endotoxin fever and the effects of prostaglandins.

Prostaglandins E1 and E2 elevated body temperature of young chicks when injected into the hypothalamus at thermoneutrality (31 degrees C). In contrast, they lowered body temperature when so injected below thermoneutrality (16degreesC): the relation of the fall in body temperature to increased heat loss and decreased heat production was examined. 2 The above effects below thermoneutrality were potentiated by pretreatment with inhibitors of prostaglandin synthetase and possible reasons for this potentation are given. 3 The O-somatic antigen of Shigella dysenteriae consistently evoked hyperthermia when injected into the hypothalamus, irrespective of whether the chicks were within or below thermoneutrality. 4 Pretreatment with prostaglandin synthetase inhibitors failed to prevent the onset of endotoxin fever; however, duration of the fever, induced by intrahypothalamic injection of the O-somatic antigen of Shigella dysenteriae was reduced. 5 The intrahypothalamic injection, belwo thermoneutrality of prostaglandins E1, E2, noradrenaline, 5-hydroxytryptamine or carbachol reversed endotoxin fever, inducing even substantial falls in body temperature. 6 While the results cast some doubts on the role of prostaglandins of the E series as mediators of endotoxin fever in chicks, they cannot be eliminated as mediators until the significance of the reduction in duration of the pyrexic response by indomethacin and 5,8,11,14-eicosatetraynoic acid, and the degree of synthesis inhibition attained, are known.

5,8,11,14-Eicosatetraynoic Acid↗

Body temperature regulation and thermoneutrality in rats.

Various concepts of thermoneutrality were considered for a proposed study of the role of hypothalamic amines in temperature regulation of rats. The classic definition, the ambient temperature over which metabolic rate is minimum and constant, gave a range of approximately 28 to 32 degrees C. However, within this temperature range rats were inactive, the inactivity apparently representing a behavioural response to heat stress and itself responsible for the reduced metabolic rate; certain thermoregulatory effectors were also activated to increase heat loss. Therefore an alternative range, 18.0 +/- 1.9 (mean +/- S.D.) to 28.1 +/- 1.0 degrees C, was defined in which rats displayed normal activity, behavioural thermoregulations being absent.

Animals↗

Behavioural, electrocortical and body temperature effects of cholera toxin.

In young chicks intrahypothalamic infusion of cholera toxin produced a dramatic and dose-dependent increase in motor activity. Similar effects were also obtained in adult fowls after injection of cholera toxin into the third cerebral ventricle, the hypothalamus or the paleostriatum augmentatum. Electrocortical changes consisted of a slight desynchronization during the hypermotor activity and were preceded, when the highest intraventricular doses were used, by a short period of slower frequency and higher amplitude potentials. Intraventricular and intrahypothalamic but not intrastriatal injection of cholera toxin produced a typical biphasic hyperthermic response.

Animals↗

Picrotoxin convulsions and GABA metabolism after injection of anticonvulsants in chicks.

Two clinically effective anticonvulsants, phenobarbitone and diazepam, protected 5-day old chicks against picrotoxin convulsions without reducing brain GABA-transaminase activity or raising brain GABA concentration. Ethanolamine-O-sulphate and amino-oxyacetic acid, in doses which inhibited GABA-transminase by at least 63% and approximately doubled brain GABA concentration, did not significantly affect the ED50 for picrotoxin convulsions. The ED50 for picrotoxin convulsions was significantly raised by di-n-propylacetate (800 mg/kg) which inhibited GABA transaminase activity by 6% and elevated brain GABA concentration by 26%.

4-Aminobutyrate Transaminase↗

The real bladder electromyogram.

The nature of bladder electrical activity was investigated in anaesthetised cats and 1 baboon. A time-locked muscle response to sacral ventral root stimulation was most clearly detected within a 10-40 Hz frequency band, the response preceding the rise in intravesical pressure. During reflex voiding only activity in the 10-40 Hz band was consistently related to reflex voiding and to the small contractions leading up to voiding. It is concluded that only a very limited part of the wide band electrical activity recorded from the bladder can be considered genuine electromyogram and that the 10-40 Hz frequency band probably excludes the worst of the artefact. Possible sources of artefact and their relation to changes in intravesical pressure are presented in Table I.

Animals↗

Enhancement of picrotoxin convulsions in chicks and mice by the prior intraperitoneal injection of hypertonic GABA or mannitol.

Effects of i.p. injection of hypertonic solutions of GABA and mannitol on convulsant activity and latency to reduced or enhanced depending on whether picrotoxin was given i.p. or given i.v. or s.c. The principal cause of these changes appeared to be altered rates of absorption of picrotoxin. There was no evidence that cerebral dehydration afforded protection against picrotoxin.

Aminobutyrates↗

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↗